CCBIO Seminars

Planned spring dates 2026:

January 29, 2026 – Katrin Kleinmanns

Speaker: Katrin Kleimanns, CCBIO researcher in the Bjørge and Mc Cormack groups.
Title: Translational PDX models as a platform to advance therapy in ovarian cancer
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Line Bjørge

February 19, 2026 – Donald Gullberg

Speaker: Professor Donald Gullberg, CCBIO PI and the Department of Biomedicine, University of Bergen
Title: Novel integrin models to study tissue and tumor fibrosis
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

March 26, 2026 – Hussain Abbas

CCBIO/cMYC seminar
Speaker: Hussain Abbas, MD Anderson Cancer Center, USA
Title: TBA
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

April 23, 2026 – Richard Dillon

CCBIO/cMYC seminar
Speaker: Richard Dillon, Clinical Senior Lecturer in Cancer Genetics in the Department of Medical & Molecular Genetics, School of Basic & Medical Biosciences, at King's College London and Consultant Haematologist at Guy’s Hospital, London, UK
Title: TBA
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

May 28, 2026 – Christer Betsholtz

Speaker: Christer Betsholtz, Uppsala University and Karolinska Institute, Sweden
Title: TBA
Time: 14:30
Place: Auditorium 4, BBB
Chairpersons: Henriette Aksnes, Department of Biomedicine, and Lars Muhl, CCBIO

June 11, 2026

Speaker: TBA
Title: TBA
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: TBA

Fall dates 2025:

August 28, 2025

Speaker: Professor Dr. Jochen Hess, University Hospital Heidelberg, Germany
Title: Sex-related disparities in the pathogenesis and therapy of head and neck cancer 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Dana Costea

September 25, 2025

Speaker: Maria Ulvmar, Senior Lecturer/Associate Professor at the Department of Medical Biochemistry and Microbiology; Infection and Immunity, Uppsala University, Sweden.
Title: Decoding Tumor-Draining Lymph Nodes: New Insights into Tumor Immunity and Biomarker Discovery 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

November 13, 2025

Speaker: Vincenzo Ciminale, Istituto Oncologico Veneto, Padova, Italy
Title:  "STRESS FOR SUCCESS”: UNLOCKING VENETOCLAX SENSITIVITY IN T-ALL THROUGH THE mTORC1–ISR–BMF AXIS 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

November 27, 2025

Speaker: Simon Joosse, University Medical Center Hamburg-Eppendorf (UKE), Germany
Title: Precision in a drop: Liquid Biopsy for personalized oncology
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Karl-Henning Kalland

December 11, 2025

Speaker: Luiza Mihaela Ghila, Researcher at the Department of Clinical Science, Medical Faculty, University of Bergen
Title: Cell plasticity in bladder urothelium
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

Spring dates 2025:

12.06.25, Franziska Görtler

Speaker: Franziska Görtler, Computional Biology Unit, UiB/Department of Oncology and Medical Physics, Haukeland University Hospital
Title: Digital deconvolution of bulk gene expression data
Time: 14:30
Place: The auditorium in Armauer Hansens Hus
Chairperson: Vladan Milosevic

Abstract: The talk will focus on the challenges in determining the cell type populations in bulk RNASeq probes like closely related cell types, small cell type proportions, hidden background contributions as well as cell type-specific regulations due to disease. We will present our three deconvolution algorithms DTD, ADTD and HIDE, providing machine learning solutions. We will verify our algorithms both on simulated data as well as on bulk RNASeq data from the Cancer Genome Atlas. 

Finally, we will introduce Deconomix – a comprehensive toolbox for the cell-type deconvolution of bulk transcriptomics data based on our algorithms, available as a Python package and as a standalone graphical user interface for easy and user-friendly access.

Franziska Görtler, PhD, is since 2023 a researcher at the Department of Oncology and Medical Physics, Haukeland University Hospital, with Prof. O. Straume's and Prof. J. Lorens' groups. Her research mainly focuses on algorithm development for immune cell deconvolution in tissues. She was 2024 awarded FRIPRO funding for early career researchers from the Research Council of Norway. Through loss-function learning optimisation, she investigates the dissection of the cellular distributions and the cell-type specific regulation patterns in spatial transcriptomics data.

She is the responsible bioinformatician in a randomised phase II clinical trial study on melanoma, focused on biomarker detection, machine learning algorithm development, and single-cell and spatial transcriptomics data. She did her postdoc in the Computational Biology Unit, Department of Biological Sciences, UiB, and her PhD in Bioinformatics at the University of Regensburg, Germany, on Loss-Function Learning for Digital Tissue Deconvolution. 

22.05.25, Marcus Buschbeck

Speaker: Marcus Buschbeck, Josep Carreras Leukaemia Research Institute, Barcelona, Spain.
Title: Mining the chromatin regulatory space for drug targets in myeloid malignancies
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell, Mathias Ziegler

Abstract: Epigenetic information is written in chromatin. But how exactly do epigenetic mechanisms operate at the molecular level? How does the environment influence these processes? How does nuclear metabolism impact chromatin structure and the cell’s epigenetic memory?

These are the questions we address in the lab. We combine basic research and applied research. In our basic research, we like to dissect molecular mechanisms of chromatin regulation and evaluate if this knowledge has an application in cancer. We have a long-standing interest in histone variants with macrodomains. In our more applied projects, we screen for novel drug targets for blood cancers and to understand their molecular mode of action. I will divide my talk into two halves and first present results showing how we identified CBP as sensitizer for azacytidine-based therapy. In the second part, I will present novel data that establish a histone variant as novel first-of-its-kind drug target in acute myeloid leukemia.

Keywords: histone variants, drug targets, combinatorial therapies, leukemia, 3D genome, chromatin regulation, myelodysplastic syndromes.

More information at: https://buschbecklab.org

24.04.25, Stein-Erik Gullaksen

Speaker: Stein-Erik Gullaksen, CCBIO/UiB
Title: Deep single cell immune and signaling profiling hours after starting treatment predict response to treatment in patients with Chronic myeloid leukemia
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

Abstract: Chronic myeloid leukemia (CML) is a myeloproliferative stem cell disorder driven by a single molecular abnormality that arises from a reciprocal translocation fusing the Breakpoint Cluster Region (BCR) gene Abelson (ABL) gene. The resulting BCR::ABL1 protein is a constitutively activated tyrosine kinase that drives uncontrolled growth of myeloid cells in the bone marrow. CML is effectively treated with small molecule BCR::ABL1 inhibitors, and up to 20% of the patients reach treatment-free remission after 5-7 years. Most patients require lifelong daily TKI treatment, with treatment side effects reducing quality of life at significant socioeconomic costs.

Using mass cytometry, we profiled single cells from longitudinal peripheral blood samples from patients CML enrolled in two international clinical trials. We found that treatment with tyrosine kinase inhibitors (TKIs) inhibited intracellular signaling in patients as early as one hour after the first dose. Each TKI had a unique signaling signature reflecting its kinase specificity profile. Using machine learning algorithms, we were able to predict the response to treatment after one year based on these early measurements. 

We envision that early single cell immune and signaling profiling may in the future within days rather than months be used to for treatment optimization, securing optimal response and limiting toxicity.

Biosketch: Stein-Erik Gullaksen holds an M.S. in Nanotechnology from the University of Bergen (UiB) and defended his PhD at the UiB in 2018, focusing on high dimensional single cell analysis of blood samples using mass cytometry. This work was performed under the supervision of Professor Bjørn Tore Gjertsen. Gullaksen continues this work in his current postdoctoral position at the Medical Department, Helse Bergen HF, and is associated with the K.G. Jebsen Centre for Myeloid Blood Cancer (C-MYC) and the Centre of Cancer Biomarkers (CCBIO). 

27.03.25, Göran Karlsson

Speaker: Göran Karlsson from Lund University, Sweden
Title: Exposing the stem cells of CML using single-cell genomics
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Stein-Erik Gullaksen

Since 2014, Göran Karlsson is an Associate Professor in Molecular Hematology at Lund Stem Cell Center with a focus on stem cells in hematopoiesis and disease. He established the single-cell core facility at Lund University, and consequently has a strong research focus on hematopoietic- and cancer stem cell heterogeneity, areas where single-cell methods can provide groundbreaking insights.

Here, Göran will present how single-cell analysis of chronic myeloid leukemia patients reveals coexistence of CD35+CD26- healthy stem cells and CD26+CD35- CML stem cells, and how the ratio between these impacts TKI response.

20.02.25, Eirik Malinen

Speaker: Eirik Malinen, associate professor in biophysics and medical physics at the University of Oslo / Oslo University Hospital.
Title: Proton therapy - bridging cancer medicine and physics
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell 

Eirik Malinen is Head of the Department of Radiation Biology, Institute for Cancer Research, Oslo University Hospital. He has a PhD in radiation biophysics holds an adjunct professorship at the Department of Physics, University of Oslo. His research has mostly been on radiotherapy of cancer, either with a clinical or pre-clinical focus. He has been a member of several national committees evaluating and planning the introduction of proton therapy in Norway, and has initiated pre-clinical and translational research efforts in this field.

Abstract: The talk with briefly explain the principles behind proton therapy of cancer and address the need to bridge physics and cancer medicine to improve this type of treatment. We will present the possibilities for pre-clinical research (cells, animals) in a proton therapy beamline like the ones at the centers in Oslo and Bergen. Recent results from experiments on combining proton therapy with immunotherapy and comparing normal tissue responses, including cytokine profiles, for protons and X-rays will be presented. Finally, the talk will include some plans from translational studies under planning for soft tissue sarcoma.

30.01.25, Austin James Rayford

Speaker: Austin James Rayford, University of Bergen
Title: A conserved culprit: Targeting dual AXL-mediated mechanisms of immunotherapy resistance in lung cancer patients
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

Abstract: Lung cancer is a leading cause of cancer-related morbidity and mortality worldwide, and is also responsible for most cancer-related deaths in Norway. Non-small cell lung cancer (NSCLC) accounts for around 80% of lung cancer cases. The introduction of targeted therapies and immune checkpoint inhibitors (ICIs) has revolutionized the treatment of NSCLC in recent years, particularly due to the remarkable clinical efficacy of ICIs observed in a subset of patients. However, innate and acquired resistance to ICIs remains a barrier to durable clinical benefit, and the complex molecular mechanisms mediating resistance are still poorly understood. 

AXL, a receptor tyrosine kinase, is upregulated by normal and malignant cells in many tissues during chronic inflammation and wound-healing, and is also a central negative feedback regulator of innate immunity. Although many studies have implicated AXL in both tumor-intrinsic and immune-mediated mechanisms of ICI resistance, current data on AXL expression in tumor and immune cells in clinical NSCLC specimens is lacking, while its prognostic and predictive role in the context of ICI treatment and the ability of AXL-inhibiting drugs to potentiate ICI efficacy remains elusive. 

In this work, we first showed that AXL expression in tumor cells was associated with aggressive phenotypic features, an immunosuppressive tumor microenvironment and poor survival in a real-world cohort of NSCLC patients treated with ICI monotherapy. We then demonstrated that the addition of bemcentinib, a selective small-molecule AXL inhibitor, to ICI therapy in a multi-national clinical trial of advanced pretreated NSCLC patients resulted in improved clinical benefit compared to standard-of-care treatments, particularly within subgroups with AXL-positive and STK11-inactivated tumors expected to have the worst prognosis. In murine models, bemcentinib sensitized STK11-mutant NSCLC tumors to ICI treatment via AXL-targeting in dendritic cells, suggesting an additional tumor-cell extrinsic mechanism that supports the efficacy of bemcentinib-ICI treatment observed in patients with STK11-loss. Taken together, these findings provide a strong scientific rationale for current and future clinical trials incorporating AXL inhibitors with ICI therapy to improve NSCLC patient outcomes.

Austin Rayford received his BSc. in Chemical Biology in 2015 from the University of California, Berkeley. After working for 2 years at Roche Molecular Systems he moved to Bergen and completed his MSc. in Biomedical Sciences in Jim Lorens’ group. Austin began working for BerGenBio in 2019 in the Exploratory Biomarkers team and completed an industrial PhD project under Jim Lorens co-funded by BerGenBio and the Norwegian Research Council. As a current Researcher in the Lorens Lab and CCBIO, he continues to explore how AXL inhibitors can potentiate the efficacy of standard-of-care therapies in advanced NSCLC and melanoma patients.

12.12.24, Frances Balkwill

Speaker: Professor Frances Balkwill OBE, FMedSci, Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, UK.
Title: Cells are Us – experiences in science communication and public engagement
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

Fran Balkwill is Professor of Cancer Biology at Barts Cancer Institute, Queen Mary University of London, and Deputy Centre Lead in the Centre for Tumour Microenvironment. She is especially interested in translating knowledge of cancer biology into new biological treatments for cancer. Much of her work focuses on the tumour microenvironment of ovarian cancer. After publishing a multi-level profile of the human ovarian cancer microenvironment, her lab has developed a platform of new mouse ovarian cancer models as well as human multi-cellular tissue culture models. They are now using these to research biological therapies that may prevent relapse and increase patient survival.  

Abstract: Since her first postdoctoral position, Fran Balkwill has had a parallel career in public engagement and informal science learning; this will be the focus of her talk. Fran will describe her experience of science journalism and writing science books for children. She will also explain how she founded and directs an informal biomedical science learning centre, Centre of the Cell which was the first science centre be located within biomedical research laboratories. Centre of the Cell seeks to positively impact on educational, career and health choices of young people and families with its digital interactive STEM Pod, workshops and shows in Neuron Pod, outreach, mentoring and volunteering opportunities. There have been more than 254,000 participants in Centre of the Cell activities since opening in September 2009. 

28.11.24, Janine Erler

Speaker: Professor Janine Erler, leader of the Erler Lab, a cancer biology research group at the Biotechnology Research and Innovation Centre (BRIC) at the University of Copenhagen.
Title: Targeting the metastatic niche
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

Abstract: "Metastasis is responsible for over 90% of cancer patient deaths, and is a process strongly regulated by the extracellular matrix (ECM). Studies have shown that the ECM can promote or restrict cancer progression, and that targeting cell-ECM interactions at the primary tumour can disrupt tumour growth and invasion as well as improve drug response. 
 
We developed a method called In Situ Decellularisation of Tissues (ISDoT) to isolate structurally intact 3D ECM organ scaffolds from healthy and tumour-bearing tissue. This has enabled us to study the metastatic niche in great detail, and map ECM proteins to the metastatic niche for further characterisation. We have used the information gained to target cell-ECM interactions at the metastatic niche, which has disrupted metastatic growth in each instance. We then developed the ISDoT method to use the ECM scaffolds as a bioreactor to culture cells, and have been able to model metastatic colonisation and outgrowth. 
 
Our studies show that interfering with cell-ECM interactions can indeed prevent metastatic growth. We aim to translate these findings into the clinic to benefit cancer patients.In addition, we run a precision medicine program for patients with metastatic cancer to provide optimal treatment to patients."

About Janine Erler: Janine Erler is a Professor and Group Leader at BRIC, University of Copenhagen, and CEO of NEUmiRNA Therapeutics. She graduated as BSc with Honours in Molecular Genetics in Biotechnology from the University of Sussex (UK) in 2000 and was awarded a PhD in Molecular Pharmacology from the University of Manchester (UK) in 2003 for her research on hypoxia-regulated resistance of cancer cells to chemotherapy. Between 2004 and 2008, Janine was a postdoctoral training fellow at Stanford University (USA), where she started working on hypoxia-regulated metastasis. She then started her own independent research group in 2008 at the Institute of Cancer Research in London (UK). Janine moved her lab to BRIC (University of Copenhagen, DK) in 2012 and became a tenured full Professor in 2016. She has received numerous awards for her research, and has filed two patents and started two companies. Her research is focused on how the tumour microenvironment drives metastasis. In particular, Janine has pioneered research into extracellular matrix remodelling during cancer progression. 

In 2022, Janine took on the role of CEO of NEUmiRNA Therapeutics, a startup developing disease-modifying RNA therapies for neurological disorders. Since then, she has secured €2M in investment and €3M in soft funding including a prestigious Michael J Fox Foundation grant and a Eurostars consortium grant. Janine signed a Term Sheet in July with 3 leading European investors for a Series A round of €30M.

Janine’s focus, both at BRIC and at NEUmiRNA, is on interdisciplinary translational research.

31.10.24, Karen Rosnes Gissum

Speaker: Karen Rosnes Gissum, UiB
Title: Navigating Ovarian Cancer Complexities: A Shared Decision-Making Approach
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

Karen Rosnes Gissum is a trained oncology nurse with clinical experience in the Gynecologic Cancer Section at the Women's Clinic (KK). She holds a master’s degree in Evidence-Based Practice and completed her doctorate at the Centre for Cancer Biomarkers (CCBIO) and the Department of Clinical Science (K2) at the University of Bergen (UiB). She currently serves as the head of the Cancer Center for Education and Rehabilitation in the Cancer Department at Haukeland University Hospital.

Abstract: Background: Ovarian cancer presents significant challenges due to its severity and complexity. Despite advancements in precision oncology, prognosis remains poor, and patients experience a difficult journey marked by side effects that burden the healthcare system. Beyond medical expertise, patients require compassionate communication and holistic care from healthcare providers. While extensive research exists on ovarian cancer as a disease, there is limited information on the illness experience and perspectives of patients and healthcare professionals.

Aims: This project aimed to explore how patients and healthcare professionals perceive and respond to the illness trajectory of ovarian cancer.

Methods: Using phenomenological methodology and a qualitative design, we conducted five focus group discussions with a patient group (n=4), nine individual interviews with gynecologists (n=9), and five focus groups with nurses in gynecological oncology (n=26).

Results: Patients experience a profound disruption, confronting identity loss and estrangement from their bodies, often struggling to articulate these challenges and seeking supportive relationships with healthcare providers. Gynecologists and nurses view ovarian cancer as a severe and devastating disease. Nurses aim to provide holistic care, while gynecologists focus on disease treatment and technological solutions. However, healthcare professionals’ understanding of the patient illness experience remains limited, constrained by emotional challenges and systemic time pressures that hinder empathy and connection.

Conclusion and Implications: This project reveals the complexity of managing ovarian cancer from both patient and provider perspectives. Phenomenological insights underscore the need for holistic, patient-centered care that acknowledges the emotional and physical needs of ovarian cancer patients beyond medical interventions.

26.09.24, Marit Valla

Speaker: Marit Valla, Associate professor in pathology at the Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, NTNU, and consultant pathologist at St. Olavs Hospital.
Title: Artificial intelligence: A revolution within medical image analysis
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Agnete Engelsen

Abstract: In this talk, Valla will mainly focus on the use of artificial intelligence (AI) in pathology. She will present research results within digital pathology and AI analysis in breast and lung cancer, and show examples of AI-based image analysis in other fields of medicine. 

Marit Valla leads the research group Artificial intelligence and digital pathology in cancer (AICAN) which studies the use of artificial intelligence in the interpretation of histopathological slides from cancer. AICAN is a cross disciplinary research group involving NTNU, St. Olavs hospital, Levanger hospital and SINTEF. They use artificial intelligence in the interpretation of histopathological slides from cancer. The group's goal is to establish methods able to predict biological properties and prognosis in breast and lung cancer. They use established biobanks from NTNU/St. Olavs hospital, and collect tissue from collaborating partners nationally and abroad.

29.08.24, Mari Kyllesø Halle

Speaker: Mari Kyllesø Halle, UiB
Title: Decoding the Landscape of Cancer Vulnerabilities in high-risk Cervical Cancer
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Stein-Erik Gullaksen

Short bio: Mari Kyllesø Halle is a molecular biologist with the Bergen Gynecological Cancer Research Group (CCBIO). She has recently initiated a four-year project funded by the Norwegian Cancer Society aiming to decode the landscape of vulnerabilities in high-risk cervical cancer. By utilizing CRISPR-Cas12 dependency and drug sensitivity screens, followed by in vitro and in vivo drug testing, she seeks to identify new treatments for high-risk cervical cancer patients. Mari has extensive experience in biomarker detection and multi-omics analysis within uterine cancers.

Abstract: Following funding of a four-year research project (Norwegian Cancer Society) focusing on rare histologies we are fine-mapping rare cervical cancer (CC) tumors alongside corresponding relapse biopsies by assembling all genomic, transcriptomic, radiomic, molecular, and clinicopathological patient data collected since 2001. To increase power of detecting targetable alterations in rare subgroups, we teamed up with Prof. Santin from Yale University (Connecticut, US) who collected and sequenced 65 NETs, including 10 NETs from our cohort, identifying 100 common oncogenic drivers recently published in PNAS. We will perform preclinical targeted drug testing towards these drivers at Yale. In parallel, we will establish our own organoid library from all consenting CC patients admitted to Haukeland University Hospital (HUH) during the project period, perform CRISPR-Cas12 dependency screens and design drug sensitivity panels based on identified drivers. Subsequently, we are utilizing the extensively characterised local (UiB) CC patient cohort (approaching 650 patients) to identify subtype-specific clinically relevant response markers. 

Firstly, we have started investigating targets for antibody drug conjugates (ADCs), which represent a new group of cancer drugs providing promising response rates across multiple cancer types. 525 primary and 194 metastatic cervical cancer lesions were investigated for membrane expression of the ADC targets TF, TROP2 and NECTIN4 in relation to clinicopathological data and patient outcome. 
TF, TROP2, and NECTIN4 showed tumor specific expression and were overexpressed (3+) in 29%, 37% and 4% and highly expressed (≥2+) in 48%, 68% and 12% of the tumors, respectively. TROP2 negative expression associated with poor outcome (p=0.02). High TF and NECTIN4 was predominantly observed in squamous tumors (p<0.001) of low-grade histology (p<0.042) and squamous- or adenosquamous- histology (p<0.001). High TROP2 expression predominated within tumors with vascular space invasion (p=0.009) and squamous-, adenosquamous- or undifferentiated- histology (p<0.001). High TF and TROP2 expression were maintained also within the metastatic lesions. 

Conclusions so far: TF, TROP2 and NECTIN4 are highly expressed in cervical cancer. High expression levels are maintained within metastatic and recurrent lesions. Clinical trials evaluating the safety and efficacy of ADCs are highly relevant in cervical cancer.  

20.06.24, Synnøve Yndestad 

Speaker: Synnøve Yndestad, Department of Clinical Science, University of Bergen
Title: Homology Repair Deficiency in Breast Cancer; Lessons from the  PETREMAC trial
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Carina Strell

Abstract: Inactivating mutations in BRCA1/2 disrupts the cells ability to repair double strand breaks by Homologous Recombination Repair (HRR), and tumors without HRR capacity are commonly refered to as beeing Homology Repair Deficient (HRD). HRD causes replication stress and genomic instabilitiy and tumors with HRD therefore have a characeristic genomic scar.

By targeting the repair of single strand breaks by inhibiting PARP, we can induce synthetic letahlity and cell death in cells with HRD. The PARP inhibitor olaparib was approved by the FDA in january 2018 for breast cancer patients with germline BRCA-mutated HER2-negative metastatic breast cancer previously treated with chemotherapy either in the neoadjuvant, adjuvant, or metastatic setting. Olaparib has fewer side effects and is better tolerated than chemotherapy, and replacing chemotherapy with olaparib may spare patients from severe side effects.

Germline BRCA-mutations is not the only route to a HRD tumor. Germline mutations in other HRR genes such as PALB2, somatic mutations in HRR genes as well as epigenetic alterations can cause inactivation of HRR genes leading to HRD. The majority of patients suffering from breast cancer with the characterstic HRD genomic scar, does not have a germline BRCA-mutation. This indicates that more patients could benefit from olaparib treatment, and there is a need to identify the exact mechanism that rendes the tumor sensitive to PARP inhibition. 

Triple-Negative Breast Cancer (TNBC) is an aggressive subtype of breast cancer with poor prognosis that had few treatment options besides chemotherapy before the recent introduction of immunotherapy. TNBC has a high degree of genomic instability and frequently show the genomic signatures associated with HRD.

The PETREMAC trial was a multicenter phase II trial headed from Bergen that included treatment naïve stage II/III breast cancer patients. The patients were stratified to eight different neoadjuvant treatment regimens based on ER, PGR and HER2 expression as well as TP53 mutation status. The TNBC patients were given 10 weeks olaparib monotherapy treatment regardless of germline BRCA1/2 status. Only a minority of theese was found to have germline HRR mutations, but still 56,3% responded to olaparib monotherapy. 
We have explored defects in the HRR pathway in both TNBC and across the other breast cancer subtypes in PETREMAC to pinpoint alterations beyond germline mutations that may predict response to olaparib. We found alterations in a limited number of genes, fulfilling a strict definition of HRR genes to correlate strongly to loss of RAD51 foci, a functional test of HRD. We found that the main driver of HRD in breast cancer across subtypes was not due to germline or somatic mutations, but inactivation of HRR through BRCA1 promoter methylation.

30.05.24, Antonio Curti - cancelled due to illness

Speaker: Antonio Curti, University of Bologna, Italy
Title: Driver mutations and immune microenvironment in acute myeloid leukemia (AML)
Time: 14:30
Place: Auditorium 4, BBB
Chairperson:  Bjørn Tore Gjertsen

Abstract: Acute myeloid leukemia (AML) is a heterogeneous clonal disease deriving from a rare population of bone marrow leukemic stem cells. Although new and potent drugs have recently entered the clinical stage, the 5-year patient overall survival is largely unsatisfactory, reaching 30% and dropping to 5-10% in the elderly. Therefore, there is an urgent and unmet need for effective new treatment modalities for AML. In the last years, cancer immunotherapy is gaining much interest due to its unique characteristics, such as the absence of conventional drug resistance mechanisms and low grade of toxicity. In AML, the immunotherapy field is evolving and expanding. However, despite a strong rationale, clinical results have not been satisfactory, and several questions need to be answered for a full exploitation of immune interventions in AML. Among them, the immunological effects of intrinsic driver AML gene mutations on the immune microenvironment and their relevance for immunotherapy are still poorly investigated. Based on these premises, the aim of the talk is to move from the current state of art of immunotherapy in AML and discuss recent biological findings, which strongly indicate the specificity of bone marrow immune microenvironment as a critical issue for an effective biology-driven development of immunotherapies in AML. In that, the contribution of cell intrinsic driver mutations, such as FLT3 and TP53, in dictating the adaptation and changes in immune microenvironment, especially at the metabolic level, will be discussed by showing unpublished results of the group. 

25.04.24, Ingvild Sandøy

Speaker: Ingvild Sandøy, BCEPS
Title: The Bergen Centre for Ethics and Priority Setting in Health
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Roger Strand

Abstract: Resource restrictions in health care are inevitable, and all countries need to ration which health services are funded. If explicit mechanisms are not put in place, new technologies and services such as new vaccines and treatments often end up primarily benefiting those with more resources. Traditional economic evaluation methods of interventions focus on overall health effects and do not consider impacts on then distribution of health and income. There is also a dearth of data on the equity impact of interventions as randomized controlled trials also tend to focus on overall effects. Existing ethical frameworks for priority setting emphasise either efficiency or fairness, and do not integrate the two aspects. 

BCEPS, which was awarded status as a Centre of Excellence from 2023 by the Research Council of Norway, aims to refine ethical frameworks, conduct primary research and improve models to guide fair priority setting. BCEPS is organised around four work streams: 1. Innovative Methods to evaluate the impact of interventions on both health and income. 2. A “Rationing Lab” to determine the impact of alternative ethical frameworks on population health and income. 3. Equity Impact Studies using analytic epidemiologic designs to evaluate health interventions. 4. Core Analytics for Disease Control Priorities. In this presentation, Ingvild Fossgard Sandøy, the Deputy Director of BCEPS, will present some of the plans for the new centre.

05.04.24, CCBIO Special Career Seminar: From startup to pharmaceutical industry

Speakers: Gro Gausdal, PhD, CEO, Bjørgvin Therapeutics Group AS; Camille Claudius, MD, HD, Head of Medical Affairs, Astellas Nordics; and Ann Theres Poblenz, PhD, Medical Affairs Therapy Area Lead, Oncology, Astellas Nordics.
Title: From startup to pharmaceutical industry
Time: 11:30
Place: Auditorium B302, Sentralblokka 3rd floor
Chairperson: Bjørn Tore Gjertsen

Program:

• Introduction: "Career Opportunities in biotech and startups", by Gro Gausdal, PhD, CEO, Bjørgvin Therapeutics Group AS. Gro has more than 10 years experience as a scientific researcher and director at a small biotech and is now taking the step forward as CEO in a new startup. How prepared will you be for industry career with a PhD in Medical Cell Biology? And why take the chance to go for a start up?
   
• "Career Opportunities in the Pharmaceutical Industry", by Camille Claudius and Ann Theres Poblenz.
  Camille Claudius, MD, HD, Head of Medical Affairs, Astellas Nordics: Camille is a medical doctor who has done research in gynaecology and neurobiology amongst others. In 2002 she joined the pharmaceutical industry, having worked in many roles in both global, national and regional positions in clinical development, medical affairs and clinical trial operations. Before joining Astellas as the Head of Medical Affairs, she was the Country Medical Director at Amgen. Prior to that, she spent ~15 years in the headquarters of Novo Nordisk Global as an International Medical Director of different areas in Global development.  She is a board member of several board in Life Science.
  Ann Theres Poblenz, PhD, Medical Affairs Therapy Area Lead, Oncology, Astellas Nordics: Ann Theres completed her PhD thesis on apoptosis in CNS before transitioning to research in breast, and prostate cancer (with focus on bone metastases), and multiple melanoma at MD Anderson Cancer Center.  In 2005, she entered the pharmaceutical industry. Prior to her current role at Astellas, she served as the Country Medical Lead for Oncology at MSD in Denmark. Before that, she worked as a Medical Science Liaison in the United States and later held positions as a Medical Affairs Strategy Lead and Country Medical Affairs Director at Merck/MSD in the United States, focusing on pembrolizumab in hematology, women’s cancer and melanoma, as well as CINV.

21.03.24, Mika Kontro

Speaker: Mika Kontro, MD, PhD is an adjunct professor and a consultant in clinical hematology at the Helsinki University Hospital Comprehensive Cancer Center. 
Title: Functional Screening for Precision Medicine Approaches in Acute Myeloid Leukemia
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

Mika Kontro, MD, PhD is an adjunct professor and a consultant in clinical hematology at the Helsinki University Hospital Comprehensive Cancer Center. Mika Kontro earned his PhD thesis, entitled “Individualizing therapy for acute leukemia”, in 2017.
He currently works as K. Albin Johannson Cancer Research Fellow (Finnish Cancer Institute) and as a group leader in FIMM. He has a strong background in running clinical trials and was selected at 2017 for European Hematology Association Clinical Research Training program (CRTH). Mika Kontro currently chairs the Finnish AML group and is a board member of the Nordic AML Group. Currently he leads a prospective multi-center AML trial VenEx utilizing ex-vivo drug sensitivity testing for individualized patient care.

Abstract: Dr. Mika Kontro will discuss the methods for personalizing AML therapies using functional screening. He will provide an overview of the current data implementation and share insights from ongoing prospective trials employing functional screening. Furthermore, Dr. Kontro will focus on the VenEx trial, which utilizes ex vivo drug sensitivity testing to identify AML patients who can benefit from the azacitidine-venetoclax regimen.

22.02.24, Diane Bielenberg

Speaker: Diane Bielenberg, Assistant Professor, Harvard Medical School, Boston Children's Hospital, Boston , Massachusetts, USA.
Title: Neuropilin-2 is Immune Suppressive During Early Stages of Carcinogenesis 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Dana Costea  

25.01.24, Vibeke Fosse

Speaker: Vibeke Fosse, CCBIO, MS in veterinary companion animal oncology and veterinary surgeon, and currently a PhD candidate in the McCormack and Bjørge groups.
Title: Comparative oncology:  a valuable model for cancer immunotherapy research 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Emmet McCormack

Vibeke Fosse, MS in veterinary companion animal oncology and veterinary surgeon, and currently a PhD candidate in the McCormack and Bjørge groups. Her project is on the development of targeted fluorescence image-guided surgery, with a focus on using clinically relevant animal models for translation. In particular, she is developing a comparative oncology approach, using pets with cancer as models for development of therapies for human disease.

Abstract: The field of cancer immunotherapy seeks to modulate the immune system to recognise and kill tumour cells. Manipulation of the immune system holds significant promise to create durable responses and improve outcomes in cancer patients. The recent advances in immunotherapeutics for human patients have stimulated an increased interest in veterinary oncology as a powerful tool in cancer immunotherapy research, acting as an important link between mouse models and human clinical studies. The strategy of using veterinary cancer patients as a model for human disease is often referred to as «comparative oncology». Naturally occurring cancers in companion dogs and humans share many features including histological appearance, tumour genetics, biological behaviour, and response to conventional treatment. In addition, pets are exposed to the same environmental factors as their owners, and dogs have a similarly high incidence of cancer as people. Thus, comparative oncology presents an opportunity to advance the understanding of cancer biology, prevention, and treatment, which will benefit dogs as well as humans. However, one of the challenges in comparative oncology is the lack of well-established investigational tools.

Our research group is currently developing novel cell-based immunotherapeutic options for dogs with cancer, with the overall goal of translating the treatments to both adult and paediatric cancer patients.  The novelty of this approach means that there is a lack of species-specific reagents, necessitating molecular cloning of dog-specific immunotargets, which is performed in collaboration with the group of Dr. Sébastien Wälchli at the Translational Research unit at Oslo Universitetssykehus. In this seminar, I will introduce the concept of comparative oncology and the promise this model holds for advancing cancer treatments for humans. 

26.01.23, Bjørn Tore Gjertsen

Bjørn Tore Gjertsen, CCBIO PI, Professor of Hematology at the Department of Clinical Science at the University of Bergen, Research Chief and Consultant Hematologist at Helse Bergen Health Trust.
Title: Early response evaluation by single cell signaling profiling in myeloid leukemia
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Erling Høivik  

Abstract: Aberrant pro-survival signaling is a hallmark of cancer cells, but the response to chemotherapy is poorly understood. We investigate the initial signaling response to standard induction chemotherapy in acute myeloid leukemia (AML) patients, using multi-dimensional mass cytometry. Through supervised and unsupervised machine learning approaches, we find that reduction of extracellular-signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) phosphorylation in the myeloid cell compartment 24h post-chemotherapy is a significant predictor of patient 5-year overall survival. Validation by RNA sequencing and proteomics show induction of MAPK targets in patients with high phospho-ERK1/2 24h post-chemotherapy. Single cell signaling profiling seems to be a valuable tool for early response evaluation in AML. We compare this response to chemotherapy with targeted kinase inhibitor therapy in chronic myeloid leukemia and discuss the potential of functional signaling analyses in precision oncology diagnostics.

References:

1. Gausdal G, Gjertsen BT, McCormack E, et al. Abolition of stress-induced protein synthesis sensitizes leukemia cells to anthracycline-induced death. Blood. 2008;111(5):2866-2877. doi:10.1182/blood-2007-07-103242
2. Gullaksen SE, Skavland J, Gavasso S, et al. Single cell immune profiling by mass cytometry of newly diagnosed chronic phase chronic myeloid leukemia treated with nilotinib. Haematologica. 2017;102(8):1361-1367. doi:10.3324/haematol.2017.167080
3. Tislevoll BS, Hellesøy M, Fagerholt OHE, et al. Early response evaluation by single cell signaling profiling in acute myeloid leukemia. Nat Commun. 2023;14(1):115. Published 2023 Jan 7. doi:10.1038/s41467-022-35624-4  

23.02.23, Lucy Yates – CANCELLED due to illness.   

23.03.23, Michael Rogers

CCBIO Special Seminar with Michael Rogers, Harvard Medical School and the Vascular Biology Program, Boston Children's Hospital
Title: “Neuro-immune communication in endometriosis, a novel therapeutic target?” 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Agnete Engelsen

Abstract: Endometriosis is a painful and debilitating inflammatory disease that affects approximately 10% of reproductive-age women.  Treatment options are currently limited to NSAIDs, hormones, and surgery.  For ~30% of patients, none of these options are effective and for many, symptom relief is only temporary.  Because neuroimmune communication plays a role in several inflammatory conditions, we sought evidence for a role for neuroimmune communication in endometriosis-associated pain and lesion growth.
To that end, we leveraged our mouse model of endometriosis-associated pain.  We found that: 

• Mouse and human lesions are highly innervated by peptidergic nociceptors.  In lesion-bearing mice, dorsal root ganglia (DRGs) showed activation of peptidergic nociceptors.  
• Calcium imaging of mouse DRG neurons showed that mouse endometriosis lesions directly activate nociceptors.  Lesion-secreted VEGF and PLGF induce neuropeptide release by cultured DRG neurons.
• Targeted ablation of TRPV1+ nociceptors by genetic (TRPV1-cre/DTA) or chemical (RTX) means reduced not only mechanical and spontaneous pain, but also lesion size, suggesting that neuropeptide release contributes to lesion maintenance and/or growth.
• Blocking TRPV1+ nociceptor signaling reduced neuropeptide release in vitro and mechanical and spontaneous pain, and lesion size in mice.
• RTX-treatment reduced F4/80+Ly6C+ cells both in the peritoneal cavity (PerC) and lesions.  In co-culture, CGRP stimulated mouse PerC macrophages to release soluble factors that stimulate endometriosis epithelial cell growth.  CGRP also impaired macrophage efferocytosis.  Depleting resident macrophages with clodronate reduced endometriosis lesion size.  
• Blocking CGRP-RAMP1 signaling with 4 different drugs reduced pain and lesion size on our mouse model.

We conclude that neuroimmune communication mediates lesion growth and pain in our endometriosis model.  This implies that blocking neuroimmune communication may be effective in treating endometriosis.  A salient example of such an approach would be CGRP pathway antagonists currently used for migraine.

30.03.23, Edward R. Smith

CCBIO Special Seminar with Edward R. Smith, Harvard Medical School and the Vascular Biology Program, Boston Children's Hospital
Title: "Learning from tumor to treat stroke"
Time: 11:30
Place: Auditorium B301, Sentralblokken 3rd floor, Haukeland University Hospital
Chairperson: Agnete Engelsen

Short bio: Dr. Smith is a professor at Harvard Medical School and the R. Michael Scott endowed chair in neurosurgery at Boston Children’s Hospital.  He serves as the co-director of the Cerebrovascular Surgery and Interventions Center, vice-chair of the #1-ranked department of pediatric neurosurgery in the US and leads a translational research laboratory in the Vascular Biology Program, focusing on development of non-invasive biomarkers and novel therapies for brain tumors and stroke.  Dr. Smith heads one of the largest pediatric cerebrovascular programs in the country, and innovations from his research and clinical efforts have been incorporated in current national guidelines, with the goal of improving patient outcomes.

Abstract: Brain tumors and stroke are two of the leading causes of death in the United States and remain significant challenges to clinicians and scientists making efforts to develop treatments.  Historically, translational research on these two conditions has been separate, with distinct areas of focus.  However, with recent insights obtained from both the operating room and the laboratory, there has been a growing recognition that there may be shared mechanisms that are co-opted by both seemingly disparate diseases, offering novel insights relevant to potential therapeutic advances.

In this lecture, a review of the impact of axon guidance factors – proteins that influence the growth of the brain and associated vasculature in embryonic development – in the pathogenesis of brain tumors and stroke conditions in childhood is presented.  Emphasis on the interconnected aspects of normal and pathologic growth programs in the central nervous system will be highlighted, with discussion centered on the importance of multidisciplinary research teams.  At the conclusion of the lecture, the audience should be able to discuss the role of axon guidance factors in the pathogenesis of these diseases and identify opportunities for future research relevant to innovating new therapies.

30.03.23, Martin Götte

Dr. Martin Götte, University of Münster, Germany
Title: "The multifunctional nature of Syndecan-1 in breast cancer"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

Abstract: The transmembrane proteoglycan syndecan-1 modulates a multitude of physiological processes via binding of its heparan sulfate carbohydrate chains to numerous ligands relevant to tumor progression and inflammation. Syndecan-1 is a classical coreceptor for growth factors, angiogenic factors and chemokines, and acts as a cell and matrix adhesion receptor. It modulates integrin function, proteolysis and tumor angiogenesis. The striking resistance of syndecan-1-deficient mice to mammary tumorigenesis has been linked to a potential role in cancer stem cell function, and we could provide evidence for a role for syndecan-1 in human tumor-initiating cells. New data from our laboratory provide a link of syndecan-1 to radiation resistance in breast cancer. In this seminar, I will present recent data which demonstrate a role for syndecan-1 in the inflammatory microenvironment, and possible molecular mechanisms linked to therapeutic resistance and recurrence.

27.04.23, Linda Lindström

Linda Lindström, Associate Professor in Cancer Epidemiology and group leader at the Department of Oncology and Pathology, Karolinska Institute, Sweden
Title: "Breast cancer inter and intra-patient heterogeneity and long-term risk to develop distant metastatic disease"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

Abstract: Most breast cancer patients are diagnosed with hormone-dependent (estrogen receptor-positive, ER+) breast cancer and anti-hormonal (endocrine) treatment is standard of care. Unlike most other cancers, the risk of fatal disease remains stable beyond 5 to 10 years after diagnosis, and half or more of all breast cancer metastases will be diagnosed long-term after this initial follow-up. The tumor biological factors underlying long-term risk are poorly understood, but clinically important in particular for younger premenopausal patients with a long post cancer life expectancy but also decades of fear from disease recurrence. Young women with breast cancer also have a worse prognosis as compared to older postmenopausal women, and menopausal status itself has been suggested to be an independent risk factor related to the hormonal milieu. In my research group, our focus is on long-term risk and how risk and endocrine treatment benefit is influenced by menopausal status and tumor biology including standard tumor markers, intra-tumor heterogeneity, and tumor microenvironment. 

_{Johansson A, Dar H, van 't Veer LJ, Tobin NP, Perez-Tenorio G, Nordenskjöld A, Johansson U, Hartman J, Skoog L, Yau C, Benz CC, Esserman LJ, Stål O, Nordenskjöld B, Fornander T, Lindström LS. Twenty-Year Benefit From Adjuvant Goserelin and Tamoxifen in Premenopausal Patients With Breast Cancer in a Controlled Randomized Clinical Trial. J Clin Oncol. 2022. PMID: 35862873.} 

_{Yu N, Iftimi A, Yau C, Tobin NP, van ’t Veer L, Hoadley KA, Benz CC, Nordenskjöld B, Fornander T, Stål O, Czene K, Esserman LJ, Lindström LS. Assessment of long-term distant recurrence-free survival associated with tamoxifen therapy in postmenopausal patients with Luminal A or Luminal B breast cancer. JAMA Oncol. 2019. PMID: 31393518.} 

_{Lindström LS, Yau C, Czene K, Thompson CK, Hoadley KA, Van’t Veer LJ, Balassanian R, Bishop JW, Carpenter PM, Chen YY, Datnow B, Hasteh F, Krings G, Lin F, Zhang Y, Nordenskjöld B, Stål O, Benz CC, Fornander T, Borowsky AD, Esserman LJ; STO Trialists Group. Intra-tumor heterogeneity of the estrogen receptor and the long-term risk of fatal breast Cancer. J Natl of Cancer Inst, (JNCI). 2018. PMID: 29361175.} 

25.05.23, JianFeng Chen

JianFeng Chen, Professor at the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
Title: "Control of lymphocyte homing by two-way tuning of integrin activation"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

Abstract: Integrins are a family of α/β heterodimeric adhesion receptors that mediate cell-cell, cell-matrix interactions and bidirectional signaling across the plasma membrane. α4 integrins (α4β7 and α4β1) are primarily expressed on leukocytes. By interacting with their ligands expressed on high endothelial venules, α4 integrins mediate the recruitment of leukocytes from blood circulation to lymphoid organs and inflamed tissues, thereby playing essential roles in immune surveillance and host defense. α4 integrins have been implicated in many inflammatory diseases, such as Crohn′s disease, ulcerative colitis and multiple sclerosis. The function of integrins is dynamically regulated by their activation and signaling. Studying the mechanism of integrin activation and signaling is important for understanding the process of lymphocyte homing and the development of new therapeutics for these inflammatory diseases. This talk will focus on our most recent findings on novel endogenous activator and inactivator for α4 integrins and their roles in regulating lymphocyte trafficking and gut immunity.

15.06.23, Tuula Salo

Tuula Salo, University of Helsinki
Title: "Personalized oral cancer treatment assays"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Dana Costea   

Abstract: Oral squamous cell carcinoma (OSCC) is an agressive cancer with high mortality rate, poor quality of life of survivors and only limited treatment modalities in addition to surgery and irradiation. Based on our and other's studies the following prognostics features, such as depth of invasion, tumour budding, intraneural invasion, tumour stroma ratio, tumour infiltration lymphocytes, and their association with clinical features should be considered in determining the optimal treatment protocol of OSCC patients. We have recently evaluated the ability of five published web-based tools to predict the clinical behaviour of oral tongue resection and biopsy samples. One tool predicted 5- (AUC 0.723) and the other 10-year (AUC 0.858) cancer-related mortality with sensitivity of 82.1%, and the third tool predicted the loco-regional recurence with an accuracy of 82.0% and specificity of 97.4%. Web-based tools may be helpful to predict the clinical behaviour of oral tongue cancer. For personalized oral cancer treatment, we have tested the reliability of our rapid cancer treatment-testing assays: human uterus tumour derived myogel-coated plates; zebrafish xenografts and 3D microfluidic chips. Chemo-, radio- and targeted-therapy tests of primary and metastatic lymph node samples and peripheral blood mononuclear cells isolated from the patients' blood were used for the analyses of three OSCC patients. The assays were fast: it took only around one week to get the responses of the patient's mimicking treatments. The cancer cells' sensitivity to the ex vivo treatments was compared with the patients' clinical response. Primary and metastatic lymph node tissue-derived DNA samples from two patients underwent also whole exome sequencing to compare the mutational profiles of the samples. Our test results were in line with patients' responses in 77% of zebrafish xenograft assays and 55% of Myogel-coated wells' assays. Immunotherapy testing was done using one metastatic patient sample which matched the patients' response. Our preliminary results of three OSCC patients show the possible potential of applying in oral cancer patients our personalized cancer treatment testing assays, specifically zebrafish xenografts and microfluidic ships, for planning the most effective chemo-immuno-radiation therapies to the patients. However, still more OSCC patient cases with possible improved methods should be tested to show if these assays could be considered for clinical use in the future.

31.08.23, Juan Rodríguez Vita

Juan Rodríguez Vita, Centro de Investigacíon Príncipe Felipe, Valencia, Spain.
Title: "Hyaluronic acid is a master regulator of tumor stroma"
Time: 14:30
Place: Auditorium 4, BBB
Chairpersons: Line Bjørge and Emmet McCormack

Dr. Juan Rodríguez Vita obtained his PhD at the FJD in Madrid (Spain), and after postdoctoral periods at the CIML in Marseille (France) and the IDIBAPS in Barcelona (Barcelona), he is currently a Project leader in the Vascular Signaling and Cancer Division at the DKFZ in Heidelberg (Germany). He started his own group at the CIPF in Valencia (Spain) on September 2021. His research focuses on deciphering the communication signals between tumor cells and stroma. 

Abstract:  Tumor cells use signals to communicate and educate the tumor stroma. These signals are often present in the extracellular matrix (ECM). I will show you how tumor cells take advantage of one of the components of this ECM, hyaluronic acid (HA), to modify their stroma in order to generate a more immunosuppressive environment and increase their metastatic potential. HA can be synthesized as low molecular weight-HA (LMW-HA) or high molecular weight-HA (HMW-HA). Firstly, I will describe how HMW-HA produced by ovarian cancer cells, when recognized by macrophages, depletes membrane cholesterol from their plasma membranes. Cholesterol depletion alters IL-4 signaling and amplifies its responses. Secondly, I will show how tumor cells precondition monocytes even before they arrive into the tumor microenvironment, by regulating HA receptors. Notch1 receptors (N1ICD) are frequently activated in Endothelial cells (ECs) within human tumors. Using VECadherin-CreERT2 transgenic mice to induce gene recombination exclusively in adult ECs, we explored the role of Notch signaling in ECs in vivo. RbpjiΔEC (VECad-rERT2xRbpjflox) mice inhibit the canonical Notch signaling upon tamoxifen administration. Thanks to these mice, we were able to demonstrate that Notch signaling in endothelial cells leads to a CXCL2 dependent regulation of CD44 (and HA receptor) in monocytes, which facilitates tumor-associated macrophages education by tumor cells. Finally, I will explain how all this led us to study the role of HA in Pancreatic ductal adenocarcinoma (PDAC) where ECM can make up to 90 % of the desmoplastic tumor mass and HA is one if its main components. We found that Hyaluronan and proteoglycan link protein 1 (HAPLN1), which crosslinks HA with proteoglycans, is an important regulator of HA actions. We found that HAPLN1 induces a Hyperplastic phenotype in tumor cells, which promotes an immune-modulatory microenvironment that favors disease progression in vivo.

28.09.23, Oddbjørn Straume

Oddbjørn Straume, CCBIO, University of Bergen and Haukeland University Hospital.
Title: "Predictive markers of response to immune checkpoint blockade in melanoma - experience from a randomized clinical trial"  
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: to be announced

26.10.23, Arne Östman

Arne Östman, Karolinska Institute, Sweden
Title: "Spatially enriched multi-marker human CAF-subsets linked to treatment response, prognosis, driver mutations, immune features and micro-niches"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

Abstract: Tumor biology studies, mostly relying on mouse cancer models, imply functionally distinct subsets of cancer-associated fibroblasts (CAFs) impacting on malignant cells and immune cells. Also, studies in physiological settings uncover fibroblast subsets with instructive functions. Identification and molecular definition of clinically relevant CAF subsets are highly warranted. This presentation discusses studies towards the ultimate goal of identification of CAF subsets to be exploited as biomarkers or drug targets. A general theme of studies is in-depth analyses of clinical samples.

For the overall question of across-tumor-type consistent CAF subsets, an ongoing study is identifying “consensus CAF subsets” by integrated analyses of multiple single cell RNA seq data sets from mouse and human tumors of different cancer types. Interestingly, signatures representing emerging subsets also identify these subsets in external datasets from other tumor types (“EuroCAF group”, in prep.).

Regarding biomarker potential of CAFs, analyses of tissue samples from two randomized trials on radiotherapy (RT) identified associations between CAFs and RT benefit, such that high stromal PDGFRbeta expression is associated with reduced RT benefit. These findings have biomarker as well as combination therapy implications (Strell et al, Clin Can Res, 2021; Strell et al al, Br Can Res Treat, 2021). 

For higher resolution in situ analyses of the human CAF landscape, multiplex-based profiling was done in two lung cancer collections, each with more than 300 cases, identifying 15 marker-defined CAF subsets. Two subsets, with contrasting expression of FAP and PDGFRA, showed significant and opposite associations with driver mutations, immune features and outcome (Pellinen et al, JNCI, 2023). 

Finally, ongoing explorative studies in colorectal cancer (CRC), integrating single cell RNA seq and multiplex staining, identified four multi-marker-defined subsets. Preliminary analyses of six CRC cases show contrasting non-random spatial associations of these subsets with proliferating T-cells, with highly proliferative cancer areas and cancer areas with high T-cell infiltration. Analyses in a larger cohort of 200+ CRC cases are ongoing for validation of spatial properties and niche-associations of the subsets, and for analyses of outcome associations (Huang et al, in prep.).

Ongoing IMC-based characterization of the tissue architecture of breast cancer, with special focus on CAFs, will also be introduced.

Collectively, studies hopefully contribute to turning CAFs into a cell type of diagnostic and therapeutic significance.

23.11.23, Christopher Elnan Kvistad

Christopher Elnan Kvistad, Neuro-SysMed, University of Bergen and Haukeland University hospital, Bergen, Norway
Title: "A brief history of the (failing) neural regeneration in the human CNS (central nervous system)"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

Christopher Elnan Kvistad is a neurologist and PhD. He has a postdoc in treatment with mesenchymal stem cells in MS, is PI in the SMART-MS study and a clinical career stipend from Helse Vest within the field of stem cell based neuroregeneration. 

Abstract: The failure of axons to regenerate is a major obstacle for functional recovery following CNS injury from various etiologies. Why is this? What has research shown us and what is the status today? The following lecture will try to answer these questions in a brief recapitulation of the research progress from 1600 BC until today.  

14.12.23, Thomas H. Barker

Thomas H. Barker, Professor in Biomedical Engineering, the University of Virginia, Charlottesville, USA
Title: “Targeting the Matrix in a matrix-centric disease: The holy grail of Fibrosis therapeutics?”
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

Abstract: Idiopathic Pulmonary Fibrosis (IPF) and other lung interstitial diseases (ILDs) represent a diverse set of clinical scenarios that all culminate in the excessive deposition of extracellular matrix (ECM) in the lung, i.e. progressive fibrosis.  Fibroblasts are the arbiters of the gross ECM remodeling that characterizes these diseases, and it is believed that targeting the emergence of fibroblasts and their signaling represents the most tractable approach for disease treatment.  Indeed, most pipeline therapeutics are focused on mechanisms of alveolar epithelial cell EMT, fibroblast activation and myofibroblast differentiation (eg. TGF activation and WNT downstream signaling).  These emerging approaches are significantly more advanced than the current standard of care yet remain somewhat myopic to the underlying ECM’s dominant impact on epithelial cell, endothelial cell, pericyte and fibroblast behaviors, which underpin both TGFb and WNT signaling.  Despite fibrosis being best characterized by ECM deposition, no current or pipeline therapeutics target this foundational piece of the fibrosis puzzle.  This is in large part due to the gross similarities in ECM composition between fibrotic and normal tissue.  While the stoichiometries may differ, the molecular signatures are highly similar making targeting a fraught enterprise.  Over the past decade or more my group has explored the emergence and impact of alternative conformations of the critical ECM protein fibronectin in tissue repair and remodeling.  In this seminar, I will review our findings that demonstrate a modest and pathophysiologically relevant force-driven conformational change in fibronectin’s integrin binding domain can drive numerous disease phenotypes and yet can be leveraged to specifically target fibrosing tissues with the potential to reverse fibrotic remodeling.

20.01.22, Donald Gullberg

Title: "α11β1, a mesenchymal collagen-binding integrin with a central role in tissue- and tumor fibrosis"
Time: 14:30 CANCELLED DUE TO ILLNESS
Place: 

17.02.22, Kaisa Lehti

Kaisa Lehti, Department of Biomedical Laboratory Science, Norwegian University of Science and Technology (NTNU), Trondheim
Title: “Crosstalk of desmoplastic tumor microenvironment and ovarian cancer in metastasis and therapy resistance”
Time: 14:30
Place: 
Chairperson: Line Bjørge

Short bio: Kaisa Lehti is professor of cell and molecular biology at NTNU and group leader at Karolinska Institutet, Stockholm. She focuses on translational ovarian cancer research, phenotypic plasticity and microenvironment-dependent cell signaling mechanisms in tumor invasion, metastasis and drug resistance. Her group has developed clinically relevant ex vivo models of primary cells, tumoroids and tissue explant cultures as well as in vivo tumor models. Results using these models have revealed potent markers and targetable mechanisms of fibrotic extracellular matrix (ECM) remodeling, oncogenic cell signaling and transmembrane protease - adhesion receptor crosstalk. In this research, collaboration between basic researchers and clinicians provide the basis for the development of significant study models and mechanistic results with potential to pave a way for improved cancer treatments. 

Abstract: Aggressive tumors are driven by complex crosstalk between cancer cells and the tumor microenvironment (TME). To date, great efforts are invested to cancer intrinsic programs for precision cancer therapy. Yet, heterogeneous cancer cells at specific TMEs develop resistance to the drugs developed for mechanisms in cancer cells alone. An unresolved challenge thus remains in the mechanisms governing the multicellular crosstalk and aggressive cancer phenotypes in the 3D TMEs. In this seminar, I will discuss our approaches using tumor & stromal cells and tissues collected longitudinally from patients with ovarian cancer (OC), the lethal gynecological malignancy with progressively chemotherapy-resistant metastases, to explore the development of therapy resistance. By examining OC transcriptome and histology, we have described the fibrotic ECM heterogeneity at primary tumors and distinct metastatic sites, prior and after chemotherapy. This data guides us in the development of clinically relevant ex vivo models for molecular mechanistic research. From there, the results are starting to suggest distinct stromal and tumor strategies and biomarker candidates for ECM and fibrosis pathway targeting to overcome therapy resistance.

31.03.22, Shin Kaneko

Shin Kaneko, Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto City, Japan
Title:  iPSC-based killer cell regeneration for cancer immunotherapy
Time: 14:30
Place: Webinar in Zoom
Chairperson: Jim Lorens

Abstract: For T cell immunotherapy, the important points for good clinical benefit is to keep antigen-specificity, younger memory function and a high quantity of T cells. Although CD19 CAR- T-cell immunotherapy has had tremendous success, some patients do not respond well because of insufficient quality and quantity of the patient’s T cell for CAR modification and CAR-T function in the body. iPS reprogramming technology can instill anti- cancer T cells a younger phenotype, clonality and quantity. Also, in cases using non-T cell derived non-antigen-specific iPS cells, antigen-specific receptor modification of the iPSC can give cancer-specificity to the differentiated T cells. To establish such a regenerative and rejuvenated T cell immunotherapy, we developed a system to efficiently produce T cells from iPS cells. In this presentation, we will introduce basic research and clinical development of iPSC-based immune cells modified by CAR.

References

1. Kawai Y, et al. Generation of highly proliferative, rejuvenated cytotoxic T cell clones through pluripotency reprograming for adoptive immunotherapy. Molecular Therapy 29(10):3027-3041.2021.    
2. Wang B, et al. Generation of hypoimmunogenic T cells from genetically engineered allogeneic human induced pluripotent stem cells. Nature Biomedical Engineering 2021(5):429-440.2021.    
3. Iriguchi S, Yasui Y, Kawai Y, et al. A clinically applicable and scalable method to regenerate T-cells from iPSCs for off-the-shelf T-cell immunotherapy. Nature Communications 2021(12) Article number: 430.2021.   
4. Ueda T, et al. Non-clinical efficacy, safety, and stable clinical cell processing of iPSC-derived anti-GPC3 CAR-expressing NK/ILC cells. Cancer Science 111(5):1478-1490.2020.
5. Xu H, Wang B, et al. Targeted Disruption of HLA Genes via CRISPR-Cas9 Generates iPSCs with Enhanced Immune Compatibility. Cell Stem Cell, 24(4):566-578.e7.
6. Minagawa A, et al. Enhancing T Cell Receptor Stability in Rejuvenated iPSC-Derived T Cells Improves Their Use in Cancer Immunotherapy. Cell Stem Cell. 23(6):850-858.e4.2018.    
7. Nishimura T, et al. Generation of rejuvenated antigen-specific T cells by reprogramming to pluripotency and redifferentiation. Cell Stem Cell. 12(1):114-26.2013

Bio: Professor Kaneko his MD and PhD degrees from the University of Tsukuba School of Medicine and completed residency in Internal Medicine at University of Tsukuba Hospital. After working as a Fellow of the Japan Society for the Promotion of Science in 2002 and a lecturer in the Department of Hematology, University of Tsukuba, he worked at the San Rafaele Institute in Italy from 2005 to 2008. After returning to Japan in 2008, he became an Assistant Professor at the Institute of Medical Sciences, University of Tokyo, an Associate Professor at the Center for iPS Cell Research and Application, Kyoto University in 2012, and a professor at the University of Tsukuba under the cross-appointment system with Kyoto University from 2020.

Professor Kaneko received the Japan Society for Hematology Young Investigator’s Award in 2002, the Japan Society for Gene Therapy Encouragement Award in 2010, and the Japan Society for Regenerative Medicine Innovation Award in 2012.
https://www.cira.kyoto-u.ac.jp/e/research/kaneko_summary.html

28.04.22, Therese Sørlie

Therese Sørlie, Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, and Institute of Clinical Medicine, University of Oslo
Title: FGFR1 as a biomarker and target for therapy in hormone receptor positive breast cancer
Time: 14:30 (Note: Auditorium 1 this time)
Place: Webinar in Zoom
Chairperson: Lars A. Akslen

Bio: Therese Sørlie is the Head of department of Cancer Genetics and Professor II at the Institute of Clinical Medicine, University of Oslo. Her research field is breast cancer, DCIS and risk prediction. Dr. Sørlie was instrumental in the pioneering studies that defined the molecular subtypes of breast cancer, now part of clinically approved classification systems. Since then her studies focus on progression in the earliest stages of tumorigenesis under the hypothesis that progression occurs differently among the different subtypes. Recently, Dr Sørlie’s group has focused on a subgroup of hormone receptor positive breast cancer, namely FGFR1 amplified luminal A and B breast cancer. In the seminar she will discuss how FGFR1 might be a therapeutic target in FGFR1–signalling dependent tumors and may reverse endocrine resistance. She will also briefly present current efforts to study spatial heterogeneity in DCIS. 

Title of the talk: “FGFR1 as a biomarker and target for therapy in hormone receptor positive breast cancer”

Abstract: Luminal breast cancer (expressing estrogen receptor and/or progesterone receptor) accounts for approximately 75% of all breast cancers tumors and are associated with relatively good survival due to efficient treatment with endocrine therapy.  Despite this, a significant proportion (up to 40 %) will in the longer term, develop resistance to therapy and disease recurrence. Many different growth factor receptors and signaling pathways are involved in breast cancer development and progression and in development of resistance. One such growth factor receptor, Fibroblast growth factor receptor 1 (FGFR1), is amplified in up to 27% of luminal cancers (highest in luminal B subtype) and is an independent prognostic marker associated with short overall survival rates. In this seminar, I will discuss our ongoing project on FGFR1 and its potential as a biomarker and target for therapy in luminal breast cancer. Through in vitro and in vivo experiments, we have shown that targeting FGFR1 inhibits cell proliferation and slows down tumor growth and may also re-sensitize resistant cells to hormone treatment. 

10.06.22, CCBIO Special Seminar with Sheila Jasanoff and Stephen Hilgartner

The 2022 Holberg Laureate, Sheila Jasanoff (Harvard University) in conversation with Stephen Hilgartner (Cornell University). Jasanoff and Hilgartner are internationally leading scholars in Science and Technology Studies (STS) and have done extensive research on the social dimensions and politics of biomedicine and biotechnology (among other fields).
Title: Can science make sense of life?
Time: 09.30-10.15
Place: Store Auditorium, Haukeland University Hospital
Chairperson: Roger Strand

This is the first time the Medical Faculty has the opportunity to welcome a Holberg prize winner, so use this opportunity to gain new insights on your research!

The Holberg Prize is awarded annually to scholars who have made outstanding contributions to research in the humanities, social sciences, law or theology, and the objective of the prize is to increase awareness of the value of academic scholarship from these fields. Science and Technology Studies (STS) pioneer Sheila Jasanoff received the prize for her groundbreaking research in the field. 

In this CCBIO Special Seminar, you will meet Sheila Jasanoff (Harvard University) on stage in conversation with Stephen Hilgartner (Cornell University). Jasanoff and Hilgartner are internationally leading scholars in Science and Technology Studies (STS) and have done extensive research on the social dimensions and politics of biomedicine and biotechnology (among other fields). What is STS and what insights does it have to offer to medical and health researchers and practitioners? And, to allude to the title of Prof. Jasanoff's latest book, what is the answer to the question "Can Science Make Sense of Life?"

Speakers:

Sheila Jasanoff, Pforzheimer Professor of Science and Technology Studies, Harvard Kennedy School

Sheila Jasanoff is Pforzheimer Professor of Science and Technology Studies at the Harvard Kennedy School. A pioneer in her field, she has authored more than 130 articles and chapters and is author or editor of more than 15 books, including The Fifth Branch, Science at the Bar, Designs on Nature, The Ethics of Invention, and Can Science Make Sense of Life? Her work explores the role of science and technology in the law, politics, and policy of modern democracies. She founded and directs the STS Program at Harvard; previously, she was founding chair of the STS Department at Cornell. She has held distinguished visiting appointments at leading universities in Europe, Asia, Australia, and the US. Jasanoff served on the AAAS Board of Directors and as President of the Society for Social Studies of Science. She is a member of the Council on Foreign Relations. Her honors include the SSRC’s Hirschman prize, the Humboldt Foundation’s Reimar-Lüst award, a Guggenheim Fellowship, an Ehrenkreuz from the Government of Austria, and foreign memberships in the British Academy and the Royal Danish Academy. She holds AB, JD, and PhD degrees from Harvard, and honorary doctorates from the Universities of Twente and Liège.

Stephen Hilgartner, professor at the Department of Science & Technology Studies (S&TS) at Cornell University

Stephen Hilgartner studies the social dimensions and politics of contemporary and emerging science and technology, especially in the life sciences. His research focuses on situations in which scientific knowledge is implicated in establishing, contesting, and maintaining social order -- a theme he has examined in studies of expertise, property formation, risk disputes, and biotechnology. His most recent book, Reordering Life: Knowledge and Control in the Genomics Revolution (MIT Press, 2017), examines how new knowledge and new regimes of control took shape during the Human Genome Project. Hilgartner’s book on science advice—Science on Stage: Expert Advice as Public Drama—won the Rachel Carson Prize from the Society for Social Studies of Science. He is also a co-editor of two recent books: Science & Democracy: Making Knowledge and Making Power in the Biosciences and Beyond (Routledge, 2015) and Handbook of Genomics, Health and Society (Routledge, 2018). Hilgartner is a Fellow of the American Association for the Advancement of Science

13.06.22, Torsten O. Nielsen

Torsten O. Nielsen MD/PhD FRCPC, Professor of Pathology & Laboratory Medicine, MD/PhD Program Director, Faculty of Medicine, University of British Columbia, Canada.
Title: Breast Cancer Biomarker Development: Intrinsic Subtypes, Ki67 and Proteomics
Time: June 13, 2022 at 13.00
Place: The auditorium in Armauer Hansens Hus, Haukelandsveien 28, Bergen
Chairperson: Lars A. Akslen

Abstract: Torsten Nielsen is a clinician-scientist pathologist from the University of British Columbia, whose research programs focus on breast cancer and sarcomas. Prof. Nielsen will discuss how some of the world's earliest cancer transcriptomics experiments, through a series of subsequent validation and functional studies, were systemically translated into new diagnostic tools and therapeutic strategies in cancer. In particular, he will tell the story behind breast cancer intrinsic subtyping and the development of the PAM50 classifier, its conversion into a nanoString-based diagnostic, and how this since has been applied to clinical trials to develop predictive markers for breast cancer, including new data on triple negative subtyping and capecitabine benefit. As one of the leaders of the International Ki67 Working Group, Prof. Nielsen will also describe current evidence and recommendations for Ki67 assessment in breast cancer, showing new results being presented at ASCO 2022 from a prospective clinical trial using this marker to guide the need for adjuvant radiation therapy. Finally, he will present very recently-published work on applying proteomics technologies to formalin-fixed breast cancer surgical specimens and how this new technology contributes to the molecular classification of breast cancer.

Research field: Professor Nielsen is a clinician-scientist pathologist who has chosen to dedicate his career to translating basic science of cancer into new diagnostics and new therapies. His research has to date has focused on breast cancer and sarcomas. He provides pathology input into translational cancer research, bringing his skills in genomics and biomarker development into clinical trial design and the development of diagnostics that truly improve patient care. 

Main achievements: Major accomplishments include development of the PAM50 algorithm and FDA-cleared Prosigna assay; leading international standardization of Ki67 testing; and key work uncovering the biology of three kinds of sarcoma each of which led to new diagnostics and clinical trials of new therapies. Read more here: https://pathology.ubc.ca/faculty/torsten-nielsen/

25.08.22, Carina Strell

Carina Strell, Department of Clinical Medicine and CCBIO, University of Bergen  Welcome seminar for Carina Strell who has received a TMS Starting Grant and will be establishing a research group on breast cancer here with us at the UiB. 
Title: Perspectives on early breast cancer – molecular biology and epidemiology
Program: 

• Opening by Lars A. Akslen
• Remarks by the Trond Mohn Foundation, Faculty of Medicine and Department of Clinical Medicine (K1)
• Presentation by Carina Strell: Tumor-Stroma Interactions Driving Progression and Therapy-Resistance of DCIS
• Presentation by Therese Sørlie: Intrinsic subtypes and spatial heterogeneity in Ductal Carcinoma In Situ
• Presentation by Solveig Hofvind: Early detection of breast cancer in a screening and registry perspective
• Discussion and closing remark

Time: 13:00
Place: Auditorium in Armauer Hansens Hus
Chairperson: Lars A. Akslen

Carina Strell received in December 2021 a Trond Mohn Foundation starting grant for her project Understanding Early Breast Cancer Evolution in Space and Time (EvoMaps). Strell has a long-term collaboration with the Akslen group, and her project will be embedded at CCBIO, commencing in Bergen in 2022. She aims to establish a competitive research group within the field of early breast cancer, investigating the biological mechanisms behind why some women experience recurrent and/or treatment resistant disease while others do not. The hypothesis is that breast cancer progression and therapy response is not only dependent on the tumor cells alone, but also on the surrounding tissue microenvironment. Through adaptation of the in-situ sequencing technique to the Hyperion Imaging System at CCBIO, Strell will perform a systematic exploration of the genetic properties of tumor cells in relation to their surrounding microenvironment over the course of disease progression and the development of treatment resistance. The overall aim of this project is to uncover and map new mechanisms of early breast cancer evolution, and to improve current diagnostic tools for breast cancer patients, reduce the treatment burden for women with early-stage breast cancer and thus improve their quality of life and spare them treatment related comorbidities.

29.09.22, Klaus Pantel

Speaker: Klaus Pantel, Director of the Institute of Tumor Biology, Center for Experimental Medicine, UKE Hamburg. 
Title: "The promise of ctDNA and CTCs in the evaluation of cancer treatment efficacy"
Time: 12:30
Place: digtal event in Zoom
Chairperson: Agnete Engelsen

Over the past ten years, circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) have received enormous attention as new biomarkers and subject of translational research. Join us in a Zoom webinar to hear Professor Pantel, considered as the father of the term liquid biopsy, give a talk on the application of CTCs and ctDNA in cancer research.

27.10.22, Ingeborg Tinhofer-Keilholz

Speaker: Dr. Ingeborg Tinhofer-Keilholz, Department of Radiooncology and Radiotherapy, Charité-Universitätsmedizin Berlin.
Title: "Advanced animal-free preclinical models for head and neck cancer." 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Dana Costea

Inge Tinhofer-Keilholz is in the research field of head neck squamous cell carcinoma; molecular mechanisms of resistance to radiotherapy, chemotherapy and targeted treatment; development of biomarkers for improved patient stratification and personalized treatment. She has has published 124 scientific papers, and coordinates the research activities of the Charité Comprehensive Cancer Center Working Group Head and Neck Cancer. Since 2015, she is Translational Research Representative from the EORTC HNC Group and since 2020 she is member of the ESMO Faculty (HNC Group). She serves as reviewer for several high-impact journals including Lancet Oncology, Clinical Cancer Research, Annals of Oncology, and European Journal of Cancer.

Seminar focus:  To describe the generation, advantages and limitations of advanced animal-free preclinical models for head and neck cancer; To present recent achievements from preclinical model studies with respect to biomarker development and therapeutic target identification.

Abstract: Comprehensive molecular characterization of head and neck squamous cell carcinoma (HNSCC) has led to the identification of distinct molecular subgroups with fundamental differences in biological properties and clinical behavior. Despite improvements in tumor classification and increased understanding about the signaling pathways involved in neoplastic transformation and disease progression, current standard-of-care treatment for HNSCC mostly remains to be based on a stage-dependent strategy whereby all patients at the same stage receive the same treatment. Preclinical models that closely resemble molecular HNSCC subgroups that can be exploited for dissecting the biological function of genetic variants and/or altered gene expression will be highly valuable for translating molecular findings into improved clinical care. In the seminar, I will discuss existing and novel information on primary two- and three-dimensional ex vivo tumor cultures from HNSCC patients. I will review their value in elucidating the basic biology of HNSCC, the molecular mechanisms of treatment resistance and their potential for the development of novel molecularly stratified treatment.

24.11.22, Donald Gullberg

Speaker: Donald Gullberg, CCBIO PI and Prosessor at the Department of Biomedicine, University of Bergen
Title: "Advances in fibroblast biology"
Time: 14:30
Place: Auditorium 4, BBB
 

Abstract: In the past year a number of interesting publications relating to fibroblasts biology, of relevance to both fibrosis and cancer biology, have been published. In my lecture I will discuss these new findings and relate them to our own research on a major collagen-binding integrin present fibroblasts, alpha11beta1.

15.12.22, Tim Coorens

Speaker: Tim Coorens
Title:  "Using somatic mutations to reconstruct the life histories of normal and cancer cells"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson:Camilla Krakstad

Abstract: From fertilization onwards, individual cells of the human body continuously experience DNA damage and accumulate somatic mutations. As mutations in the genome are reliably passed on to a cell’s progeny, the somatic genome of a cell becomes a record of its life history and a means to infer its relationship to any other cell of the same individual. In essence, somatic mutations connect all cells together into one large phylogenetic tree of human development with the zygote at the root. Besides recording the cell division, migration and differentiation of early development, somatic mutations can also delineate aberrant, premalignant expansions and shed light on the evolution of a cancer in response to treatment. 
In this seminar, I will discuss the surprising insights that we have recently gained by using somatic mutations as natural lineage markers. Covering the timescale from early development to cancer evolution, I will present my findings on (1) patterns of embryogenesis in the human body¹ and placenta², (2) early precursor clones to Wilms tumor³, a childhood kidney cancer, and (3) a surprising case of lineage switch leukemia in response to CAR-T cell therapy⁴. 

^{1.    Coorens THH, Moore L et al. Extensive phylogenies of human development inferred from somatic mutations. Nature 597, 387-392 (2021).
2.    Coorens THH, Oliver TRW et al. Inherent mosaicism and extensive mutation of human placentas. Nature 592, 80–85 (2021).
3.    Coorens THH et al. Embryonal precursors of Wilms tumor. Science 366, 1247–1251 (2019).
4.    Coorens THH et al. Clonal origin of lineage switch leukaemia following CAR-T cell and blinatunomab therapy. In preparation}

Short bio: Tim’s work focuses on the use of somatic mutations to reconstruct the developmental history of normal cells and cancers, including reconstructing patterns of early embryogenesis, tracing the origins of pediatric tumors, and inferring mechanisms of resistance in cancers. He completed his PhD at the Wellcome Sanger Institute, UK, under the auspices of Mike Stratton, Iñigo Martincorena and Sam Behjati. He is currently an EMBO Postdoctoral Fellow in Gaddy Getz’s lab at the Broad Institute of MIT and Harvard. See publications.

28.01.21, Arne Östman

Arne Östman, Department of Oncology-Pathology, Karolinska Institute (KI), Sweden, and CCBIO affiliated international investigator.
Title: "Cancer-associated fibroblasts; novel subsets associated with tumor biology features, outcome and response to treatment"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Lars A. Akslen

Short bio: Professor Arne Östman received his PhD in 1990 on platelet-derived growth factor from the Ludwig Institute for Cancer Research, Uppsala University, Sweden. He is currently a professor at the Karolinska Institute (KI).

Professor Östman’s research is focused on the biology of the tumor micro-environment with special focus on tumor-associated fibroblasts and their role in cancer progression. Professor Östman was vice-coordinator of STRATCAN, a government-funded initiative for the development of excellent cancer research at KI (2010-2018), and acted as coordinator for the Swedish Research Council-supported STARGET center of excellence 2006-16. Since 2020, he is a member of the Nobel Assembly.

Abstract: Cancer-associated fibroblasts (CAFs) constitute a prognosis-associated heterogeneous cell population occurring in most solid tumors. According to model studies, CAFs exert multiple regulatory functions, including regulation of malignant cells, vascular cells, and immune cells. In-depth profiling of CAFs in clinical samples thus appears as a valid strategy for biomarker identification and for the discovery of novel associations indicative of clinically relevant cellular cross-talk.

Analyses of the CAF-markers PDGFaR and PDGFbR have demonstrated that these proteins are independently expressed, and the abundance of these markers shows differential prognosis associations, indicating that they mark functionally distinct CAF subsets.

PDGFbR was also explored as a candidate marker for RT sensitivity through analyses of a randomized trial-derived breast DCIS collection. Notably, significant interactions between marker and treatment were detected in the analysis in such a manner that PDGFbR-high breast DCIS displayed no significant benefit of RT. Ongoing analyses in a tissue collection of invasive breast cancer provide similar, but weaker, associations between RT benefit and high PDGFR expression in invasive breast cancer.

Ongoing studies using single-cell RNA seq of human colorectal cancer CAFs have identified 2 main classes, subdivided into five subsets with distinct and strong survival associations.  Results from ongoing analyses regarding subset-specific associations with driver mutations and immune features will be discussed.

Finally, multiplex-staining has been employed on a large lung cancer collection. These ongoing studies are identifying novel multi-marker-defined CAF subsets showing compartment- and subset-specific survival associations. Also in this setting, analyses are ongoing regarding associations with driver mutations and immune.

Collectively, studies provide novel evidence for clinically relevant heterogeneity of CAFS, supporting the overall concept that these cells should be further explored for the development of biomarkers of clinical utility and drugs with novel mechanisms of action.

25.02.21, Mark LaBarge

Mark LaBarge, Department of Population Sciences, Beckman Research Institute at City of Hope, Duarte, CA, USA
Title: "Epigenetic priming in mammary epithelia underlies susceptibility to age-related cancers: causes, consequences, and countermeasures"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Agnete Engelsen

Short bio: Mark LaBarge is a Professor and cell biologist in the Department of Population Sciences at the Beckman Research Institute at City of Hope National Medical Center, which is near Los Angeles in California, USA. Dr. LaBarge’s work focuses on understanding how aging makes mammary epithelia more susceptible to cancer initiation.  His lab uses combinations of primary cell and organoid culture with technologies for precision manipulation of the microenvironment to deeply characterize the effects of aging in human mammary epithelia, and to probe the functional consequences of those changes. In recognition of his work, Dr. LaBarge is the recipient of the Era of Hope Scholar Award, and he is the Associate Director and co-founder of the Center for Cancer and Aging at City of Hope.

Mark is also one of CCBIO's international affiliated investigators.

Abstract: Aging causes molecular changes that manifest as stereotypical phenotypes yet aging-associated diseases progress only in certain individuals. At lineage-specific resolution, we show how directional and variant age-dependent changes are integrated in mammary epithelia to generate a stereotypical phenotype in luminal epithelial cells - the cancer cell of origin for age-related breast cancers. Strikingly,  >94% of all the age-related directional changes in the entire mammary epithelium occur only in luminal epithelial cells, whereas neighboring myoepithelial cells exhibit little obvious change. Increased variance in DNA methylation leads to epigenetic priming for future events that are more directly related to cancer progression, such as demethylation of ESR1-binding regions in DNAm-regulatory CXXC5 in older luminal cells and luminal-subtype cancers. Acceleration of age-dependent directional changes in luminal lineage-specific transcription factors, such as ELF5, distinguished women who were at exceedingly high risk of breast cancer thus establishing a connection between specific age-dependent changes and cancer susceptibility. At the proteome level up-regulation of basal markers in luminal cells, including KRT14 and AXL, are a prominent consequence of aging, and DDR1-PEAK1 was identified as an age-dependent signaling kinase in luminal cells, which revealed a potential age-dependent vulnerability for targeted ablation of cancer cells of origin. We hypothesize that increased variance with age in gene expression and DNA methylation explains why some women get breast cancer and others do not, and that some specific directional changes will help to distinguish the women who go on to get age-dependent cancer from those who do not. We are exploring age-dependent changes for applications as risk biomarkers and prevention targets.

25.03.21, Randolph Watnick

Randolph Watnick, Vascular Biology Program, Boston Children's Hospital, and Department of Surgery, Harvard Medical School, Boston, MA, US
Title: "Identification of a novel paracrine acting stimulator of tumor growth and progression via modulation of Tsp-1 in the tumor microenvironment"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Lars A. Akslen

Bio: Randy Watnick received his PhD in biochemistry and biophysics from Columbia University in 1999, and was a postdoctoral fellow with Dr. Robert Weinberg, Whitehead Institute, Cambridge, MA, until 2003. Dr. Watnick is currently assistant professor at the Department of Surgery, Harvard Medical School and research associate in the Vascular Biology Program (VBP) at Boston Children’s Hospital.

Dr. Watnick’s expertise is in tumor stromal interactions, regulators of metastasis and gene regulation in epithelial and mesenchymal cells. His research group studies the regulation of angiogenesis, proliferation and motility in both epithelial cells and fibroblasts. The team has identified a novel suppressor of metastasis, prosaposin, which acts both locally and distally by stimulating the expression and activity of p53, which then stimulates the expression of Tsp-1. Significantly, prosaposin also inhibits both primary tumor growth and metastasis when administered in a systemic fashion, thus making it a potential therapeutic agent to stem the metastatic dissemination of human tumors. Dr. Watnick’s group has also developed a therapeutic peptide derived from prosaposin, which has been licensed to Vigeo Therapeutics and is currently in clinical trials in the United States.

Dr. Watnick has a longstanding collaboration with Lars A. Akslen on several projects, which among other has made important findings related to the role of Notch1 in breast cancer initiation and progression. Their collaboration on the tumor microenvironment has led to important observations related to CD36, CD47 and prosaposin expression in pancreatic cancer and their correlations to outcome and patient survival.

Abstract: In the earliest stages of tumor development, epithelial tumors (carcinomas) are physically confined to the area of the tissue in which they form. These nascent lesions (carcinomas in situ) are sequestered from the tissue parenchyma by the basement membrane. Within the tissue parenchyma lie a myriad of cell types comprised of fibroblasts, immune and inflammatory cells and endothelial cells. Upon invasion across the basement membrane and into the tissue parenchyma, tumors must manipulate the expression of pro- and anti-tumorigenic proteins such that pro-tumorigenic factors are produced in vast excess to anti-tumorigenic proteins.  One such anti-tumorigenic protein is Thrombospondin-1 (Tsp-1).  We have previously demonstrated that stimulation of Tsp-1 in the tumor microenvironment (TME) potently inhibits tumor growth and progression and in some cases induces tumor regression.  Here, we identify a novel tumor-mediated mechanism to repress the expression of Tsp-1 in the TME via secretion of the serine protease PRSS2.  We demonstrate that PRSS2 represses Tsp-1, not via its enzymatic activity, but by binding to the low-density lipoprotein receptor-related protein 1 (LRP1).  These findings describe a novel activity for PRSS2 as well as novel ligand and activity for LRP1 and represent a potential therapeutic strategy to treat cancer by blocking the PRSS2-mediated repression of Tsp-1.

29.04.21, Ian Mills

Ian Mills, Centre for Cancer Research and Cell Biology, Queen's University Belfast, Northern Ireland, and Nuffield Department of Surgical Sciences, University of Oxford, UK
Title: "Non-oncogene addiction and the stress phenotype of prostate cancer cells"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Karl-Henning Kalland

Abstract: Prostate cancer is a high incidence male cancer and a significant cause of cancer-specific mortality. In the course of the last two decades genomics has identified a complex landscape of mutational changes associated with prostate cancers within individual patients and across patient cohorts.  This multi-focal heterogeneity has made it difficult to identify oncogenic driver mutations in early-stage disease, although there is evidence for clonal selection as prostate cancer progresses to metastasis.  By contrast there is significant evidence of high-incidence transcriptional, epigenetic and metabolic changes in early-stage prostate cancer.  The phrase ‘non-oncogene addiction’ refers to a dependency on biological processes supported by genes and proteins that are not individually able to fully transform cells but are able to create a cancer permissive state. Given that mutational selection occurs in the progression to advanced/metastatic prostate cancer, we hypothesize that non-oncogene addiction may be particularly significant in the earlier stages of prostate cancer development and in localized disease.  In this seminar I will provide some examples of these processes and refer in particular to transcriptional processivity, the unfolded protein response and nucleolar function.  I will discuss the challenges and opportunities in assessing their activity and in perturbing them to impact on prostate cancer progression.

Short bio: Professor Ian Mills earned his PhD in Molecular and Cellular Physiology at the University of Liverpool in 2000. He is currently Professor of Translational Prostate Cancer Biology at Queen’s University of Belfast and John Black Associate Professor of Prostate Cancer at the University of Oxford. In addition he is a Visiting Scientist at Cambridge Cancer Research UK Institute, an Honorary Visiting Fellow in the Department of Oncology at the University of Cambridge and an Affiliate Member of the Centre for Molecular Medicine Norway (NCMM). Since 2018 he is Affiliated Professor at Centre for Cancer Biomarkers (CCBIO), University of Bergen.

His work on prostate cancer is focusing on the impact of transcriptional and chromatin dysregulation on metabolism and stress response pathways, aiming to understand the interplay between these biologies and radiotherapy response, as well as on the development of new pre-clinical models of prostate cancer. He is working to understand how these biological processes synergize with treatment stress to influence the evolution of prostate cancers, investigating this alongside complementary research teams led by computational biologists, surgical clinician scientists, pathologists and bone biologists. 

27.05.21, Ellen Pure

Ellen Pure, Department of Biomedical Sciences, University of Pennsylvania, USA
Title: "Flanking solid tumors via immune-mediated disruption of desmoplastic stroma"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Donald Gullberg

Abstract: Solid tumors are dependent on cues intrinsic to malignant cells as well as on extrinsic factors derived from non-malignant components of the tissue/tumor microenvironment, overall ecology of the host and environmental factors. Malignant transformation and disease progression involves co-evolution of malignant cells and the vascular, neural, immune and stromal compartments of the cancer neo-organ. At the site of primary tumor, as well as sites of metastasis, this results in transition from the tumor resistant environment of normal tissue to establishment of a pro-tumorigenic niche and involves angiogenesis, innervation and transition from immune surveillance to immune escape. Activation of spatially and temporally diverse populations of stromal cells referred to collectively as cancer associated fibroblasts (CAFs), and dynamic extracellular matrix remodeling, are increasingly recognized as an essential hub in the complex network of communications within the tumor microenvironment that drives tumorigenesis and disease progression. The mechanisms of activation and effector functions of a pro-tumorigenic and immune suppressive subpopulation of fibroblast activation protein (FAP) expressing CAFs will be discussed.  In addition, proof-of-concept that this subpopulation can be therapeutically targeted at a cellular or molecular level will be presented.   

Short bio: Ellen Puré is Professor and Chair, Department of Biomedical Sciences, University of Pennsylvania School of Veterinary Medicine. The laboratory of Ellen Puré is studying the cellular and molecular basis of inflammation and fibrosis, with a particular focus on the role of stromal cells and extracellular matrix (ECM), in the context of chronic inflammatory diseases and cancer. Two molecules studied in some detail in her lab are CD44 and fibroblast activation protein (FAP), a stromal cell surface protease, widely used as a marker for cancer-associated fibroblasts.

10.06.21, Andrew Leask

Andrew Leask, School of Dentistry, University of Saskatchewan, Saskatoon, SK, Canada
Title: "Microenvironmental control of fibrosis: a central role for the CCN family of matricellular proteins"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Donald Gullberg

Short bio: Dr. Leask has a BSc from the University of British Columbia and a PhD from the University of Chicago. After a CIHR Postdoctoral fellowship at Stanford, he was recruited to FibroGen as a Staff Scientist. He then went to the Royal Free Hospital in London, UK, before becoming Professor at the University of Western Ontario. Since 2019 he has been Professor at the University of Saskatchewan. According to Google Scholar, he has published >175 peer-reviewed papers (out of ~220 total), have an h index of 63, and have been cited over 17800 times.  His group has made substantial progress in the understanding of the molecular mechanisms underlying fibrosis, prinicipally using scleroderma as a model system. He is also currently Editor-in-Chief of Journal of Cell Communication and Signaling (IF=3.8), the official journal, published by Springer Nature, of the International CCN Society. He is also on several scientific boards including the American Society of Matrix Biology, the Canadian Skin Research and the International CCN Society. 

Abstract: Inflammation is associated with chronic health conditions including the autoimmune connective tissue disease scleroderma (SSc), the metabolic disorder nonalcoholic steatohepatitis (NASH) and the skin cancer, melanoma.  Although the etiology of these diseases is likely to differ, in all three indications, inflammation triggers a fibrotic response, characterized by excessive production of extracellular matrix (ECM), that results in organ failure and, often, death.  Similarly, activated cancer-associated fibroblasts (CAFs) in the tumor stroma generate a stiff ECM reminiscent of a fibrotic microenvironment that is essential for promoting metastasis. The cells responsible for generating a fibrotic microenvironment are myofibroblasts, highly adhesive/contractile connective tissue cells that arise from resident fibroblasts in response to pro-inflammatory signals. 

We and others hypothesize that a shared feed-forward mechanism, namely an autocrine pro-adhesive/contractile signaling loop acting via integrins/focal adhesion kinase (FAK), leads to the activation and perpetuation of myofibroblasts and, hence, fibrosis. More specifically, we propose, downstream of FAK, that a persistently activated hippo/YAP/TAZ mechanotransduction pathway, initially activated in response to inflammation, is necessary to initiate and maintain the fibrotic phenotype.  Moreover, we have shown that collagen-lineage fibroblasts are required for this process.

CCN1 and 2, members of the pro-adhesive CCN family of matricellular proteins, is a prototypical hippo/YAP/TAZ targets that, in a context-dependent fashion, mediate fibrosis in a variety of models. Conversely, the related protein CCN3, which is reciprocally regulated to CCN2, is antifibrotic. Our idea is that this is a general pathway responsible for all fibrotic conditions, including scleroderma, cancer metastasis, NASH and idiopathic pulmonary fibrosis and thus strategies targeting CCN proteins will have wide therapeutic value. 

26.08.21, Hege F. Berg

Hege F. Berg, Krakstad group, University of Bergen
Title: “Endometrial cancer model systems to improve treatment”
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Harsh Dongre

Hege is a PhD candidate in her last year in the Krakstad group, in the research field Preclinical models for endometrial cancer. She has established a collection of patient-derived endometrial cancer organoids and organoid-based xenograft models.

Organoid models have proven to be highly useful in cancer research and models have been established from several cancer types. This seminar present the group's recent work to establish genetically stable models from all types of endometrial cancer. The work was recently published in Communications Medicine (https://rdcu.be/cqT0a).

Abstract: Endometrial cancer is the most common malignancy of the female reproductive system in countries with high developmental index. Standard treatment for endometrial cancer is surgery, with adjuvant chemotherapy given for high risk or advanced disease. Still, 15-20% of patients experience recurrence. Alternative treatment options for this patient group are few and targeted drugs have not yet reached the clinic for endometrial cancer patients. To bridge the gap between bench and clinic, more advanced cellular models are emerging, such as 3D tumor organoids that mimic the molecular features of the matched patient tissue. Multiple co-clinical trials have demonstrated similar drug responses between patients and their corresponding organoid model, implying a great potential of organoids in translational research. Cancer modeling and the establishment of a new preclinical platform for endometrial cancer will be discussed. This includes the establishment of patient-derived endometrial cancer organoids and organoid-based xenograft models. The models are profiled at DNA, RNA and protein levels, and molecular features mimic the corresponding patient tissue. The clinical relevance of these models is further evaluated by treatment with conventional chemotherapy and are currently used in testing of targeted therapies.

30.09.21, Emmet McCormack

Emmet McCormack, Department of Clinical Science / CCBIO, University of Bergen
Title: "Imaging preclinical tumour models: improving translational power"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Bjørn Tore Gjertsen

Bio: Emmet Mc Cormack is professor of pharmaceutics at the university of Bergen, adjunct professor at university of Tromsø and principal investigator at CCBIO. His research focusses primarily on development of preclinical models of cancer, particularly haematolgical malignancies, ovarian and pancreatic cancers, combined with the development of preclinical imaging modalities.

Abstract: The current dogma of rushing novel pharmaceuticals through inappropriate preclinical models is one of the major reasons for the limited clinical penetration of novel drugs. Despite this, the preclinical step in drug development is generally overlooked and models are chosen to fit the desired result, rather than using them as valuable tools to drive clinical development. Here I will present our groups ongoing work on development, characterisation and application of clinically relevant models and multimodal molecular imaging strategies, and how we believe judicious application of these technologies can expedite clinical development of novel therapeutics.

28.10.21, Sebastian Marwitz

Sebastian Marwitz, PI at the Lung Research Center, Borstel, Germany
Title: "A pathway and spatial biology approach to NSCLC"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Donald Gullberg

Abstract: 

Lung cancer is the leading cause of cancer-related death worldwide and many patients have despite recent developments an unfavorable prognosis which results in an ongoing need for new or combined therapeutic approaches targeting molecular pathways or cellular functions. The transforming growth factor beta (TGFB) pathway is pleiotropically involved in a multitude of processes at the cellular level and is considered as either pro or anti-tumorigenic, depending on the microenvironment and stage of carcinogenesis. The talk will be focused on TGFB signaling as well as spatial biology approaches in lung cancer.

Background:

• 2021: Principal Investigator at German Center for Lung Research; Spatial biology platform
• 2019: Scientist, Reseach Center Borstel – Leibniz Lung Center, Pathology
• 2018 – 2019: Visiting Researcher, Earle A Chiles Research Institute, Portland, OR, USA
• 2014 – 2018: Scientist, Reseach Center Borstel – Leibniz Lung Center, Pathology
• 2010 – 2014: PhD student, University of Lübeck
• 2008 – 2010: Msc, Christian-AlbrechtsUniversity Kiel
• 2005 – 2008: Bsc, University of Hamburg

Area of scientific interest: Pathway biology, spatial biology, cancer, lung diseases

Webpage: https://fz-borstel.de/index.php/en/

Linkedin:linkedin.com/in/sebastian-marwitz

Twitter: @MarwitzS

25.11.21, Emily Arner

Emily Arner, the Brekken lab, UT Southwestern Medical Center, Texas, USA
Title: "AXL-TBK1 driven nuclear AKT3 stabilizes snail/slug to promote EMT"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Jim Lorens

Dr. Emily Arner has received her PhD from UT Southwestern under the mentorship of Dr. Rolf Brekken and is a post-doctoral fellow in the lab of Dr. Kimryn Rathmell at Vanderbilt University Medical Center. Dr. Arner received an F99/K00 pre-doctoral to post-doctoral transition award from NCI.  She is interested in cancer cell plasticity/metastasis and finding novel targets to inhibit this process. 

Abstract: Epithelial-to-mesenchymal transition (EMT) contributes to tumor cell survival, immune evasion, migration, invasion, and therapy resistance. Across human cancer, tumors that are high grade, poorly differentiated, and have undergone EMT carry a worse prognosis with a higher likelihood of metastasis. AXL, a receptor tyrosine kinase, drives EMT and is implicated in tumor progression, metastasis, and therapy resistance in multiple cancer types including pancreatic cancer and breast cancer. TANK-binding kinase 1 (TBK1) is central to AXL-driven EMT yet, the mechanism of how TBK1 induces EMT remains unclear. Here, we report that AXL activation stimulates TBK1 binding and phosphorylation of AKT3. TBK1 activation of AKT3 drives binding to slug/snail, protection of snail/slug from proteasomal degradation and translocation of the complex to the nucleus. We show that nuclear translocation of AKT3 is required for AXL-driven EMT and metastasis. Congruently, nuclear AKT3 expression correlates with worse outcome in aggressive breast cancer. These results suggest that AKT3 nuclear activity is an important feature of AXL-driven epithelial plasticity and that selective AKT3 inhibition represents a novel therapeutic avenue for treating aggressive cancer.

16.12.21, Eystein Jansen

Eystein Jansen, UIB, Bjerknes Centre for Climate Research
Title: "Climate Research in Bergen - Strategic choices and challenges that paved the way"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Lars A. Akslen

In the last seminar of the year, we traditionally look at our research from a slightly different perspective. Perhaps there are somethings to learn from the strategic choices and challenges of another field?

Short bio: Professor in paleoclimatology, UiB, Academic Director Academia Europaea Bergen Knowledge Hub, Vice Director SapienCE Centre of Excellence, Member of the ERC Scientific Council. 
Research field: Climate change and climate dynamics. Past climate changes and role of the ocean in the climate system. 
Main achievements: Founding Director of the Bjerknes Centre for Climate Research, Coordinating Lead Author/Lead author of the Intergovernmental Panel on Climate Change (IPCC) 4th and 5th Assesment report. 
Motivation: Climate change is a key challenge for humanity with long-term impacts on all aspects of society and with potential negative ramifications on sustainability, ecosystems, economies, global health, peace and stability. After this challenge started to be recognised in the 1990-ies, Bergen has become an internationally recknowned centre for climate research. What is the current status for climate change and our efforts to mitigate them, and what were the factors behind the strong build-up of climate research here in Bergen? 

Abstract: Through the Bjerknes Centre for Climate Research, Bergen has become an international powerhouse for research on the climate system and the centre has within its 20 year history grown from 40 to 250 people. How did this development come about? What strategic decisions were behind this development and how has the Centre navigated in a field of mixed science and politics? What are the research challenges ahead and what is the status for our climate after the recent Glasgow climate summit?

09.01.20, Cancer in the News

CCBIO Special Seminar on the topic Cancer in the News. Speakers: Irmelin W Nilsen, UiB, Mille S Stenmarck, UiB, Tine Dommerud, Aftenposten and Knut Helland, UiB.
Time: 13:00
Place: Auditorium 4, BBB
Chairperson: Roger Strand

30.01.20, Johannes A. Eble

Johannes Eble, Institute of Physiological Chemistry and Pathobiochemistry, Cells in Motion Interfaculty Centre, University of Münster, Germany.
Title: "Beating around the bush, yet hitting the point: CAFs and vasculogenic mimicry vessels as anticancer targets"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

31.01.20, Iain Johnston

CCBIO Special Seminar with speaker Iain Johnston, Department of Mathematics, University of Bergen.
Title: "HyperTraPS: Learning pathways of disease (and cancer) progression from data."
Time: 15:15
Place: Auditorium H113, Hospital main building
Chairperson: Line Bjørge

20.02.20, Rameen Beroukhim

Rameen Beroukhim, Associate Professor of Medical Oncology at the Dana-Farber Cancer Institute and Harvard Medical School, and Associate Member of the Broad Institute.
Title: "Ancestry-associated features in cancer" 
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Camilla Krakstad

19.03.20, Akinyemi Ojesina - CANCELLED - 

Akinyemi Ojesina, Assistant Professor in the Department of Epidemiology at the University of Alabama at Birmingham (UAB), and an Adjunct Faculty Investigator at the HudsonAlpha Institute for Biotechnology.
Title: "Interplay of Microbial Influences and Genomic Alterations in Cancer"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Camilla Krakstad

30.04.20,  CANCELLED  

Title: TBA
Time: 14:30
Place: Auditorium 4, BBB
Chairperson:

28.05.20, JianFeng Chen

Professor JianFeng Chen, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.
Title: Regulation of immune cell trafficking by extracellular microenvironment
Time: 10:00
Place: Digital event, as a webinar in Zoom
Chairperson: Donald Gullberg.

11.06.20, Biaoyang Lin

Biaoyang Lin, Zhejiang University, China.
Title: "Critical roles of Chitinase 3-like 1 (CHI3L1) in inflammation, fibrosis and cancer"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Karl-Henning Kalland.

27.08.20, Ritva Heljasvaara

Ritva Heljasvaara, University of Oulu, Finland
Title: "Novel roles of collagens and a11 integrin in solid cancers"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Donald Gullberg

24.09.20, Joyce Bischoff

Joyce Bischoff, Professor of Surgery at Harvard Medical School with a primary appointment in the Vascular Biology Program and Department of Surgery at Boston Children’s Hospital.
Title: "Endothelial Anomalies in Vascular Tumors and Vascular Malformations"
Time: 14:00
Place: Digital event, as a webinar in Zoom
Chairperson: Elisabeth Wik

28.09.20, Hong Chen

CCBIO Special Seminar with speaker Hong Chen, Principal Investigator and Research Associate at Vascular Biology Program in Boston Children’s Hospital and Associate Professor at Harvard Medical School.
Title: “Endocytic Adaptor Protein Epsin is a Gatekeeper of the Quiescent Endothelium”
Time: 14:00
Place: Digital event, as a webinar in Zoom
Chairperson: Elisabeth Wik

30.09.20. Edward R. Smith

CCBIO Special Seminar with speaker Edward R. Smith, professor of neurosurgery at Harvard Medical School, the R. Michael Scott Chair in Neurosurgery at Boston Children’s Hospital and the Co-Director of the Cerebrovascular Surgery and Interventions Center.
Title: “Learning from tumor to treat stroke”
Time: 14:00
Place: Digital event, as a webinar in Zoom
Chairperson: Elisabeth Wik

01.10.20, Mike Rogers

CCBIO Special Seminar with Mike Rogers, Assistant Professor of Surgery, Harvard Medical School and Research Associate, Vascular Biology Program, Boston Children's Hospital.
Title: “Metastasis without a tumor”
Time: 14:00
Place: Digital event, as a webinar in Zoom
Chairperson: Elisabeth Wik

21.10.20, Mini Symposium on Endometrial Cancer

Title: "Endometrial cancer - How will new molecular knowledge influence the way we are treating our patients?"
Speakers: Alicia Leon del Castillo, Leiden, Alexandra Leary, Paris, Mansoor R Mirza, Copenhagen, Katrine Woie, Bergen, and Ane Gerda Zahl Eriksson, Oslo.
Time: 15:00 - 17.00
Place: Digital event, as a webinar in Zoom
Chairpersons: Camilla Krakstad and Line Bjørge

05.11.20, Huocong Huang

Speaker: Huocong Huang, Department of Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA
Title: Heterogeneity of cancer-associated fibroblasts in pancreatic cancer
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Jim Lorens

26.11.20, Fréderic Amant

Speaker: Professor Frédéric Amant, KU Leuven, Belgium and University of Amsterdam, the Netherlands.
Title: “Exploiting patient-derived preclinical models to identify biomarkers of response/resistance to therapy in (high grade) gynecological cancers”
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Camilla Krakstad

17.12.20, Jean Paul Thiery

Speaker: Jean Paul Thiery, Bioland Laboratory, Guangzhou Regenerative Medicine and Health, People’s Republic of China, and CCBIO, University of Bergen, Norway
Title: "Epithelial mesenchymal transition in carcinoma; therapeutic intervention"
Time: 14:30
Place: Digital event, as a webinar in Zoom
Chairperson: Agnete Engelsen

31.01.19, Cord Brakebusch
Cord Brakebusch, Biotech Research and Innovation Center (BRIC), University of Copenhagen, Denmark
Title:  "Epigenetic control of skin inflammation"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

06.02.19, Opening Symposium for the Hyperion Imaging System

CCBIO Special Seminar
Introduction to the research possibilities offered by the Hyperion Imaging System and examples of groundbreaking research in a high level keynote lecture by Dr. Dario Bressan, Head of the IMAXT Laboratory, CRUK Cambridge Institute, University of Cambridge, UK.
Link to info and abstracts.
Time: 13:00
Place: Auditorium 2, BBB

21.02.19, Diane Bielenberg

Diane Bielenberg, Assistant Professor, Vascular Biology Program, Boston Children’s Hospital, Department of Surgery, Harvard Medical School
Title: "Targeting Neuropilin Pathways to Inhibit Metastasis"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Elisabeth Wik

28.03.19, Gaoxiang Ge

Gaoxiang Ge, Shanghai institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China
Title: "Extracellular Matrix Remodeling in Tissue Homeostasis and Diseases"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

25.04.19, Øystein Rekdal

Øystein Rekdal, PhD, from Lytix Biopharma AS and The Arctic University of Norway, Tromsø
Title: "From Bench to Bedside with a first in class oncolytic peptide"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Bjørn Tore Gjertsen

23.05.19, Valerie Weaver

Valerie M. Weaver, Center for Bioengineering and Tissue Regeneration, Department of Surgery, University of California San Francisco (UCSF), San Francisco, CA, USA
Title: "Forcing tumor risk, transformation and aggression"
Place: Auditorium 4, BBB
Chairperson: Lars A. Akslen

06.06.19, Joanna Phillips

Joanna Phillips, UCSF Department of Neurological Surgery, Helen Diller Cancer Center, University of California San Francisco, CA, USA
Title: "GBM heterogeneity and extracellular regulation of oncogenic signaling"
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Marion Kusche-Gullberg

15.08.19, Innovation in Cancer Therapy

CCBIO Special Seminar. Speakers from Alden Cancer Therapy II, BerGenBio, DC Prime, KINN Therapeutics, Pfizer Norway, PubGene, SINTEF
Time: 12:30
Place: Auditorium 4, BB-building
Chairperson: Bjørn Tore Gjertsen

05.09.19, Sushma-Nagaraja Grellscheid

Sushma-Nagaraja Grellscheid, Associate Professor at the Department of Biological Sciences (BIO), University of Bergen, on the topic of RNA splicing.
Title: Understanding alternative splicing regulation in health and disease.
Time: Thursday September 5th at 14:30
Place: Auditorium 4, BB-building
Chairperson: Agnete Engelsen

18.09.19, Bruce Baguley

CCBIO Special Seminar with invited speaker Professor Bruce Baguley, University of Auckland, Auckland Cancer Society Research Centre, New Zealand
Title: Do human cancer cell lines really behave in the same way as clinical tumor material?
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Jim Lorens

26.09.19, Karl Kadler

Professor Karl Kadler, Director at the Wellcome Trust Centre for Cell-Matrix Research, Manchester, UK.
Title: Circadian control of the secretory pathway is a central mechanism in tissue homeostasis
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Donald Gullberg

04.10.19, Clinical trials in the future

CCBIO Mini Symposium. Speakers:
Fredrik Öhrn, Gothenburg: Design of clinical trials in the future
Donal Landers, Manchester: Digital experimental medicine in Oncology
Ketil Widerberg, Oslo: How artificial intelligence can improve clinical trials
The Norwegian Cancer Society: Use of patients as co-scientists / Decision aids
Time: 12:30
Place: Auditorium 4, BBB
Chairpersons: Line Bjørge and Hani Gabra.

31.10.19, Daniela Elena Costea

Daniela Elena Costea, Associated Investigator at CCBIO and Professor in tumor pathology, Department of Clinical Medicine, Faculty of Medicine, University of Bergen.
Title: “My sabbatical year at University of California, San Diego: Conditional expression of HPV16 E6/E7 onco-proteins and PIK3CA is sufficient to initiate HPV-associated carcinogenesis.”
Time: Thursday October 31st at 14:30
Place: Auditorium 4, BB-building
Chairperson: Lars A. Akslen

28.11.19, Speaker Curzio Ruegg

Professor Curzio Ruegg, Department of Medicine, Faculty of Science, University of Fribourg, Switzerland.
Title: Chemotherapy-induced immunological dormancy in breast cancer
Time: 14:30
Place: Auditorium 4, BBB
Chairperson: Oddbjørn Straume

12.12.19, Speaker Srinivas Malladi

CCBIO Special Seminar with Dr. Srinivas Malladi from the Department of Pathology, UT Southwestern, Dallas.
Title: Metastatic Latency - Models and Mechanisms
Time: 14:30
Place: Birkhaugsalen, 3rd floor Sentralblokken
Chairperson: James Lorens

12.12.19, Speaker Anders Goksøyr

Professor Anders Goksøyr, Department of Biological Sciences (BIO), University of Bergen.
Title: From feminized fish to obese mice – On endocrine and metabolic disruption in wildlife (and the lab). 
Time: 14:30
Place: Birkhaugsalen, 3rd floor Sentralblokken
Chairperson: Lars A. Akslen

01.02.18, Helge Wiig

Professor Helge Wiig, Department of Biomedicine, Faculty of Medicine, University of Bergen.
Time: 14:30
Chairperson: Lars A. Akslen
Title: "Lessons from a black box –The extracellular microenvironment and lymphatics in malignant tissue"

22.02.18, Ole Frithjof Norheim

Professor Ole Frithjof Norheim, physician and professor in medical ethics at the Department of Global Public Health and Primary Care, University of Bergen, and adjunct professor at the Department of Global Health and Population, Harvard TH Chan School of Public Health. Norheim is also a CCBIO associate investigator.
Time: 14:30
Chairperson: Roger Strand
Title: "Can biomarkers improve priority setting for new, expensive cancer drugs?"

22.03.18, Aaron Meyer

Assistant Professor Aaron Meyer, Department of Bioengineering, University of California at Los Angeles (UCLA).
Time: 14:30
Chairperson: Jim Lorens
Title: "Engineering more precise and potent TAM-targeted therapies"

26.04.18, Ian Mackenzie

Professor Ian Mackenzie from the Centre for Cell Biology and Cutaneous Research, the Blizard Institute, Queen Mary University of London.
Time: 14:30
Chairperson: Anne Christine Johannessen
Title: "Stem cell plasticity in head and neck cancers”

31.05.18, Aurora Martinez

Professor Aurora Martinez from the Department of Biomedicine, Faculty of Medicine, University of Bergen.
Time: 14:30
Chairperson: Camilla Krakstad
Title: "Pharmacological chaperoning: a potential treatment for genetic diseases, including some cancer syndromes."

07.06.18, Arvid Lundervold

Professor Arvid Lundervold from the Department of Biomedicine, Faculty of Medicine, University of Bergen.
Time: 14:30
Chairperson: Lars A. Akslen.
Title: "Computational imaging and machine learning in biomedicine"

30.08.18, Edna Cukierman

Edna Cukierman from the Department of Cancer Biology, Fox Chase Cancer Center, Philadelphia, PA, USA
Time: 14:30
Chairperson: Donald Gullberg.
Title: “Oncogenic synapses; stromal regulators of pancreatic cancer, metabolic support and innate immunosuppression”.  

19.09.18, Bruce Zetter, Merle Jacob, Lars A. Akslen and Roger Strand

CCBIO Special Seminar. Statements and reflection around the concept of excellence in research, incl. Harvard experiences. The seminar is organized as part of the CCBIO/Harvard INTPART partnership.
Time: 13.00
Title: "What is Scientfic Excellence?"

20.09.18, Michael Rogers and Bruce Zetter

CCBIO Special Seminar. The seminar is organized as part of the CCBIO/Harvard INTPART partnership.
Time: 09.00-12.00
Michael Rogers: "Validation of Anthrax Toxin Receptor 2 (Antxr2/CMG2) as a Target for Small Molecule Antiangiogenic Therapy."
Bruce Zetter: "Drug discovery for treating metastatic cancers."
Read more here.
 

27.09.18, Staffan Strömblad

Staffan Strömblad from the Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden
Time: 14:30
Chairperson: Donald Gullberg.
Title: "Novel cell-matrix adhesion structures"

03.10.18, Marsha Moses, Roland Jonsson, Roopali Roy, Anne Blanchard

CCBIO Special Seminar. The seminar is organized as part of the CCBIO/Harvard INTPART partnership.
Time: 13.00-16.00
Title "The Importance of Mentoring for Career Development". The seminar will consist of short presentations, panel discussion and interactions with the audience.
Note that location is not Aud. 4 at BBB this time, but B302 at Haukeland Univ. Hospital, Sentralblokka (main building), 3rd floor.

25.10.18, Arne Östman

Professor Arne Östman, Karolinska Institutet, Sweden, and also CCBIO international affiliated researcher.
Time: 14:30
Chairperson: Lars A. Akslen.
Title:  "Prognostic and response-predictive potential of tumor-stroma cell subsets."

29.11.18, Frédéric Amant

Frédéric Amant from the Center for Gynecologic Oncology, Netherlands Cancer Institute and Academic Medical Center, Amsterdam, The Netherlands. Professor Amant is also one of CCBIO's international affiliated researchers.
Time: 13:30 (Note: one hour earlier than usual)
Chairperson: Elisabeth Wik.
Title: "Cancer during pregnancy: a multidisciplinary approach in an INCIP research setting"

13.12.18 - Cedric Zeltz

Cedric Zeltz, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Time: 14:30
Note: Auditorium is Birkhaugsalen this time, at Sentralblokken (Haukeland University Hospital main building), 3rd floor.
Chairperson: Donald Gullberg.
Title: "Importance of the tumor microenvironment in non-small cell lung cancer: Examples of stromal proteins as potential therapeutical targets"

26.01.17, Norman J. Maitland

Norman J. Maitland, Department of Biology, University of York, UK.
Time: 14:30
Chairperson: Karl-Henning Kalland
Title: Modelling of cell fate and differentiation using tissue-derived human prostate epithelial cells

23.02.17, Øystein Bruserud

Øystein Bruserud, the Leukaemia Research Group, Department of Clinical Science, University of Bergen, Norway.
Time: 14:30
Chairperson: Bjørn Tore Gjertsen
Title: Classification and prognostication of acute myeloid leukemia – the past, the present and the future

16.03.17, Klas Wiman

Klas Wiman, the Department of Oncology-Pathology, Karolinska Institute, Sweden.
Chairperson: Bjørn Tore Gjertsen
Title: Targeting missense and nonsense mutant p53 in cancer – from molecular biology to the clinic

27.04.17, Robert Lafyatis - CANCELLED

Robert Lafyatis, Division of Rheumatology and Clinical Immunology,University of Pittsburgh Medical Center, USA.
Chairperson: Donald Gullberg
Title: Understanding cellular heterogeneity and fibrosis in systemic sclerosis skin using single cell RNAseq: SFRP2/DPP4 and FMO1/LSP1 define two major fibroblast populations in normal skin

11.05.17, Ulf Landegren

Ulf Landegren, Department of Immunology, Genetics and Pathology, Uppsala University, Sweden.
Chairperson: Rolf Kåre Reed
Title: Molecular tools for high performance analyses of proteins and nucleic acids

15.06.17, Kalle Sipila

Kalle Sipila, Centre for Stem Cells and Regenerative Medicine, King's College London, UK
Chairperson: Donald Gullberg
Title: Integrative genomic and functional analysis of human primary oral SCC cells

28.09.17, Nuno M. Coelho

Nuno M. Coelho, Matrix Dynamics Group, University of Toronto
Chairperson: Donald Gullberg
Title: DDR1 expression, collagen-dependent activation and signalling in cancer and tissue fibrosis

26.10.17, Jan Jacob Schuringa

Jan Jacob Schuringa, Department of Experimental Hematology, Cancer Research Centre Groningen, University Medical Centre Groningen, The Netherlands
Chairperson: Bjørn Tore Gjertsen
Title: Towards identification and targeting of leukemic stem cells and (epi)genetically distinct subclones using humanized niche xenograft mouse models

03.11.17, CCBIO Special Seminar, Rameen Beroukhim

Rameen Beroukhim, Department of Medical Oncology and Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Chairperson: Lars A. Akslen
Title: Structural variations in the cancer genome

23.11.17, Satu Mustjoki

Satu Mustjoki, Hematology Research Unit Helsinki, Department of Clinical Chemistry and Hematology, University of Helsinki and Helsinki University Hospital Comprehensive Cancer Center, Finland
Chairperson: Bjørn Tore Gjertsen
Title: Immunogenicity in hematological malignancies and immunological effects of targeted therapy

12.12.17, CCBIO Special Seminar, Randolph Watnick

Randolph Watnick, the Department of Surgery, Harvard Medical School and the Vascular Biology Program at Boston Children’s Hospital, USA.
Chairperson: Lars A. Akslen
Title: A novel mechanism governing tumor initiation and cancer stem cell function.

28.01.2016, Jean-Christophe Bourdon

Jean-Christophe Bourdon, Division of Cancer Research, Jacqui Wood Cancer Centre, University of Dundee, United Kingdom. 
Time: 14:30
Host: Bjørn Tore Gjertsen
Title: A decade of research on p53 sumarised.

25.02.2016, Olivier De Wever

Olivier De Wever, Laboratory of Experimental Cancer Research, Ghent University, Belgium.
Time: 14:30
Host: Donald Gullberg
Title: Communication in the tumor environment: diagnostic and therapeutic opportunities.

17.03.2016, Lutz P. Müller

Lutz P. Müller, MD; Clinic for Internal Medicine IV - Hematology / Oncology, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
Time: 14:30
Host: Donald Gullberg
Title: Growth promotion of colorectal cancer by mesenchymal stromal cells – when and how?

28.04.2016, Krister Wennerberg

Krister Wennerberg, Institute for Molecular Medicine Finland, University of Helsinki, Finland.
Time: 14:30
Host: Bjørn Tore Gjertsen
Title: Targeting cancers using individual systems medicine

26.05.2016 CCBIO Special Seminar

Speaker: Anne Blanchard and invited speakers
Time: 14:30
Host: Roger Strand
Title: Pharma and public cancer biomarker research in the transition from a blockbuster model to personalised medicine

16.06.2016, Gwendalyn J. Randolph

Gwendalyn J. Randolph, Division of Immunology, School of Medicine, Washington University in St. Lois, USA.
Time: 14:30
Host: Rolf K. Reed
Title: The Lymphatic vasculature in immunity and inflammatory disease

25.08.2016, Jonathan M. Irish

Jonathan M. Irish, Department of Cancer Biology, Vanderbilt University, Nashville, TN, USA
Time: 14:30, Auditorium 2.
Host: James Lorens
Title: Decoding human tumor microenvironments and healthy tissues using high dimensional single cell mass cytometry

29.09.2016, Herbert Schiller

Herbert Schiller, Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Helmholtz Zentrum München, Neuherberg, Germany
Time: 14:30, Auditorium 4.
Host: Donald Gullberg
Title: Multi-dimensional proteomics of the extracellular matrix in regeneration and fibrosis

27.10.2016

27.10.16 is cancelled, new date will be announced.
Time: 14.30, Auditorium 2
Hosts: Jan Håvik and Donald Gullberg

10.11.2016, CCBIO/OCC Network Meeting

A joint R&D Network titled "Personalized Cancer Therapy: Repurposing and in vitro drug screens"

Time: 10:30-17.00, aud. 4 till lunchbreak, aud. 2 after lunchbreak, BB-building.

01.12.2016, Jean-Paul Thiery

Jean-Paul Thiery, Centre for Cancer Biomarkers CCBIO, The University of Bergen, Yong Loo Lin School of Medicine National University of Singapore, University Paris Denis Diderot, Paris, France and Comprehensive Cancer Center Institut Gustave Roussy, Villejuif, France.
Title: "Epithelial cell plasticity in carcinoma: Harnessing mechanisms controlling biomechanics and progression of malignancy for the design of new therapeutic strategies"

Time: 14.30, Auditorium 4
Host: James B. Lorens

15.12.2016, Kenneth Hugdahl

Kenneth Hugdahl, Department of Biological and Medical Psychology, University of Bergen.
Excellence in science: Experience with ERC Advanced Grants
Time: 14:30, Auditorium 4.
Host: Lars Akslen

22.01.2015, John Cairns

John Cairns, Centre for Cancer Biomarkers (CCBIO), Department of Economics, University of Bergen, and Department of Health Services Research and Policy, London School of Hygiene and Tropical Medicine, United Kingdom.
Time: 14:30
Host: Roger Stand
Title: "Assessing the cost-effectiveness of bevacizumab in the treatment of metastatic melanoma"

19.02.2015, Anne Christine Johannessen

Anne Christine Johannessen, Centre for Cancer Biomarkers (CCBIO), Department of Clinical Medicine, University of Bergen.
Time: 14:30.
Host: Roger Stand
Title: "Oral cancer – ongoing research with special focus on tumour microenvironment"

26.03.2015, Hani Gabra

Hani Gabra, Department of Surgery and Cancer, Imperial College London, UK.
Time: 14:30.
Host: Helga Salvesen
Title: "OPCML, a tumour suppressor and novel systems regulator of tyrosine kinase signalling in ovarian and other cancers"

08.04.2015, Rik Thompson and John Haley

CCBIO special seminar with keynote speakers:

Rik Thompson, Queensland University of Technology, Brisbane Australia. See more introduction here to Rik Thompson.

John D. Haley, Stony Brook School of Medicine New York, SBU Cancer Center and SBU Proteomics Center.

Title: "Tumor plasticity and drug resistance”
Host: James Lorens.
Time: 14:00-16.00.

30.04.2015, Lorena Arranz

Lorena Arranz, Stem Cell Aging and Cancer Research Group, Department of Medical Biology, UiT The Arctic University of Norway, Tromsø

Title: Neuroglial dysregulation of the haematopoietic stem cell niche in myeloid leukaemias
Time: 14:30.
Host: Bjørn Tore Gjertsen

28.05.2015, Neil C. Henderson

Neil C. Henderson, MRC Centre for Inflammation Research, University of Edinburgh, UK.

Title: Targeting of pericytes and tissue myofibroblasts during organ fibrogenesis
Time: 14:30.
Host: Donald Gullberg

11.06.2015, Robert S. Kerbel

A combined CCBIO and BBB seminar

Robert S. Kerbel, Biological Sciences Platform, Sunnybrook Research Institute, Toronto, and Department of Medical Biophysics, University of Toronto, Canada

Title: Antiangiogenic therapeutics in oncology: Overview, update, and future directions
Time: 14:30
Host: Oleg Tsinkalovsky

27.08.2015, Roya Navab

Speaker: Roya Navab, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada

Title: Integrin α11β1 regulates cancer stromal stiffness and promotes tumorigenicity and metastasis in non-small cell lung cancer
Time: 14:30.
Host: Donald Gullberg

24.09.2015, Bruce Baguley

Speaker: Bruce Baguley, the Auckland Cancer Society Research Centre, The University of Auckland, New Zealand.

Title: The importance of being... a receptor tyrosine kinase.
Time: 14:30.
Host: Jim Lorens

15.10.2015, Matthew G. Krebs

Combined BBB and CCBIO Seminar.

Speaker: Matthew G. Krebs, Clinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, UK.

Title: Circulating biomarkers in early phase drug development for lung cancer.
Time: 14:30.
Host: Bjørn Tore Gjertsen

22.10.2015, Eric Sahai

Speaker: Eric Sahai, the Francis Crick Institute, London.

Title: The role of CAFs in therapy failure. Intravital imaging reveals how stroma dictates heterogeneous responses to targeted therapy.
Time: 14:30. (NB: In Auditorium 1 at BBB this time.)
Host: Donald Gullberg

26.11.2015, Patrick Schöffski

Speaker: Patrick Schöffski, the Laboratory of Experimental Oncology, the Department of Oncology, KU Leuven, Belgium.

Title: “Modelling mesenchymal malignancies: development of patient-derived xenografts of soft tissue sarcomas and gastrointestinal stromal tumours and in vivo-drug testing with direct implications for clinical research (bedside to bench and back)”
Time: 14:30.
Host: Bjørn Tore Gjertsen

17.12.2015, Jarle Breivik

Speaker: Jarle Breivik, Dept. of Behavioural Sciences in Medicine, Faculty of Medicine, University of Oslo

Title: "Cancer and aging: Facing realities and an uncertain future".
Time: 14:30.
Host: Lars A. Akslen

30.01.2014, Karl-Henning Kalland

Centre for Cancer Biomarkers (CCBIO), Department of Clinical Science, University of Bergen:
Heterogeneity and reprogramming plasticity of cancer cells – therapeutic possibilities.

20.02.2014: Roger Strand

Centre for Cancer Biomarkers (CCBIO) and Centre for the Study of the Sciences and the Humanities (SVT), University of Bergen:
Crossing the Styx

20.03.2014, Cédric Gaggioli

Institute for Research on Cancer and Aging (IRCAN), Nice, France:
Production of LIF cytokine by cancer cells and fibroblasts contributes to the establishment of a pro-invasive tumor microenvironment.

24.04.2014, Angela Nieto

Instituto de Neurociencias Consejo Superior de Investigaciones Científicas (CSIC)–Universidad Miguel Hernández (UMH), San Juan de Alicante, Spain:
Epithelial plasticity in development and disease

22.05.2014, Emmet McCormack

Department of Clinical Science, University of Bergen:
Pharmacological inhibition of the SIRT1 deacetylase with the small molecule inhibitor Tenovin-6 enhances ablation of FLT3-ITD+ LSC in combination with TKI treatment.

28.08.2014, Inge Jonassen

Centre for Cancer Biomarkers and Computational Biology Unit, Department of Informatics, University of Bergen:

Towards characterizing tumour microenvironments – experimental and computational approaches.

02.10.2014, Zena Werb

Department of Anatomy, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA:

New insights into mechanisms underlying breast cancer metastasis

30.10.2014, Boris Hinz

Laboratory of Tissue Repair and Regeneration, University of Toronto, Canada

Myofibroblasts can have it all: matrix mechanics, integrins, and pro-fibrotic growth factor activation

27.11.2014, Bjørn Tore Gjertsen

Department of Clinical Science, University of Bergen

Oncogene-addicted cancer: chronic myelogen leukemia as a model of a tyrosine kinase driven malignancy

18.12.2014, Arne Östman

Department of Oncology-Pathology, Karolinska Institutet,
Stockholm, Sweden

Impact of PDGFR-regulated fibroblasts and pericytes on tumor progression, prognosis and drug response

29.8.2013: Lars A. Akslen

Director of CCBIO.

CCBIO: Current concepts and challenges in cancer research.

26.9.2013: Helga B. Salvesen

Co-Director of CCBIO.

Individualized therapy based on molecular alterations in gynecologic cancer.

31.10.2013: Oddbjørn Straume

CCBIO. Angiogenic biomarkers in malignant melanoma.
 

25.11.2013: Sonja Loges

University Hospital Hamburg-Eppendorf, University Comprehensive Cancer. Center II, Medical Clinic & Institute of Tumor Biology. CCBIO Special Lecture:
Role of Gas6 - Axl axis in malignant interaction with the host.
 

28.11.2013: Bjørn Tore Gjertsen

CCBIO. Phosphoprotein signaling in acute myeloid leukemia.

About the CCBIO Seminars
The CCBIO Seminar series covers the full spectrum of research areas within CCBIO's research focus. Talks are held mainly by invited international speakers. Before each semester, it is possible to suggest speakers for the next semester of CCBIO Seminars. CCBIO provides financing for inviting speakers. The CCBIO Seminars series is part of a master- and a PhD course programme, BMED380 and CCBIO902 respectively, and is open to all that are interested in biomedical and biosciences research. Registration to the courses can be done at StudentWeb (for students requiring ECTS). Audience not requiring ECTS registration, does not need to register.

Place, time, transport
The seminars are normally held at BBB, Jonas Lies vei 91, 3rd floor, in auditorium 4, usually at 14.30 one Thursday per month. The auditorium is up the stairs on the right hand side after passing the reception at the BBB main entrance or is straight on when coming via the pedestrian bridge from Haukeland Hospital. For transport from downtown Bergen, you can consider using the Campusbussen.

CCBIO Special Seminars: Please inform us about your guests
If a renowned scientist within a relevant field is going to visit your group and would be willing to give a talk under the umbrella of the CCBIO Special Seminars, please let us know. If approved as a Special Seminar, CCBIO will provide part of the financing and assist with marketing. Contact Donald Gullberg if you have suggestions for speakers for the CCBIO Seminars at the scheduled dates or for a CCBIO Special Seminar outside these dates.

If you want to suggest a speaker to any of the open slots, please get in touch with Carina Strell per email. In the email, you should include the following information: A short motivation, topic suggestion, a short bio of 4-5 lines, affiliation, CV or publication list and webpage of the speaker. CCBIO will select speakers among those suggested, using the following criteria: scientific excellence, topic of general interest, topic diversity. For CCBIO Special Seminars, please include what date you suggest for the talk. We prefer you to arrange for booking of one of the auditoria in the BB-Building for the CCBIO Special Seminar.

Travel costs and reimbursement
CCBIO will contribute with costs for the selected speakers up to 50% of the total costs for travel, lodging and sustenance/dinner. CCBIO's total contribution is capped at 15.000 NOK for overseas speakers and 8.000 NOK for European speakers. The rest will need to be covered by your funds. For flights, hotel and reimbursement you need to interact with your own department's administration according to your own department's procedures. After all the costs have been paid and you know the full amount, your financial officers can forward CCBIO’s part of the cost to CCBIO's financial coordinator Sara.Olsen@uib.no.

Your responsibilities as a host
If CCBIO agrees to your proposed guest speaker, you will be acting as host.

This involves sending the following to Eli.Vidhammer@uib.no :

• The short bio of 4-5 lines, affiliation, webpage of the speaker with bio and publication list, immediately after your candidate has been accepted by CCBIO.
• A seminar title (as soon as possible after accepting, it can be changed later) as well as an abstract (approx. ½ a page; to be provided at the latest two weeks before the seminar).
• You must inform the speaker 1) to give a general introduction at the start, 2) that the audience is composed of students, postdocs and faculty with diverse backgrounds, 3) to limit the lecture to approx. 45 min.

In terms of logistics, following up your guest and the seminar itself, you need to:

• Act as a liaison between the speaker and your own department's administration regarding transport and accommodation for the guest as well as reimbursement of travelling costs.
• Arrange a social program for the guest during his/her stay.
• Setup of the ppt.-presentation in the auditorium together with the speaker in due time before the start of the seminar. In case you prefer technical assistance, please contact Torstein Ravnskog at least one day in advance.
• Ask the speaker to give a general introduction at the beginning of the talk placing his/her work/results into a broader perspective. Informing him/her that the lecture should not greatly exceed 45 minutes.
• Chair the seminar which includes introducing the speaker and leading the discussion.
• Snap some photos during the seminar, or make sure someone else does, for use in the CCBIO Annual Report, to be sent to Eli.Vidhammer@uib.no along with a short text about the seminar (topic, speaker, interesting points raised in the talk...)

If a renowned scientist within a relevant field is going to visit your group and would be willing to give a talk under the umbrella of CCBIO's Special Seminars, please let us know. If approved as a Special Seminar, CCBIO will provide financing and assist with marketing as well as ordering pizza for an informal get-together following the talk. 

Contact Carina Strell if you have suggestions for speakers for the CCBIO Seminars at the scheduled dates and Geir Olav Løken if you would like to suggest a CCBIO Special Seminar outside these dates. In the email, you should include the following information: Affiliation, CV or publication list and webpage of the speaker and a short motivation. CCBIO will select the speakers among those suggested, using the following criteria: scientific excellence, topic of general interest, topic diversity.

Please see the menu point "Call for proposals, financing and information for hosts" above for practicalities.

For CCBIO Special Seminars you or your group need to book of one of the auditoria in the BB-Building (preferably Auditorium 4, or elsewhere if the BBB auditoria are not available) and to ensure that you have access to the room you have booked.