M.F. Bijlsma PhD

PhD M.F. Bijlsma

Positions

PhD Candidate, Associate Professor, Research Associate

Main activities

Research

Specialisation

The biology of upper GI cancers

Focus of research

My lab studies the biology that underlies the growth and therapy resistance of pancreatic and esophageael cancer. Models in my lab range from cell culture systems, mouse experiments, biobanking and the analysis of predictive and prognostic markers and profiles in large cohorts. Most of these have been generated through our live biobanking. 

One of the most typical features of upper GI cancers is the abundance of non-cancerous cells and material – the stroma. The stroma exerts both tumor-promoting as well as -limiting properties. We aim to identify which signals mediate critical tumor-stroma crosstalk, and whether we can use this to target tumor growth and drug resistance. In addition, we develop blood-borne markers to stratify patients for stroma-targeting treatments.

Many events that shape the developing embryo are regulated by the Hedgehog proteins. In the adult body, activity of these proteins is limited, but reactivation of the pathway is thought to contribute to pancreatic cancer. Several lines of research in my lab deal with the production and transport, but also the reception and interpretation of this ligand.

To construct the relevant experimental models needed to study cancer, I have founded the AMC biobank pancreatic carcinoma – BioPAN and co-coordinate the esophageal BiOES biobank. For these biobanks we accrue and store blood samples, tissue, and clinical data. Analyses on these materials include expression profiling and measurements of serum markers. BioPAN closely collaborates with the nation-wide PancreasParel biobank of which I am the coordinator, and the AMC-VUmc Liquid Biopsy Center that I co-head. Our expression profiling efforts have enabled us to identify subgroups of patients that differ in their clinical outcome and other clinically important parameters. 

The lethality of pancreatic cancer relies on the presence of so called cancer stem cells. Current tools to identify these cells have serious shortcomings. We have adapted tracing methods to trace the offspring of a single cell in tumors grown from these cells. These allow us to study the population of cancer stem cells that are thought to contribute to pancreatic cancer growth.