Heterocellular interactions in the tumour microenvironment

Cancelled due to illness

The next CanCell seminar scheduled for Friday 1st of March at 14:00 hrs is unfortunately cancelled due to illness

Invited Speaker: Claus Jørgensen, Systems Oncology Group Leader, Cancer Research UK Manchester Institute

Introducing 'young shot' talk: 

Royjar Khezri, Tumour-Host Biology Group, CanCell, UiO & Department of Molecular Cell Biology, ICR, OUH



Tumours are complex systems defined by heterotypic interactions between cancer and stromal cells. Pancreatic ductal adenocarcinoma is characterised by an extensive desmoplastic reaction, which on average constitutes ~85% of the tumour volume. Tumour cells co-opt host cells, such as fibroblasts and myeloid cells, which leads to a pathological remodelled extracellular matrix and cell to cell interactions ultimately changing tumour cell function and response to therapy. The rules governing tumour-stromal interactions are currently not clearly defined. Recently we described an oncogene-driven signalling axis, whereby cancer cells co-opt stromal fibroblasts to alter secreted signals ultimately leading to increased signalling pathway activation in the cancer cells (Tape et al Cell 2016). To further our understanding of tumour-stroma interactions, and to better understand the impact of tumour cell diversity, we established a model of intra-tumoral heterogeneity in PDA. Intriguingly we find both differences in stromal fibroblast co-option across individual clones and ensuing tumour cell response to reciprocal signals.  Together our data suggests that clonal tumour cell populations differentially engage nearby stromal cell populations, which may further complicate selection of therapies.

Published Jan. 25, 2019 4:39 PM - Last modified Feb. 20, 2019 7:54 AM