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Mr. Hemant Kocher

Research Institution: Centre for Tumour Biology - Barts Cancer Institute

Award: £114,000   Duration: 3 years

Project Title: FGF Signalling in pancreatic cancer

Research Aims: To date, the pancreatic cancer stroma (the characteristic scar tissue around this cancer) has not been targeted, in the search for a potential cure. This scar tissue may serve as a ‘rich soil’ in which the cancer (seed) grows (seed and soil hypothesis). Also, the scar tissue may prevent the patient’s own immune system, as well as anti-cancer agents, from reaching and killing the cancer cells. We have identified that the cells within this ‘soil’ produce local hormones, which can benefit the cancer growth. We have identified one such family of related molecules called the FGF (Fibroblast Growth Factor(s)), of which FGF-10 in particular may drive the tumour growth. How FGF acts on cancer cells is not well understood.

In this proposal we shall use various complementary biological methods in the laboratory to establish conclusively the importance of FGF signalling pathway in pancreatic cancer and confirm these findings in patient samples obtained with ethical approval. These studies will help us design a range of putative ‘druggable’ targets to be used in the medium to long term (5-10 years) to abrogate the abnormal FGF signalling. Thus if we can modify these local hormones to affect cancer growth and allow anti-cancer agents to act upon the cancer cells, potentially we may find a cure for pancreatic cancer. We believe that therapies designed to stop FGF working properly could stop pancreatic cancers developing into a fatal disease.

The goal of the study is to show that FGF signalling pathways are a useful target for directing anti-cancer therapies, by co-targeting the stroma.