Disrupting tumour defences in pancreatic cancer

At Barts Cancer Institute in London, Worldwide Cancer Research scientist, Dr Angus Cameron, is working hard to find ways to pull down cancers defences and make it vulnerable to treatment. By understanding how healthy cells in and around the tumour support the growth of cancer, his team hope to uncover new treatments for pancreatic cancer.

Our lab is focused on the interaction between normal cells and cancer cells. And we are specifically interested in pancreatic cancer. The biology of pancreatic cancer is quite unusual because tumours are largely made up of fibrotic tissue, which is full of a normal cell type called fibroblasts. In fact, cancer cells often only make up 10-20% of the mass of a pancreatic tumour.

Dr Angus Cameron Barts Cancer Institute, United Kingdom

In pancreatic tumours, these fibroblasts are hijacked by the cancer cells and help them to spread into the nearby tissue.

They also act as a protective shield, preventing drugs from being able to penetrate into the tumour, and preventing cells of the immune system from accessing the tumour where they can help to eradicate cancer cells.

Pancreatic cancer is often diagnosed at an advanced stage when it is too late for treatments to have any real positive effect. Patients often only survive for a year or so after their diagnosis, and in many cases, the patient may only live a couple of months or even weeks. This grim picture hasn’t changed in 40 years.

Dr Cameron's project, which started in April 2018 and was funded by a partnership between Worldwide Cancer Research and Pancreatic Cancer Research Fund, is trying to specifically target the activation of fibroblasts by cancer cells in order to help make treatments such as immunotherapy and chemotherapy work better for pancreatic cancer patients

Reflecting on the achievements of the past year, Dr Cameron told us that there are three ways in which they’ve really made progress.

The first thing we’ve discovered is precisely how a type of healthy cell, called fibroblasts, are able to communicate with cancer cells, and importantly, how this changes the way the tumour behaves.

We’ve also fully established our pancreatic tumour model in mice, which we are now using to test how cutting off the communication between fibroblasts and cancer cells will affect the growth of real tumours. This is a critical step for taking our findings towards the clinic.

And finally, we’re very excited because we’ve got our drug discovery pipeline up and running. In the next few weeks, we will start screening tens of thousands of chemical compounds to look for new drugs that specially cut off the communication between fibroblasts and cancer cells. Some of these compounds will be the precursors for drugs that we will one day be able to test further and hopefully take into clinical trials.

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