LustgartenLIVE! The Best of 2021: Research Highlights

On December 14, 2021, Lustgarten Foundation leadership came together for a special year-end review of the progress we’ve made toward transforming pancreatic cancer into a curable disease. They also gave viewers a sneak peek into exciting research plans for 2022. Presenters included: David Tuveson, MD, PhD, Director of the Lustgarten Foundation Dedicated Research Lab at Cold Spring Harbor Laboratory (CSHL) Cancer Center; Elizabeth Jaffee, MD, Director, Lustgarten Clinical Accelerator Initiative; Linda Tantawi, CEO, Lustgarten Foundation; Andrew Rakeman, PhD VP of Research, Lustgarten Foundation.

Webinar Q&A

What is the risk of getting pancreatic cancer, especially for family members?

Pancreas cancer as a disease seems to have a familial predisposition 10% to maybe 20% of the time. A patient with pancreas cancer about that often would say, “I had a first degree relative who has also had pancreas cancer.” Studies of these families have led us to understand more about the causes of pancreas cancer. Some of the genes are in the cancer cells. Some of the genes are actually in other cells that can cause inflammation. We’re always trying to find new genes involving the process because it gives us an understanding, and that understanding leads to therapeutic options, as well as new early detection and prevention opportunities.

What role does the environment play on the risk of getting pancreatic cancer?

When someone says they’ve had two family members who themselves were unrelated with pancreas cancer, it could mean that there’s an environmental exposure. Environmental exposures in patients with pancreatic cancer include tobacco consumption and obesity.

Are there advancements being made for people who are at risk to either try to prevent or intercept pancreatic cancer?

We’re thinking, can we vaccinate people who might be at high risk for pancreatic cancer? It becomes a little difficult because when you look at models of pancreatic cancer development, there are a lot of early, inflammatory changes after the first genetic alteration, which is usually mutated KRAS, mutated in pre-malignant lesions that lead to pancreatic cancer. So we figured that’s a great target because we don’t have a viral infection to target. So this is acting like the “viral infection.” What we’re trying to do is not only target mutated KRAS in a vaccine, but also create that vaccine so that it has signals that can alter the developing microenvironment of the tumor. The study, which is the first of its kind, got FDA approved. It’s going to be available to a very limited population right now. The FDA still wants to show safety. So right now, we’re only allowed to test patients who have a family history and already have a pre-malignant lesion we can see on a radiographic type of exam. We know from patients who have used this vaccine that it’s safe and that we can see those killer T Cells developing after we vaccinate. We’re hoping to eventually bring this to a wider group of people if it works well.

Is there anything to say about the role of fibrosis in the development of pancreatic cancer?

The role that fibrosis plays in the pathogenesis of the disease is under intensive study. The fibrosis itself makes it difficult for blood to perfuse the tumor, and that has been tested in several clinical trials. If you were to reduce the pressure in the tumor, would patients do better? There’s ample evidence that when you reduce the pressure in the tumor, you get more things in, like more medicines. So we think fibrosis plays a role in drug delivery, and we know it plays a role in modifying the immune response in the cancer cell response. So right know it’s kind of a sign that there’s something wrong in the tumor and what we’re trying to do is instead of just getting rid of fibrosis is change it so that the part of it that makes it hard for the immune system to work or makes it easy for the cancer cells to proliferate changes. There are a lot of investigations in this space.

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