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The Silent Danger of Pancreatic Disease

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The video introduces Dr. Danny Ingle, an assistant professor at the Salk Institute who specializes in the early detection and treatment of pancreatic cancer. With a background that includes degrees from Northwestern University and UC San Diego, as well as recent publications in *Cell Stem Cell*, she utilizes patient-derived pancreatic organoids to study disease progression and develop personalized therapies. Her journey into this specific field was deeply personal; after initially studying genetics, her focus shifted rapidly toward cancer research following the diagnosis of both her father and uncle with pancreatic cancer within a decade of each other. This family history provided her with a strong motivation to understand why such diseases are so difficult to treat and detect early enough to save lives. Pancreatic cancer presents a unique challenge because it is relatively uncommon, with only about 60,000 new cases expected annually in the United States, yet it carries an extremely high mortality rate. The primary obstacle lies in screening; testing the general population for this condition is not considered cost-effective by insurance companies due to the low incidence of the disease compared to its severity. Furthermore, current diagnostic methods often yield false positives because pancreatitis and pancreatic cancer share very similar biomarkers but have vastly different outcomes. Distinguishing between these two conditions typically requires a biopsy rather than simple blood tests or CT scans, which is invasive and difficult for patients undergoing symptoms like stomach pain caused by tumors pressing on nerves or other organs. The difficulty in early detection stems from the biological timeline of tumor growth within the pancreas. Mathematical modeling and autopsy studies indicate that it takes approximately 10 to 12 years for a pancreatic cancer lesion to form, yet this slow progression does not mean the disease is easy to catch; rather, patients usually do not experience symptoms until the tumor has grown large enough to cause physical pressure or pain. By the time these noticeable signs appear, there are already trillions of cancer cells in the body, and roughly 85% of patients have developed metastatic spread where the cancer has traveled to other parts of the body. Consequently, once a patient presents with symptoms indicating advanced disease, it is often too late for effective intervention, highlighting the critical need for better early detection platforms like organoids that Dr. Ingle's research aims to advance.
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our guest for the evening, Dr. Danny Ingle. Dr. Ingle is an assistant professor at the Salk Institute specializing in the early detection and treatment of pancreatic cancer. She received her BA from Northwestern University in biology and Asian studies and her PhD in biology from the University of California, San Diego. She recently published a paper in Cell Stem Cell describing a new platform using patient-derived pancreatic organoids for disease study and development of personalized treatments. And I think this sounds like a really exciting direction. And I I we've talked about organoids a lot on the show over the years, but I think it's really important to get somebody who's really involved in the research and use of this kind of a platform to come and talk with us about how it works, the challenges, all these things. Thank you for joining me, Dr. Ingle. >> Lovely to be here. Thanks for having me. >> You're welcome. So, first off, before we get into this study and the nut of uh of the nitty-gritty of everything that you've been working on, how did you actually come to start studying pancreatic disorders in the first place? >> Uh so, I would say that my journey has actually not been super typical for a scientist. I actually went to college for music uh before switching to biology and a lot of that had to do with with like, you know, using creative part of my brain, but also figuring out that while I might not be the best test taker, I'm really good in the lab. And so, for >> [laughter] >> for how I got into the pancreas, you know, I I I started off working in genetics, but then I uh I moved into cancer pretty quickly because my dad was diagnosed with pancreatic cancer. About 10 years later, my uncle was diagnosed with pancreatic cancer. And so, for me, it's been kind of a personal motivation combined with this really scientific drive to understand why is it so hard to treat and find early. >> Why is it so hard? >> [laughter] >> I know, right? I mean, I wish I had all the answers to that. I think that you know, if you if you zoom back out and you look at the incidence of pancreatic cancer, it's it's relatively uncommon. So, there'll be about like 60 to 70,000 new cases this year. Um and so, it's a low incidence cancer, but it has a very high mortality. And so, I think part of the problem is that means that screening the general population is not what insurance companies would call cost-effective. Um which is a hard like you know, statistic and and how you know, calculus for for me to learn since I'm a patient advocate, but at the same time, you know, um false positive do do harm. And I think that's that's the big challenge. And so, that's also how I got started in pancreatitis because that's a major false positive for any test that's trying to detect pancreatic cancer. So, they're two very similar diseases in terms of their biomarkers, but their outcomes are are very very different. >> So, when somebody has is coming in with stomach pains and has the the etiology, the the presentation of certain aspects, it could be pancreatitis or pancreatic can- cancer and there's no way of knowing the difference until you go into the pancreas itself. >> That's right. And so, in order to confirm a diagnosis, it's not like you know, a simple blood test or CT scan. It it does require [clears throat] a biopsy to really understand what what the lesion is. And I think there's there's multiple challenges here. Um pancreatic cancer itself for mathematical modeling and autopsy studies takes 10 to 12 years to form. So, it's not that it moves too fast for us to find it. It's It's by the time that there are symptoms, those symptoms are usually caused because the tumor is gotten big enough to impinge on on other organs or you're starting to get um pain that's from a a tumor pressing on a nerve. And so I think at that point there's already trillions of cancer cells in your body and at that point 85% of the patients already have metastatic spread. >> Oh, wow. So once it's there, it's it's at a at a really late point. >> Yeah.