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Original Publication Date
2018
Document Type
Presentation
Abstract
Kranthi Chougoni’s research aims to improve outcomes for patients with pancreatic cancer, one of the most aggressive and deadly forms of cancer, where the average survival time after diagnosis is only two to four months. His work focuses on a protein called CtBP (C-terminal binding protein), which functions as a signaling regulator in cells. When CtBP behaves abnormally, it can drive uncontrolled cell growth and tumor formation. Previous studies have linked CtBP to several cancers, but its role in pancreatic cancer was unknown. By analyzing patient samples, Chougoni and his team discovered elevated CtBP activity in pancreatic tumors, prompting them to test chemical inhibitors designed to block CtBP function. Using mouse models that closely mimic human pancreatic cancer, they observed that reducing CtBP activity led to normal pancreatic tissue and longer survival. These promising findings suggest that targeting CtBP could slow tumor progression and extend patient survival, offering new hope for improving treatment in one of the most challenging cancers to cure.
Transcription
We might have all experienced the burden of cancer either directly or indirectly through our friends or family. In spite of advancement in medicine, research and science pancreatic cancer poses serious challenges. You will all be surprised if I tell you that pancreatic cancer patient once diagnosed survival is only 2-4 months, this is really bad. Human system for us to be hale and healthy we are made of cells and proteins which are like signaling networks. If our proteins work well, they direct the cells to divide or not divide. Whenever our proteins start behaving abnormally that's when situation of cancer arises. One such protein of our interest is CtBP (C-terminal binding Protein). We did some earlier studies with CtBP and it was as a causative factor in various cancers, when it comes to pancreatic cancer no, there was no finding so far about CtBP. We went back in time and looked at patient samples,then it was shown that pancreatic tumor samples showed high CtBP protein activity, then we decided to explore CtBP, because we have developed chemical compounds which inhibit CtBPs protein activity that could lead to tumor regression. For which we developed a mice model to test, why mice? because human genome is 80% similar to mouse. First we chose a mice model and these mice develop pancreatic tumors just like the humans. These mice if you see, the one on the left you can wild type can synthesis full protein and the other one can synthesize only half protein. When I cut the pancreas and looked at the sections, I found that when half protein was synthesized pancreas is normal and they survived longer, when full protein was synthesized they developed tumors and died early. This means if we can inhibit this protein activity through a chemical inhibitor we could possibly regress pancreatic tumors. So, we chose mice induced tumors and treat them with inhibitors. Once mice study becomes successful we want to translate it to humans. Bright side is even though we want to cure pancreatic cancer completely, but if we can extend the patients survival for 4 months to another 6 months that would be a great achievement.
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Transcription
Comments
Entrant, 4th Annual VCU 3MT® Competition, held on October 18-19, 2018.