Title

Manipulating CtBP2 Protein Activity to Target Pancreatic Ductal Adenocarcinoma [online video]

Streaming Media

Original Publication Date

2018

Document Type

Presentation

Comments

Entrant, 4th Annual VCU 3MT® Competition, held on October 18-19, 2018.

Abstract

Manipulating CtBP2 protein activity to target pancreatic ductal adenocarcinoma

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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