Events by this organizer

Abstract:
Phenotypic heterogeneity in cancer is often caused by different patterns of genetic alterations. Understanding such phenotype-genotype relationships is fundamental for the advance of personalized medicine. In this talk, I will present a computational method, named NETPHIX (NETwork-to-PHenotype association with eXclusivity) to identify subnetworks of genes whose genetic alterations are associated with drug response or other continuous cancer phenotypes. Leveraging interaction information among genes and properties of cancer mutations such as mutual exclusivity, we model the problem as a variant of connected set cover and obtain a subnetwork of associated genes using integer linear program (ILP) optimization. Applied to a large-scale drug screening dataset, NETPHIX uncovered gene modules significantly associated with responses for many drugs. We show that the identified modules provide important insights into drug action and can also be leveraged to suggest drug combinations.

Bio:
Dr. Yoo-Ah Kim is a staff scientist in the National Center for Biotechnology Information at National Institutes of Health (NCBI/NLM/NIH). Her current research focuses on algorithmic approaches in cancer network biology. Before joining NIH in 2008, she received her PhD degree in Computer Science from the University of Maryland, College Park in 2005 and was with the CSE department at the University of Connecticut, working on combinatorial optimization and graph algorithms.

Presenter: Dr. Arjun Raj from the Perelman School of Medicine, UPenn.

Abstract:Anti-cancer therapies can often kill the vast majority of tumor cells but a few rare cells remain and grow despite treatment. Non-genetic variability has emerged as a potential contributor to this behavior. However, it remains unclear what drives this variability, and what the ultimate phenotypic consequences are. We have developed a set of new single cell barcoding technologies (Rewind and FateMap) that have enabled us to show how different types of variability can translate into different drug-resistant outcomes upon treatment with drugs. In particular, we found that even a genetically and epigenetically clonal population harbors enough latent variability to produce an entire ecosystem of different resistant cell types, and show preliminary evidence suggesting that these cell types can contribute to tumor development in distinct ways.

Meeting details:

Join Zoom Meeting
https://umd.zoom.us/j/91843071125

Meeting ID: 918 4307 1125
One tap mobile
+13017158592,,91843071125# US (Washington D.C)
+19294362866,,91843071125# US (New York)

Dial by your location
+1 301 715 8592 US (Washington D.C)
+1 929 436 2866 US (New York)
+1 312 626 6799 US (Chicago)
+1 346 248 7799 US (Houston)
+1 669 900 6833 US (San Jose)
+1 253 215 8782 US (Tacoma)
Meeting ID: 918 4307 1125
Find your local number: https://umd.zoom.us/u/abASyXtwsH

Thanks,
Sushant