Delineating and exploiting the stress phenotype of cancer

Marc Mendillo, PhD, assistant professor, Department of Biochemistry and Molecular Genetics, Northwestern University, Feinberg School of Medicine

When Mar 20, 2018 from 11:00 AM to 12:00 PM (EST / UTC-400)
Where 1131 Bioinformatics Auditorium
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This event is hosted by Jill Dowen, PhD. 


A major strategy in anti-cancer efforts is to define the oncogenic signaling networks that are aberrantly activated in malignancies and to develop therapeutics that target essential nodes in these networks. Despite the dependence of tumors on such oncogenic pathways, the efficacy of these targeted therapies is often limited by the development of acquired resistance. Besides the mutated oncogenic protein, cancer cells are dependent on non-mutated, non-oncogene systems. These non-oncogene targets offer a fundamentally different therapeutic strategy aimed at the common and unusual biological requirements that characterize the malignant phenotype, rather than at any one type of oncogenic lesion. One prominent example of this "non-oncogene addiction" is the dependence of cancer cells on the protein homeostasis (proteostasis) network. Here, I will discuss our recent advances in understanding how the regulatory cir­cuitry of this ancient pro-survival network is co-opted and rewired in the cells of the tumor ecosystem to support malig­nancy. In addition, I will discuss our efforts to reveal vulnerabilities dependent on the oncogenic activation of the regulators of the proteostasis network that we can exploit as a therapeutic strategy to target cancers of diverse origin.