RAS-mediated tumor stress adaptation and the targeting opportunities it presents

Authors

Alexandra Redding, Thomas Jefferson UniversityFollow
A E Aplin, Thomas Jefferson UniversityFollow
Elda Grabocka, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

2-1-2022

Comments

This article is the author’s final published version in Disease models & mechanisms, Volume 15, Issue 2, February 2022, Pages 1-13.

The published version is available at https://doi.org/10.1242/dmm.049280. Copyright © Published by The Company of Biologists Ltd.

Abstract

Cellular stress is known to function in synergistic cooperation with oncogenic mutations during tumorigenesis to drive cancer progression. Oncogenic RAS is a strong inducer of a variety of pro-tumorigenic cellular stresses, and also enhances the ability of cells to tolerate these stresses through multiple mechanisms. Many of these oncogenic, RAS-driven, stress-adaptive mechanisms have also been implicated in tolerance and resistance to chemotherapy and to therapies that target the RAS pathway. Understanding how oncogenic RAS shapes cellular stress adaptation and how this functions in drug resistance is of vital importance for identifying new therapeutic targets and therapeutic combinations to treat RAS-driven cancers.

Recommended Citation

Redding, Alexandra; Aplin, A E; and Grabocka, Elda, "RAS-mediated tumor stress adaptation and the targeting opportunities it presents" (2022). Department of Cancer Biology Faculty Papers. Paper 187.
https://jdc.jefferson.edu/cbfp/187

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.

PubMed ID

35147163

Language

English