Hyperactivation of ERK by multiple mechanisms is toxic to RTK-RAS mutation-driven lung adenocarcinoma cells

Hyperactivation of ERK by multiple mechanisms is toxic to RTK-RAS mutation-driven lung adenocarcinoma cells

Synthetic lethality results when mutant KRAS and EGFR proteins are co-expressed in human lung adenocarcinoma (LUAD) cells, revealing the biological basis for mutual exclusivity of KRAS and EGFR mutations. We have now defined the biochemical events responsible for the toxic effects by combining pharm...

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Bibliographic Details
Main Authors: Arun M Unni, Bryant Harbourne, Min Hee Oh, Sophia Wild, John R Ferrarone, William W Lockwood, Harold Varmus
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2018-11-01
Series:eLife
Subjects:
KRAS
EGFR
DUSP6
mutual exclusivity
synthetic lethality
feedback inhibition
Online Access:https://elifesciences.org/articles/33718

Internet

https://elifesciences.org/articles/33718

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