MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically
Details
Publication Year 2020-09-10,Volume 11,Issue #1,Page 4527
Journal Title
Nature Communications
Publication Type
Journal Article
Abstract
Evasion of programmed cell death represents a critical form of oncogene addiction in cancer cells. Understanding the molecular mechanisms underpinning cancer cell survival despite the oncogenic stress could provide a molecular basis for potential therapeutic interventions. Here we explore the role of pro-survival genes in cancer cell integrity during clonal evolution in non-small cell lung cancer (NSCLC). We identify gains of MCL-1 at high frequency in multiple independent NSCLC cohorts, occurring both clonally and subclonally. Clonal loss of functional TP53 is significantly associated with subclonal gains of MCL-1. In mice, tumour progression is delayed upon pharmacologic or genetic inhibition of MCL-1. These findings reveal that MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically.
Publisher
NPG
Research Division(s)
Blood Cells And Blood Cancer
PubMed ID
32913197
Open Access at Publisher's Site
https://doi.org/10.1038/s41467-020-18372-1
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2020-10-02 10:28:02
Last Modified: 2020-10-02 10:36:02
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