Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

Igor Bado; Xiang H.F. Zhang

doi:10.1016/j.ccell.2019.12.008

Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

Igor Bado, Xiang H.F. Zhang

Research output: Contribution to journal › Comment/debate

5 Scopus citations

Abstract

Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.

Original language	English
Pages (from-to)	1-2
Number of pages	2
Journal	Cancer Cell
Volume	37
Issue number	1
DOIs	https://doi.org/10.1016/j.ccell.2019.12.008
State	Published - 13 Jan 2020
Externally published	Yes

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title = "Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition",

abstract = "Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.",

author = "Igor Bado and Zhang, {Xiang H.F.}",

note = "Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",

year = "2020",

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T2 - YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

AU - Bado, Igor

AU - Zhang, Xiang H.F.

PY - 2020/1/13

Y1 - 2020/1/13

N2 - Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.

AB - Therapeutic resistance is a major challenge in cancer treatment. In this issue of Cancer Cell, Kurppa et al. demonstrated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and MEK. This was mediated by the YAP/TEAD pathway, which drives epigenomic reprogramming and EMT to counteract apoptosis.

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U2 - 10.1016/j.ccell.2019.12.008

DO - 10.1016/j.ccell.2019.12.008

M3 - Comment/debate

C2 - 31951560

AN - SCOPUS:85078015194

VL - 37

SP - 1

EP - 2

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 1

ER -

Senesce to Survive: YAP-Mediated Dormancy Escapes EGFR/MEK Inhibition

Abstract

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