Novel mechanism of resistance to targeted therapies in lung cancer

Walter Wang; David P. Carbone; Rajeswara Rao Arasada

doi:10.1080/23723556.2018.1551015

Novel mechanism of resistance to targeted therapies in lung cancer

Walter Wang, David P. Carbone, Rajeswara Rao Arasada

Research output: Contribution to journal › Comment/debate

3 Scopus citations

Abstract

We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.

Original language	English
Article number	1551015
Journal	Molecular and Cellular Oncology
Volume	6
Issue number	1
DOIs	https://doi.org/10.1080/23723556.2018.1551015
State	Published - Jan 2 2019

Keywords

EGFR
EGFR TKI
Notch3
cancer stem cells
drug persister cells

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10.1080/23723556.2018.1551015

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title = "Novel mechanism of resistance to targeted therapies in lung cancer",

abstract = "We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.",

keywords = "EGFR, EGFR TKI, Notch3, cancer stem cells, drug persister cells",

author = "Walter Wang and Carbone, {David P.} and Arasada, {Rajeswara Rao}",

note = "Publisher Copyright: {\textcopyright} 2018, {\textcopyright} 2018 The Author(s). Published with license by Taylor & Francis Group, LLC.",

year = "2019",

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T1 - Novel mechanism of resistance to targeted therapies in lung cancer

AU - Wang, Walter

AU - Carbone, David P.

AU - Arasada, Rajeswara Rao

PY - 2019/1/2

Y1 - 2019/1/2

N2 - We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.

AB - We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.

KW - EGFR

KW - EGFR TKI

KW - Notch3

KW - cancer stem cells

KW - drug persister cells

UR - http://www.scopus.com/inward/record.url?scp=85059325062&partnerID=8YFLogxK

U2 - 10.1080/23723556.2018.1551015

DO - 10.1080/23723556.2018.1551015

M3 - Comment/debate

AN - SCOPUS:85059325062

SN - 2372-3556

VL - 6

JO - Molecular and Cellular Oncology

JF - Molecular and Cellular Oncology

IS - 1

M1 - 1551015

ER -

Novel mechanism of resistance to targeted therapies in lung cancer

Abstract

Keywords

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