Primary and acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer: An update

Ayodele Ayoola, Amit Barochia, Kiran Belani, Chandra Belani

Research output: Contribution to journalReview article

51 Citations (Scopus)

Abstract

Epidermal growth factor receptor (EGFR) is a critical target in the treatment of nonsmall cell lung cancer (NSCLC). The mutations involving EGFR are more prevalent in patients of Asian ancestry, women, never smokers, and those with adenocarcinoma histology. Primary mechanism of resistance to EGFR-TKIs includes in frame insertion mutation in exon 20, de novo T790M mutation also on exon 20, activating mutations in KRAS, loss of PTEN, and amplification of c-MET whereas acquired resistance results from development of secondary alteration in ATP domain of T790M. There are many novel targeting agents in development to overcome resistance to EGFR TKIs.

Original languageEnglish (US)
Pages (from-to)433-446
Number of pages14
JournalCancer Investigation
Volume30
Issue number5
DOIs
StatePublished - Jun 1 2012

Fingerprint

Epidermal Growth Factor Receptor
Non-Small Cell Lung Carcinoma
Protein-Tyrosine Kinases
Mutation
Exons
Insertional Mutagenesis
Histology
Adenocarcinoma
Adenosine Triphosphate
Therapeutics

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

@article{4c2511aa7a1b4401ad175bbfdf335b84,
title = "Primary and acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer: An update",
abstract = "Epidermal growth factor receptor (EGFR) is a critical target in the treatment of nonsmall cell lung cancer (NSCLC). The mutations involving EGFR are more prevalent in patients of Asian ancestry, women, never smokers, and those with adenocarcinoma histology. Primary mechanism of resistance to EGFR-TKIs includes in frame insertion mutation in exon 20, de novo T790M mutation also on exon 20, activating mutations in KRAS, loss of PTEN, and amplification of c-MET whereas acquired resistance results from development of secondary alteration in ATP domain of T790M. There are many novel targeting agents in development to overcome resistance to EGFR TKIs.",
author = "Ayodele Ayoola and Amit Barochia and Kiran Belani and Chandra Belani",
year = "2012",
month = "6",
day = "1",
doi = "10.3109/07357907.2012.666691",
language = "English (US)",
volume = "30",
pages = "433--446",
journal = "Cancer Investigation",
issn = "0735-7907",
publisher = "Informa Healthcare",
number = "5",

}

Primary and acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer : An update. / Ayoola, Ayodele; Barochia, Amit; Belani, Kiran; Belani, Chandra.

In: Cancer Investigation, Vol. 30, No. 5, 01.06.2012, p. 433-446.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Primary and acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer

T2 - An update

AU - Ayoola, Ayodele

AU - Barochia, Amit

AU - Belani, Kiran

AU - Belani, Chandra

PY - 2012/6/1

Y1 - 2012/6/1

N2 - Epidermal growth factor receptor (EGFR) is a critical target in the treatment of nonsmall cell lung cancer (NSCLC). The mutations involving EGFR are more prevalent in patients of Asian ancestry, women, never smokers, and those with adenocarcinoma histology. Primary mechanism of resistance to EGFR-TKIs includes in frame insertion mutation in exon 20, de novo T790M mutation also on exon 20, activating mutations in KRAS, loss of PTEN, and amplification of c-MET whereas acquired resistance results from development of secondary alteration in ATP domain of T790M. There are many novel targeting agents in development to overcome resistance to EGFR TKIs.

AB - Epidermal growth factor receptor (EGFR) is a critical target in the treatment of nonsmall cell lung cancer (NSCLC). The mutations involving EGFR are more prevalent in patients of Asian ancestry, women, never smokers, and those with adenocarcinoma histology. Primary mechanism of resistance to EGFR-TKIs includes in frame insertion mutation in exon 20, de novo T790M mutation also on exon 20, activating mutations in KRAS, loss of PTEN, and amplification of c-MET whereas acquired resistance results from development of secondary alteration in ATP domain of T790M. There are many novel targeting agents in development to overcome resistance to EGFR TKIs.

UR - http://www.scopus.com/inward/record.url?scp=84861042428&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84861042428&partnerID=8YFLogxK

U2 - 10.3109/07357907.2012.666691

DO - 10.3109/07357907.2012.666691

M3 - Review article

C2 - 22571344

AN - SCOPUS:84861042428

VL - 30

SP - 433

EP - 446

JO - Cancer Investigation

JF - Cancer Investigation

SN - 0735-7907

IS - 5

ER -