Use of K-Ras as a predictive biomarker for selecting anti-EGF receptor/pathway treatment

Yixing Jiang, Heath Mackley, Hua Cheng, Jaffer A. Ajani

Research output: Contribution to journalReview article

10 Citations (Scopus)

Abstract

Ras protein is a downstream regulator of multiple cellular receptor tyrosine kinases, mediating cell growth, transformation and maintenance of the malignant phenotype in several human cancers. Oncogenic gain-of-function mutations in ras frequently occur in colorectal cancer, non-small-cell lung cancer and pancreatic cancers. Recent clinical studies of colorectal cancer have revealed that the therapeutic efficacy of cetuximab, a chimeric monoclonal antibody against EGF receptor, depends on the presence of wild-type k-ras. Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib. These observations have provoked an interest in utilizing K-Ras as a predictive biomarker, allowing clinicians to direct the therapy of cancer patients based on their mutational status of the k-ras gene.

Original languageEnglish (US)
Pages (from-to)535-541
Number of pages7
JournalBiomarkers in Medicine
Volume4
Issue number4
DOIs
StatePublished - Aug 1 2010

Fingerprint

Biomarkers
Epidermal Growth Factor Receptor
Non-Small Cell Lung Carcinoma
Colorectal Neoplasms
Cells
ras Proteins
Mutation
ras Genes
Receptor Protein-Tyrosine Kinases
Cell growth
Pancreatic Neoplasms
Protein-Tyrosine Kinases
Neoplasms
Genes
Monoclonal Antibodies
Maintenance
Phenotype
Therapeutics
Growth
Clinical Studies

All Science Journal Classification (ASJC) codes

  • Drug Discovery
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Jiang, Yixing ; Mackley, Heath ; Cheng, Hua ; Ajani, Jaffer A. / Use of K-Ras as a predictive biomarker for selecting anti-EGF receptor/pathway treatment. In: Biomarkers in Medicine. 2010 ; Vol. 4, No. 4. pp. 535-541.
@article{6d7b1cf2878849319e252a66825302cc,
title = "Use of K-Ras as a predictive biomarker for selecting anti-EGF receptor/pathway treatment",
abstract = "Ras protein is a downstream regulator of multiple cellular receptor tyrosine kinases, mediating cell growth, transformation and maintenance of the malignant phenotype in several human cancers. Oncogenic gain-of-function mutations in ras frequently occur in colorectal cancer, non-small-cell lung cancer and pancreatic cancers. Recent clinical studies of colorectal cancer have revealed that the therapeutic efficacy of cetuximab, a chimeric monoclonal antibody against EGF receptor, depends on the presence of wild-type k-ras. Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib. These observations have provoked an interest in utilizing K-Ras as a predictive biomarker, allowing clinicians to direct the therapy of cancer patients based on their mutational status of the k-ras gene.",
author = "Yixing Jiang and Heath Mackley and Hua Cheng and Ajani, {Jaffer A.}",
year = "2010",
month = "8",
day = "1",
doi = "10.2217/bmm.10.74",
language = "English (US)",
volume = "4",
pages = "535--541",
journal = "Biomarkers in Medicine",
issn = "1752-0363",
publisher = "Future Medicine Ltd.",
number = "4",

}

Use of K-Ras as a predictive biomarker for selecting anti-EGF receptor/pathway treatment. / Jiang, Yixing; Mackley, Heath; Cheng, Hua; Ajani, Jaffer A.

In: Biomarkers in Medicine, Vol. 4, No. 4, 01.08.2010, p. 535-541.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Use of K-Ras as a predictive biomarker for selecting anti-EGF receptor/pathway treatment

AU - Jiang, Yixing

AU - Mackley, Heath

AU - Cheng, Hua

AU - Ajani, Jaffer A.

PY - 2010/8/1

Y1 - 2010/8/1

N2 - Ras protein is a downstream regulator of multiple cellular receptor tyrosine kinases, mediating cell growth, transformation and maintenance of the malignant phenotype in several human cancers. Oncogenic gain-of-function mutations in ras frequently occur in colorectal cancer, non-small-cell lung cancer and pancreatic cancers. Recent clinical studies of colorectal cancer have revealed that the therapeutic efficacy of cetuximab, a chimeric monoclonal antibody against EGF receptor, depends on the presence of wild-type k-ras. Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib. These observations have provoked an interest in utilizing K-Ras as a predictive biomarker, allowing clinicians to direct the therapy of cancer patients based on their mutational status of the k-ras gene.

AB - Ras protein is a downstream regulator of multiple cellular receptor tyrosine kinases, mediating cell growth, transformation and maintenance of the malignant phenotype in several human cancers. Oncogenic gain-of-function mutations in ras frequently occur in colorectal cancer, non-small-cell lung cancer and pancreatic cancers. Recent clinical studies of colorectal cancer have revealed that the therapeutic efficacy of cetuximab, a chimeric monoclonal antibody against EGF receptor, depends on the presence of wild-type k-ras. Additional studies in non-small-cell lung cancer have suggested that the k-ras mutation may be a negative predictor of response to the EGF receptor tyrosine kinase inhibitors erlotinib and gefitinib. These observations have provoked an interest in utilizing K-Ras as a predictive biomarker, allowing clinicians to direct the therapy of cancer patients based on their mutational status of the k-ras gene.

UR - http://www.scopus.com/inward/record.url?scp=77955651659&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77955651659&partnerID=8YFLogxK

U2 - 10.2217/bmm.10.74

DO - 10.2217/bmm.10.74

M3 - Review article

C2 - 20701442

AN - SCOPUS:77955651659

VL - 4

SP - 535

EP - 541

JO - Biomarkers in Medicine

JF - Biomarkers in Medicine

SN - 1752-0363

IS - 4

ER -