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 language | English (US) |
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Pages (from-to) | 535-541 |
Number of pages | 7 |
Journal | Biomarkers in Medicine |
Volume | 4 |
Issue number | 4 |
DOIs | |
State | Published - Aug 2010 |
All Science Journal Classification (ASJC) codes
- Drug Discovery
- Clinical Biochemistry
- Biochemistry, medical