Non-small cell lung cancer--genetic predictors
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
23733083
DOI
10.5507/bp.2013.034
Knihovny.cz E-resources
- MeSH
- Drug Resistance, Neoplasm MeSH
- ErbB Receptors drug effects genetics MeSH
- Oncogene Proteins, Fusion drug effects genetics MeSH
- Protein Kinase Inhibitors pharmacology MeSH
- Humans MeSH
- Biomarkers, Tumor genetics MeSH
- Lung Neoplasms drug therapy genetics MeSH
- Carcinoma, Non-Small-Cell Lung drug therapy genetics MeSH
- Proto-Oncogene Proteins c-met drug effects genetics MeSH
- Proto-Oncogene Proteins p21(ras) MeSH
- Proto-Oncogene Proteins drug effects genetics MeSH
- ras Proteins drug effects genetics MeSH
- Protein-Tyrosine Kinases drug effects genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- EML4-ALK fusion protein, human MeSH Browser
- ErbB Receptors MeSH
- Oncogene Proteins, Fusion MeSH
- Protein Kinase Inhibitors MeSH
- KRAS protein, human MeSH Browser
- Biomarkers, Tumor MeSH
- Proto-Oncogene Proteins c-met MeSH
- Proto-Oncogene Proteins p21(ras) MeSH
- Proto-Oncogene Proteins MeSH
- ras Proteins MeSH
- ROS1 protein, human MeSH Browser
- Protein-Tyrosine Kinases MeSH
BACKGROUND: Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer that is the leading cause of cancer-related mortality worldwide. Several predictive markers have been found in NSCLC patients to date but only a few are currently used for tailored therapy. METHODS AND RESULTS: PubMed and Web of Science online databases were used to search review and original articles on the most important predictive markers in NSCLC. CONCLUSION: EGFR activating mutations (exons 18 to 21) and EML4-ALK rearrangement are clinically important markers able to select NSCLC patients which benefit from EGFR or ALK tyrosine kinase inhibitors (gefitinib, erlotinib, crizotinib). Other markers, such as KRAS mutation, EGFR T790M mutation and C-MET amplification, are responsible for resistance to these inhibitors. Overcoming of this resistance as well as discovery of new potential markers and inhibitors is the main goal of ongoing research and clinical trials in NSCLC.
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