TY - JOUR
T1 - The importance of molecular profiling in predicting response to epidermal growth factor receptor family inhibitors in non-small-cell lung cancer
T2 - Focus on clinical trial results
AU - Tsao, Anne S.
AU - Papadimitrakopoulou, Vassiliki
N1 - Funding Information:
This work was supported by Boehringer Ingelheim Pharmaceuticals Inc. Writing and editorial assistance was provided by Staci Heise, PhD, of MedErgy, which was contracted by Boehringer Ingelheim Pharmaceuticals for these services. The authors meet criteria for authorship as recommended by the International Committee of Medical Journal Editors, were fully responsible for all content and editorial decisions, and were involved at all stages of manuscript development. The authors received no compensation related to the development of the manuscript.
PY - 2013/7
Y1 - 2013/7
N2 - In recent years, the epidermal growth factor receptor (EGFR) family has become a key focus of non-small-cell lung cancer biology and targeted therapies, such as the reversible EGFR tyrosine kinase inhibitors erlotinib and gefitinib. Initially, response to these agents was associated with certain demographic and clinical characteristics; subsequently, it was discovered that these subgroups were more likely to harbor specific mutations in the EGFR gene that enhanced tumor response. However, the presence of these mutations does not equate to therapeutic success. Other aspects of EGFR family signaling, including other types of EGFR mutations, EGFR protein expression, EGFR gene amplification, mediators of downstream signaling, and other receptors with similar downstream pathways may all play a role in response or resistance to treatment. The identification of these and other molecular determinants is driving the development of novel therapies designed to achieve improved clinical outcomes in patients.
AB - In recent years, the epidermal growth factor receptor (EGFR) family has become a key focus of non-small-cell lung cancer biology and targeted therapies, such as the reversible EGFR tyrosine kinase inhibitors erlotinib and gefitinib. Initially, response to these agents was associated with certain demographic and clinical characteristics; subsequently, it was discovered that these subgroups were more likely to harbor specific mutations in the EGFR gene that enhanced tumor response. However, the presence of these mutations does not equate to therapeutic success. Other aspects of EGFR family signaling, including other types of EGFR mutations, EGFR protein expression, EGFR gene amplification, mediators of downstream signaling, and other receptors with similar downstream pathways may all play a role in response or resistance to treatment. The identification of these and other molecular determinants is driving the development of novel therapies designed to achieve improved clinical outcomes in patients.
KW - Epidermal growth factor receptor tyrosine kinase inhibitor
KW - Gene amplification
KW - Hepatocyte growth factor receptor
KW - Kirsten rat sarcoma viral oncogene homolog
KW - Phosphoinositide-3-kinase
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U2 - 10.1016/j.cllc.2013.01.001
DO - 10.1016/j.cllc.2013.01.001
M3 - Review article
C2 - 23582282
AN - SCOPUS:84878774249
SN - 1525-7304
VL - 14
SP - 311
EP - 321
JO - Clinical Lung Cancer
JF - Clinical Lung Cancer
IS - 4
ER -