TY - JOUR
T1 - Acquired resistance of non-small cell lung cancer to epidermal growth factor receptor tyrosine kinase inhibitors
AU - Nurwidya, Fariz
AU - Takahashi, Fumiyuki
AU - Murakami, Akiko
AU - Kobayashi, Isao
AU - Kato, Motoyasu
AU - Shukuya, Takehito
AU - Tajima, Ken
AU - Shimada, Naoko
AU - Takahashi, Kazuhisa
N1 - Funding Information:
This work was supported by the Ministry of Education, Culture, Sports, Science and Technology of Japan .
PY - 2014/3
Y1 - 2014/3
N2 - Activation of epidermal growth factor receptor (EGFR) triggers anti-apoptotic signaling, proliferation, angiogenesis, invasion, metastasis, and drug resistance, which leads to development and progression of human epithelial cancers, including non-small cell lung cancer (NSCLC). Inhibition of EGFR by tyrosine kinase inhibitors such as gefitinib and erlotinib has provided a new hope for the cure of NSCLC patients. However, acquired resistance to gefitinib and erlotinib via EGFR-mutant NSCLC has occurred through various molecular mechanisms such as T790M secondary mutation, MET amplification, hepatocyte growth factor (HGF) overexpression, PTEN downregulation, epithelial-mesenchymal transition (EMT), and other mechanisms. This review will discuss the biology of receptor tyrosine kinase inhibition and focus on the molecular mechanisms of acquired resistance to tyrosine kinase inhibitors of EGFR-mutant NSCLC.
AB - Activation of epidermal growth factor receptor (EGFR) triggers anti-apoptotic signaling, proliferation, angiogenesis, invasion, metastasis, and drug resistance, which leads to development and progression of human epithelial cancers, including non-small cell lung cancer (NSCLC). Inhibition of EGFR by tyrosine kinase inhibitors such as gefitinib and erlotinib has provided a new hope for the cure of NSCLC patients. However, acquired resistance to gefitinib and erlotinib via EGFR-mutant NSCLC has occurred through various molecular mechanisms such as T790M secondary mutation, MET amplification, hepatocyte growth factor (HGF) overexpression, PTEN downregulation, epithelial-mesenchymal transition (EMT), and other mechanisms. This review will discuss the biology of receptor tyrosine kinase inhibition and focus on the molecular mechanisms of acquired resistance to tyrosine kinase inhibitors of EGFR-mutant NSCLC.
KW - Acquired resistance
KW - Epidermal growth factor receptor (EGFR)
KW - Non-small cell lung cancer (NSCLC)
KW - Tyrosine kinase inhibitors
UR - http://www.scopus.com/inward/record.url?scp=84896047823&partnerID=8YFLogxK
U2 - 10.1016/j.resinv.2013.07.007
DO - 10.1016/j.resinv.2013.07.007
M3 - Review article
C2 - 24636263
AN - SCOPUS:84896047823
VL - 52
SP - 82
EP - 91
JO - Respiratory Investigation
JF - Respiratory Investigation
SN - 2212-5345
IS - 2
ER -
