Emerging Molecular Dependencies of Mutant EGFR-Driven Non-Small Cell Lung Cancer.
Cells
; 10(12)2021 12 16.
Article
in En
| MEDLINE
| ID: mdl-34944063
ABSTRACT
Epidermal growth factor receptor (EGFR) mutations are the molecular driver of a subset of non-small cell lung cancers (NSCLC); tumors that harbor these mutations are often dependent on sustained oncogene signaling for survival, a concept known as "oncogene addiction". Inhibiting EGFR with tyrosine kinase inhibitors has improved clinical outcomes for patients; however, successive generations of inhibitors have failed to prevent the eventual emergence of resistance to targeted agents. Although these tumors have a well-established dependency on EGFR signaling, there remain questions about the underlying genetic mechanisms necessary for EGFR-driven oncogenesis and the factors that allow tumor cells to escape EGFR dependence. In this review, we highlight the latest findings on mutant EGFR dependencies, co-operative drivers, and molecular mechanisms that underlie sensitivity to EGFR inhibitors. Additionally, we offer perspective on how these discoveries may inform novel combination therapies tailored to EGFR mutant NSCLC.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Carcinoma, Non-Small-Cell Lung
/
Drug Resistance, Neoplasm
/
Molecular Targeted Therapy
Limits:
Humans
Language:
En
Journal:
Cells
Year:
2021
Document type:
Article
Affiliation country: