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Intratumor heterogeneity of EGFR expression mediates targeted therapy resistance and formation of drug tolerant microenvironment.
Nat Commun
January 2025
Translational Immunology Research Program (TRIMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are commonly used to treat non-small cell lung cancers with EGFR mutations, but drug resistance often emerges. Intratumor heterogeneity is a known cause of targeted therapy resistance and is considered a major factor in treatment failure. This study identifies clones of EGFR-mutant non-small cell lung tumors expressing low levels of both wild-type and mutant EGFR protein.
View Article and Find Full Text PDFDecoding the Clinical and Molecular Signatures of EGFR Common, Compound, and Uncommon Mutations in NSCLC: A Brief Report.
J Thorac Oncol
December 2024
Oncology Service, University Hospital Geneva, Geneva, Switzerland. Electronic address:
Introduction: EGFR mutations are key oncogenic drivers in lung adenocarcinoma (LUAD), predominantly affecting Asian, nonsmoking, and female populations. Although common mutations, such as exon 19 deletions and L858R, respond well to tyrosine kinase inhibitors (TKIs), uncommon EGFR mutations and compound variants exhibit variable treatment responses. This study aims to compare clinical characteristics and molecular profiles of patients with common, uncommon, and compound EGFR mutations, assessing their implications for therapy outcomes.
View Article and Find Full Text PDFReceptor Tyrosine Kinase Fusion-Mediated Resistance to EGFR TKI in EGFR-Mutant NSCLC: A Multi-Center Analysis and Literature Review.
J Thorac Oncol
November 2024
Department of Thoracic, Head, and Neck Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas. Electronic address:
Article Synopsis
- - Drug resistance in EGFR-mutant non-small cell lung cancer (NSCLC) is complicated by mechanisms like pathway reactivation and fusion of receptor tyrosine kinases (RTKs), leading to challenges in treatment with tyrosine kinase inhibitors (TKIs).
- - A study involving multiple institutions analyzed 27 patients with RTK fusions identified through genetic testing, focusing on their response to dual TKI therapy, with results showing a 24% objective response rate and an 80% disease control rate overall.
- - The majority of patients had ALK or RET fusions, and those who received dual TKI treatment had a slightly lower response rate (21.4%) but no new side effects were reported, suggesting this approach
Loss of CDKN2A Enhances the Efficacy of Immunotherapy in EGFR Mutant Non-Small Cell Lung Cancer.
Cancer Res
November 2024
Shenyang Pharmaceutical University, Shenyang, China.
Mutant epidermal growth factor receptor (EGFR) is a common driver of non-small cell lung cancer (NSCLC). While mutant EGFR has been reported to limit the efficacy of immunotherapy, a subset of EGFR mutant NSCLC patients benefit from treatment with immune checkpoint inhibitors. A better understanding of how co-occurring genomic alterations in oncogenic driver genes impact immunotherapy efficacy may provide a more complete understanding of cancer heterogeneity and identify biomarkers of response.
View Article and Find Full Text PDFAmplification in Small-Cell Lung Cancer-Transformed Tumors Following Resistance to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors.
Cancers (Basel)
October 2024
Division of Molecular Therapeutics, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
Background/objectives: Although tyrosine kinase inhibitors (TKIs) targeting EGFR-activating mutations significantly improved the outcome of EGFR-mutant NSCLC, resistance inevitably emerges. Despite the heterogeneity of these resistance mechanisms, many induce activation of MAPK signaling in the presence of EGFR-TKIs. While gene amplification is identified as a resistance mechanism that activates MAPK signaling by directly interacting with RAS, little is known about its clinicopathologic characteristics.
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