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EGFR

EGFR Exon 20 Insertion Mutations in Advanced Non-Small-Cell Lung Cancer: Current Status and Perspectives

[Biomarker Research] The authors systematically review the recent clinical research of and treatments used for epidermal growth factor receptor ex20ins mutations, summarize the latest data on emerging therapies, and discuss future prospects and treatments.

Loss of KMT5C Promotes EGFR Inhibitor Resistance in NSCLC via LINC01510-Mediated Upregulation of MET

[Cancer Research] Researchers identified that loss of an epigenetic factor, lysine methyltransferase 5C (KMT5C), drove resistance of NSCLC to multiple EGFR inhibitors, including erlotinib, gefitinib, afatinib, and osimertinib.

Janssen Announces Health Canada Approval of RYBREVANT® (amivantamab), the First and Only Targeted Treatment for Patients with Non-Small Cell Lung Cancer with EGFR Exon...

[Janssen Pharmaceutical Companies] The Janssen Pharmaceutical Companies of Johnson & Johnson announced that Health Canada has issued a Notice of Compliance with Conditions approving RYBREVANT®, a fully-human, bispecific antibody, for the treatment of adult patients with locally advanced or metastatic NSCLC.

Betacellulin Promotes Tumor Development and EGFR Mutant Lung Cancer Growth by Stimulating the EGFR Pathway and Suppressing Apoptosis

[iScience] Knockdown of betacellulin inhibited the growth of EGFR-mutant human lung adenocarcinoma cells in culture and their tumor-forming ability in mice.

Targeting Nicotinamide N-Methyltransferase Overcomes Resistance to EGFR-TKI in Non-Small Cell Lung Cancer Cells

[Cell Death Discovery] Using iTRAQ-based quantitative proteomics analysis, we identified that nicotinamide N-methyltransferase was significantly increased in epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)-resistant NSCLC cells.

The Candida albicans Toxin Candidalysin Mediates Distinct Epithelial Inflammatory Responses through p38 and EGFR-ERK Pathways

[Science Signaling] In cultured oral epithelial cells, candidalysin activated the MAPK p38, which resulted in heat shock protein 27 (Hsp27) activation, IL-6 release, and EGFR phosphorylation without affecting the induction of c-Fos.

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