Sep 15, 2021 · Osimertinib (AZD9291 or TAGRISSO) is a promising and approved third-generation EGFR tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation.

Osimertinib (AZD9291 or TAGRISSO ™) is a promising and approved third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations or …

Epidermal growth factor receptor (EGFR) signaling pathways leading to G1/S cell cycle progression activated by EGF activation. Depicted are the RAS-RAF-MEK-ERK MAPK and PI3K-AKT-mTOR pathways. EGF activation of the EGFR induces receptor dimerization and transphosphorylation of the C-terminal domain.

This review presents an overview of recent findings on various epigenetic and post-transcriptional modifications of the epidermal growth factor receptor (EGFR), which activates the oncogenes RAS and MYC.

Here, we report the functions of STAMBPL1 in modulating the stability of the protein and mRNA of the epidermal growth factor receptor (EGFR). STAMBPL1 deficiency attenuates liver tumorigenesis in vitro and in vivo. STAMBPL1 removes K63-linked ubiquitin chains from EGFR to avoid lysosome degradation upon EGF stimulation.

Sep 15, 2021 · Osimertinib (AZD9291 or TAGRISSO) is a promising and approved third-generation EGFR tyrosine kinase inhibitor (TKI) for treating patients with advanced non–small cell lung cancer (NSCLC) harboring EGFR-activating mutations or the resistant T790M mutation. However, the inevitable emergence of acquired resistance limits its long-term efficacy.

MYC is a master transcription factor critical for mediating oncogenic signal transduction and has been implicated in EGFRi resistance, suggesting that MYC targeting may overcome multiple EGFRi resistance mechanisms.

Jan 14, 2025 · This review focuses on the deregulation of EGFR, RAS, and MYC expression caused by (epi)genetic alterations and post-translational modifications. It also explores the therapeutic potential of targeting these regulatory proteins, emphasizing the importance of phenotyping neoplastic tissues to inform the treatment of cancer.

Feb 15, 2019 · Mechanistically, we showed that EGFR-I645L, an activating EGFR mutation, impaired the sensitivity of HCC to JQ1 via MAPK regulation of MYC stability. In addtion, combination of JQ1 with EGFR inhibitors significantly enhanced the …

Feb 15, 2019 · Results: We found that JQ1, a commonly used BET bromo-domain inhibitor, offered a better anti-tumor response than sorafenib in MYC-positive HCC cells by inducing apoptosis in vitro and in vivo. Unlike sorafenib, JQ1 treatment significantly impaired mitochondrial respiration and glycolysis in HCC cells.