Until now, HNSCC are treated with surgical removal of cancer tissue in primary region and lymph nodes combined with radiotherapy, cytostatic drugs and in some cases, epidermal growth factor receptor (EGFR) targeted antibody cetuximab and programmed death receptor-1 (PD-1) antibodies.
Several growth factors and their receptors, such as epidermal growth factor receptor, have been studied as prognostic biomarkers for many epithelial malignancies.
Moreover, we demonstrate that chemical inhibitors targeting specific KMTs and KDMs are able to promote or block extrachromosomal EGFR amplification, which identifies potential therapeutic strategies for controlling EGFR copy number heterogeneity in cancer, and in turn, drug response.
Therefore, proposed benzothiazole derivatives may be promising EGFR tyrosine kinase inhibitors for potential application as cancer therapy.Communicated by Ramaswamy H. Sarma.
Epidermal growth factor receptor (EGFR) and MEK inhibitors (EGFR/MEKi) are beneficial for the treatment of solid cancers but are frequently associated with severe therapy-limiting acneiform skin toxicities.
To investigate its therapeutic availability in cancer therapy, we here modified the hybrid system to stably express EGFR shRNA and confirmed the antitumor effects.
Docking analysis and molecular dynamics (MD) simulations were performed to understand the plausible structural and dynamical implications caused by somatic mutations available in the Catalogue of Somatic Mutations in Cancer database on the EGFR and anti-EGFR mAbs.
Inhibition of angiogenesis with consequent impairments in intratumoral microcirculation is one of the mechanisms through which EGFR inhibition halts the progression of cancer.
The single nucleotide polymorphisms (SNPs) of microRNA-binding sites with target genes in the EGFR pathway could lead to alteration in the combination of microRNA with target genes and contribute to the susceptibility of cancer.
Transcriptionally Active HPV and Targetable EGFR Mutations in Sinonasal Inverted Papilloma: An Association Between Low-risk HPV, Condylomatous Morphology, and Cancer Risk?
Activation of epidermal growth factor receptor (EGFR) has been reported in a variety of cancer types, including colorectal cancer (CRC), and represents a potential chemotherapeutic drug target.
<b>Purpose:</b> This study evaluates the cytotoxicity of AuNPs coated with polyallylamine (AuNPs-PAA) and conjugated or not to the epidermal growth factor receptor (EGFR)-targeting antibody Cetuximab (AuNPs-PAA-Ctxb) in normal human kidney (HK-2), liver (THLE-2) and microvascular endothelial (TIME) cells, and compares it with two cancer cell lines that are EGFR-overexpressing (A431) or EGFR-negative (MDA-MB-453).
Despite the latest advancements in cancer diagnostics and therapeutics against EGFR, the survival rates of patients with advanced head and neck cancer remain disappointing due to anti-EGFR resistance.
EGFR inhibitors from cancer to inflammation: Discovery of 4-fluoro-N-(4-(3-(trifluoromethyl)phenoxy)pyrimidin-5-yl)benzamide as a novel anti-inflammatory EGFR inhibitor.
Epidermal Growth Factor Receptor (EGFR) signaling to the Ras-MAPK pathway is implicated in the development and progression of cancer and is a major focus of targeted combination therapies.
In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.