We intended to evaluate the combination of pemetrexed/erlotinib in patients with high epidermal growth factor receptor (EGFR)-expressing (2+ or 3 on immunohistochemistry) metastatic CRC who experienced disease progression after standard chemotherapy.
Taken together, VPS33B as a tumor suppressor is easily dysregulated by chemical carcinogens and it interacts with NESG1 to modulate the EGFR/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loop and thus suppress the malignant phenotype of CRC.
Taken together, the ERBB3 kinase activity contributes to the outgrowth of ileal organoids and intestinal tumorigenesis, and the development of ERBB3 kinase inhibitors, including epidermal growth factor receptor family members, can be a potential way to target colorectal cancer.
8‑Gingerol inhibited CRC cell proliferation and migration by targeting the EGFR/signal transducer and activator of transcription/extracellular signal‑regulated kinase pathway, and the effects of 8‑gingerol depended on the expression of EGFR.
We analyzed the EGFR signaling network, which plays an essential role in colorectal cancer, and studied its dynamics within 24 h upon treatment with the EGFR blocking antibody cetuximab, representing the first cellular adaption towards therapy.
Using machine-learning methods, peptides derived from epidermal growth factor receptor and leucine-rich alpha-2-glycoprotein 1 were consistently identified as highly predictive for detecting CRC from cancer-free cases.
The present study focuses on the involvement of EGFR positive and negative feedback genes in the establishment of cetuximab (CTX) resistance in metastatic Colorectal Cancer (CRC) patients.
Adjuvant Chemotherapy With or Without Biologics Including Antiangiogenics and Monoclonal Antibodies Targeting EGFR and EpCAM in Colorectal Cancer: A Systematic Review and Meta-analysis.
Although the presence of HER2 amplifications and oncogenic mutations in KRAS, NRAS, and BRAF are associated with EGFR-targeted therapy resistance, for a large population of CRC patients the underlying mechanism of RAS-MEK-ERK hyperactivation is not clear.
Cetuximab is a chimeric monoclonal antibody against epidermal growth factor receptor (EGFR) and it is approved for treatment of human colorectal cancer and squamous cell carcinoma of head and neck.
Long Noncoding RNA LINC00265 Targets EGFR and Promotes Deterioration of Colorectal Cancer: A Comprehensive Study Based on Data Mining and in vitro Validation.
These results reveal that KRAS G13D is responsive to neurofibromin-stimulated hydrolysis and suggest that a subset of <i>KRAS</i> G13-mutated colorectal cancers that are neurofibromin-competent may respond to EGFR therapies.
The rise in epidermal growth factor receptor (EGFR; human epidermal growth factor receptor 1; HER1) expression and enhanced phosphorylation of HER2 and HER3 are associated with tumor resistance, metastasis and invasion, thus resulting in poor outcome of anti-CRC therapy.
<i>Background and Aims:</i> Numerous studies have identified <i>BRAF<sup>V600E</sup></i> mutation as a predictive factor of anti-EGFR antibodies in colorectal cancer (CRC).
CRC tissues showed increased microvascular density and EGFR expression, activated ERK signaling, and miR-7 downregulation.EGFR was a target gene of miR-7. miR-7 overexpression and EGFR silencing decreased vasculogenic mimicry density, cell migration, and cell invasion, but increased cell apoptosis.
<i>TP53, KRAS, APC</i>) has limited diagnostic sensitivity (40-60%), however, methylated DNA including <i>SEPT9, SFRP1, SDC2</i> can be applied with higher sensitivity (up to 90%) for CRC.Circulating miRNAs (e.g. miR-21, miR-92, miR-141) provide comparably high sensitivity for CRC as the circulating tumor cell mRNA markers (e.g.EGFR, CK19, CK20, CEA).