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.
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.
The combination of fluorouracil and irinotecan with a BRAF<sup>V600E</sup> and EGFR inhibitor may have synergistic action, leading to recession of secondary metastases in patients with BRAF<sup>V600E</sup>-mutated colorectal cancer.
Adjuvant Chemotherapy With or Without Biologics Including Antiangiogenics and Monoclonal Antibodies Targeting EGFR and EpCAM in Colorectal Cancer: A Systematic Review and Meta-analysis.
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.
Sixty patients with lung or colorectal cancer who were receiving EGFR inhibitors were prospectively followed for at least one year by oncologists and dermatologists.
The optimal management of hypomagnesemia (hMg) induced by epidermal growth factor receptor inhibitors (egfris) for advanced colorectal cancer is unclear.
Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer.
SIGNIFICANCE: Menin acts as a calcium-responsive regulator of SKP2 expression, and small molecule EGFR inhibitors, which induce calcium release, synergize with Menin inhibition to reduce SKP2 expression and suppress colorectal cancer.
This study, therefore, identified five candidate microRNAs, two hub genes (CTNNB1 and epidermal growth factor receptor), and seven significant target genes associated with colorectal cancer.
Broad-spectrum receptor tyrosine kinase inhibitors overcome <i>de novo</i> and acquired modes of resistance to EGFR-targeted therapies in colorectal cancer.
miR-145-5p restrained cell growth, invasion, migration and tumorigenesis via modulating RHBDD1 in colorectal cancer via the EGFR-associated signaling pathway.