The rat sarcoma viral oncogene homolog (RAS) family of closely related oncogenes (KRAS, HRAS, and NRAS) are the most frequently mutated drivers of malignant transformation. RAS family highly associates the epidermal growth factor receptor (EGFR) mainly. EGF selectively binds to EGFR and triggers the receptor to form a dimer that activates RAS. RAS transmits signals from activated trans membrane receptor EGFR to effectors in the B-raf proto-oncogene (BRAF)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway in the cytoplasm. The status of RAS proteins is a negative predictive biomarker for anti-EGFR therapy in metastatic colon cancer or other malignant tumors. In here, we report that our clinical studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma (KRAS) silent variants are of concern to be a serious problem in genomic cancer medicine.The status of rat sarcoma viral oncogene homolog (RAS) proteins is a negative predictive biomarker for anti-epidermal growth factor receptor (EGFR) therapy in metastatic colon cancer. In the phase 2 CHRONOS trial, patients with mutant gene(s) are ineligible for anti-EGFR therapy.1,2 However, our studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma (KRAS) silent variants are of concern to be a serious problem in genomic cancer medicine.
KRAS, oncogenic variant, Cancer Genome Medicine, EGFR
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