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. Although the RAS family genes were discovered as human significant tumor genes 40 years ago, the RAS proteins have proved to be challenging targets in anti-tumor drug discovery: sotorasib was only approved as the first direct inhibitor of a RAS protein for clinical use in 2021. The downstream signaling pathway of 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-epidermal growth factor receptor (EGFR) therapy in metastatic colon cancer. 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.
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