As an oncologist, we deeply understand that tumor treatment is always in the stage of development, and we need to always study tirelessly to understand the most cutting-edge development in order to bring our patients greater hope for survival. Scientists from Cancer Research UK’s Genes and Oncogenes Research Team published the Cancer Research Progress article Kinase-DeadBRAFandOncogenicRASCooperatetoDriveTumorProgressionthroughCRAF in the latest issue of Cell, which found that lethal The study found that mutated BRAF and oncogenic RAS work together to promote tumor growth and development, and was named a research highlight article in this issue of Cell. The RAS gene product is involved in the kinase signaling pathway that controls gene transcription, thereby regulating cell growth and differentiation. oncogene to oncogene. The effects of such functional alterations on cells are multifaceted, as ras is involved in many signaling pathways that control cell division and death. BRAF is an oncogene that encodes a serine/threonine-specific kinase that is an important transducer of the RAS/RAF/MEK/ERK/MAPK pathway and is involved in the regulation of multiple biological events in cells, such as cell growth, differentiation and apoptosis. Studies have shown that BRAF gene mutations exist in various proportions in a variety of human malignancies, such as malignant melanoma, colorectal cancer, lung cancer, thyroid cancer, liver cancer and pancreatic cancer, and somatic missense mutations exist in BRAF gene in about 66% of malignant melanoma and 15% of colon cancer. Approximately 80-90% of B-raf gene mutations occur at nucleotide 1799 of exon15, with a T mutation to A, resulting in the substitution of its encoded glutamate by valine (V600E). It is now believed that the V600E mutation mimics the phosphorylation process at both T599 and S602 loci, resulting in abnormal activation of the B-raf protein. BRAF and RAS are currently hot oncogenes in the field of cancer research, and in this study, scientists in the UK found for the first time that lethally mutated BRAF kinase mediates tumorigenesis in the presence of the RAS gene. The researchers found that selective inhibition of the BRAF-driven RAS-dependent BRAF-CRAF, CRAF binding process (a process that activates the MEK-ERK signaling pathway induced by the BRAF-CRAF-CRAF complex) with drugs. The above scenario does not occur when the oncogene BRAF is inhibited, suggesting that BRAF must function properly in collaboration with the oncogene RAS. Researchers conducted animal model tests with mice and found that the collaboration of the lethal kinase BRAF with the lethal kinase Braf in the RAS, which mimics the action of the above drugs, induces melanoma in mice. The most significant of these findings is the understanding of the signaling pathways involved in the development of cancer, which points the way to the development of treatment plans and drug screening for patients.