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The mechanism and consequences of BRAF inhibitor resistance in melanoma

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Abstract

BRAF V600E is a constitutive BRAF (B-raf proto-oncogene, serine/threonine kinase) mutation that accounts for more than 90% of BRAF mutations in melanoma. Vemurafenib is a BRAF V600E selective kinase inhibitor (BRAFi) that is commonly used to treat BRAF V600E melanoma patients. However, vemurafenib treatment-induced resistance occurs in about 50% of patients diagnosed with melanoma, and half of the patients have disease progression within six months. But the mechanism and the consequences of BRAF inhibitor resistance have not been fully elucidated. In this review, we summarize the mechanism and the consequences of BRAF inhibitor vemurafenib resistance in melanoma, aiming to provide a guidance for the intervention of BRAF inhibitor resistance.

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Acknowledgements

We thank Dr. Jing Li for the critical reading of the manuscript. This work was supported by the National Natural Science Foundation of China (82273460, 32260167), the Yunnan Applied Basic Research Projects (202101AV070002), a grant (Grant No. KLTIPT-2023-02) from Key Laboratory of Tumor Immunological Prevention and Treatment in Yunnan Province, Yan'an Hospital Affiliated to Kunming Medical University, Kunming and grants (Grant No. 2023Y0222) from Yunnan University.

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KG and JS were responsible for the study concept and design. KG, WB, ZZ, HX and RS drafted the manuscript. JS and JS revised and edited the manuscript. All authors contributed to this review and approved the submitted version.

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Correspondence to Junling Shen or Jianwei Sun.

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The authors declare that they have no conflict of interest.

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Golub, K., Bai, W., Zhang, Z. et al. The mechanism and consequences of BRAF inhibitor resistance in melanoma. GENOME INSTAB. DIS. 4, 266–274 (2023). https://doi.org/10.1007/s42764-023-00105-5

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  • DOI: https://doi.org/10.1007/s42764-023-00105-5

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