Progress of BRAF Gene Alteration in Non-small Cell Lung Cancer.
10.3779/j.issn.1009-3419.2024.101.01
- Author:
Libian DENG
1
;
Yaxian YANG
2
;
Jian HUANG
3
Author Information
1. Department of Pathology, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang 524002, China.
2. Guangzhou Huayin Health Medical Group Co., Ltd, Guangzhou 510700, China.
3. Department of Pathological Diagnosis and Research Center, The Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
- Publication Type:Journal Article
- Keywords:
BRAF gene;
Lung neoplasms;
Targeted therapy
- MeSH:
Animals;
Mice;
Humans;
Carcinoma, Non-Small-Cell Lung/pathology*;
Lung Neoplasms/pathology*;
Proto-Oncogene Proteins B-raf/genetics*;
Mutation;
Mitogen-Activated Protein Kinase Kinases/therapeutic use*;
Protein Kinase Inhibitors/therapeutic use*
- From:
Chinese Journal of Lung Cancer
2024;27(1):73-80
- CountryChina
- Language:Chinese
-
Abstract:
V-Raf murine sarcoma viral oncogene homolog B (BRAF) alteration is one of the most essential driver genes of non-small cell lung cancer (NSCLC). BRAF encodes serine/threonine protein kinases, and its mutations typically lead to protein compositional activation, thereby activating the mitogen-activated protein kinase kinase (MEK) signaling pathway. A promising new approach for the treatment of mutated BRAF and/or downstream MEK may provide customized treatment opportunities for BRAF driven NSCLC patients. However, combination therapy is necessary to overcome the difficulties such as short duration of benefit, poor therapeutic effect of non-V600 BRAF mutations and susceptibility to drug resistance. This article reviewed the progress in structural characteristics, related signaling pathways, mutation types of BRAF gene, and the clinical pathological relationship between BRAF mutations and NSCLC, as well as the therapy, in order to provide more evidences for clinical doctors to make treatment decisions.
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