KRAS and BRAF Double Mutations and Functional Classes of BRAF Mutations in Non–small-cell Lung Cancers

Bourhis, Amélie; Remoué, Annabelle; Uguen, Arnaud

doi:10.1016/j.cllc.2020.02.018

Cited by 4 publications

(2 citation statements)

References 15 publications

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“…For BRAF, more and more co-mutations have been found between BRAF and other genes, which also indicates that the branching cloning process occurs at the early stage of tumor evolution, which leads to the generation of BRAF co-mutations. According to literature reports, BRAF can co-occur with KRAS mutation ( 27 , 28 ), NRAS mutation ( 29 ), PTEN mutation ( 30 , 31 ), MEK2 mutation ( 32 ), PIK3CA mutation ( 33 ) and other gene mutations. And most of these BRAF co-mutations occur in melanoma and lung cancer, but also found in other tumors.…”

Section: The Activation Of Brafmentioning

confidence: 99%

“…In another patient, ROS1 rearrangement was lost during treatment, leaving only the BRAF V600E mutation ( 37 ). Through single circulating tumor cell (CTC) sequencing, researchers found that patients with ALK mutation developed acquired drug resistance after ALK-TKIs therapy ( 27 ). And the mechanism of ALK-TKIs resistance mainly included mutations of RTK-KRAS pathway and TP53 pathway independent of ALK pathway.…”

Section: The Activation Of Brafmentioning

confidence: 99%

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The Evolution of BRAF Activation in Non-Small-Cell Lung Cancer

et al. 2022

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Non-small-cell lung cancer (NSCLC) is the most common subtype of lung cancer, of which approximate 4% had BRAF activation, with an option for targeted therapy. BRAF activation comprises of V600 and non-V600 mutations, fusion, rearrangement, in-frame deletions, insertions, and co-mutations. In addition, BRAF primary activation and secondary activation presents with different biological phenotypes, medical senses and subsequent treatments. BRAF primary activation plays a critical role in proliferation and metastasis as a driver gene of NSCLC, while secondary activation mediates acquired resistance to other targeted therapy, especially for epidermal growth factor tyrosine kinase inhibitor (EGFR-TKI). Treatment options for different activation of BRAF are diverse. Targeted therapy, especially two-drug combination therapy, is an important option. Besides, immune checkpoint inhibitors (ICIs) would be another option since BRAF activation would be a positive biomarker of tumor response of ICIs therapy. To date, no high level evidences support targeted therapy or immunotherapy as prioritized recommendation. After targeted therapy, the evolution of BRAF includes the activation of the upstream, downstream and bypass pathways of BRAF. In this review, therapeutic modalities and post-therapeutic evolutionary pathways of BRAF are discussed, and future research directions are also provided.

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