BRAF
BRAF (B-Raf proto-oncogene, serine/threonine kinase) is a protein-coding gene that encodes a cytoplasmic serine/threonine-protein kinase in the RAF family.
BRAF (B-Raf proto-oncogene, serine/threonine kinase) is a protein-coding gene that encodes a cytoplasmic serine/threonine-protein kinase in the RAF family. It is a central component of the RAS–RAF–MEK–ERK mitogen-activated protein kinase (MAPK) pathway, which regulates cell proliferation, differentiation, survival, and migration. Following activation by RAS, BRAF can promote phosphorylation and activation of MEK proteins, leading to downstream ERK Signaling and changes in gene expression.
Activating BRAF mutations are important drivers in multiple Cancers. The best-known alteration is BRAF V600E, which produces a constitutively active kinase and enables MAPK signaling independently of normal upstream regulation. BRAF alterations are particularly relevant in melanoma, colorectal cancer, thyroid carcinoma, histiocytic and dendritic cell neoplasms, and other Tumors. They may serve as diagnostic, prognostic, or treatment-selection biomarkers and can influence the use of BRAF- and MEK-directed therapies. BRAF Signaling is also affected by interactions with RAS, EGFR, PTEN, and other components of growth-factor and intracellular Signaling networks.
Rebuilt from PubMed 18 Sept 2026 · no new papers today
Where the papers sit
19 papers study braf directly. Those 19 are one subject: Translational Oncology Research. Clinical oncology, cancer genomics, targeted therapy and computational molecular design are combined here, but the papers share no single disease, mechanism or research direction. No way of splitting those 19 scores better than chance. 1 new direction follows.
BRAF is regulated as a palmitoylated signaling protein, not only as a genetically altered kinase
The cholangiocarcinoma study of ZDHHC5-mediated BRAF palmitoylation found that ZDHHC5 modifies BRAF at Cys194/195, promoting its membrane localization and stability, activating ERK signaling, and driving tumor growth 42134490May. This departs from the set’s usual treatment of BRAF as a mutation-defined kinase target by assigning it a post-translationally regulated role in tumor biology. As a result, the ZDHHC5–BRAF–ERK axis, rather than BRAF mutation status alone, becomes a potential mechanism and therapeutic point of intervention.
Recent Findings on BRAF
Precision Oncology and Drug Discovery: Clinical molecular profiling stratifies BRAF-altered disease, but ctDNA sensitivity depends on disease context. Preoperative primary melanoma yielded no detectable ctDNA, whereas metastatic burden, elevated LDH, lesion count, and metabolic tumor volume predicted positivity 42714248Sep42011804Apr. Rare non-V600E/K mutations showed comparable survival with BRAF/MEK inhibitors, although response was numerically lower and structural activation varied 42003243Apr. BRAF-directed regimens produced rapid or durable responses in melanoma, hairy cell leukemia, and BRAF-mutated histiocytic/dendritic cell sarcoma, while evidence in glioma remains heterogeneous 42335571Jun42308249Jun42264920Jun42261252Jun. Sorafenib plus piroxicam also benefited canine urothelial carcinoma, with survival associated with treatment-induced hypertension and tumor CX3CL1 expression 42680778Sep. Resistance studies identify heterogeneous BRAF fusions, frequent post-EGFR-TKI emergence, and model-dependent trametinib sensitivity in colorectal cancer organoids 42546514Aug41833556Mar. Drug discovery combines conditional molecular generation, kinase-interface modeling, molecular glue degradation, and pyrimido[4,5-d]pyrimidine design to improve BRAF selectivity and address drug resistance 42489643Jul42427025Jul42447212Jul42208521May. ZDHHC5-mediated palmitoylation activates BRAF and increases MAPK inhibitor sensitivity, adding a regulatory vulnerability 42134490May. Real-world pharmacovigilance shows agent-specific cutaneous toxicity, while guidelines and spatial biomarkers refine monitoring, surgery, and treatment selection 42177750May42489130Jul42276049Jun.
Written from 19 PubMed abstracts, each one cited by PMID above. Published: 2026-08-20. Last written: 2026-09-11 by GPT. Drafted by language models from published abstracts; not medical advice.