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BIOMARKER:

BRAF L597R

i
Other names: BRAF, B-raf proto-oncogene, B-raf proto-oncogene, Serine/threonine kinase, V-Raf murine sarcoma viral oncogene homolog B, Serine/threonine-protein kinase B-Raf, Proto-oncogene B-Raf, BRAF1, RAFB1, B-raf proto-oncogene Serine/threonine-protein kinase, Murine sarcoma viral (V-Raf) oncogene homolog B1, B-raf serine/threonine-protein, 94 KDa B-raf protein, B-RAF1
Entrez ID:
29d
Identification of recurrent BRAF non-V600 mutations in intraductal carcinoma of the prostate in Chinese populations. (PubMed, Neoplasia)
The BRAF mutation may represent important genetic alteration in a subset of IDC-P, highlighting the role of MAPK signaling pathway in this subtype of PCa. To the best of knowledge, this is the first description of non-V600 BRAF mutation in setting of IDC-P, which may in part explain the aggressive phenotype seen in IDC-P and could also bring more treatment options for PCa patients with IDC-P harboring such mutations.
Journal
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BRAF (B-raf proto-oncogene)
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BRAF mutation • BRAF K601E • BRAF L597R • BRAF K601 • BRAF L597
8ms
The characteristics in Chinese NSCLC patients with different BRAF mutation classes (ESMO 2023)
Furthermore, TP53, LRP1B, STK11, SPTA1and MAGI2 were significantly over-mutated in Class II and III (p<0.06) and SETD2 is over-mutated in Class I (p<0.001), might suggesting relatively poor prognosis in NSCLC patients. Conclusions The characteristics of Chinese NSCLC were further explored, including BRAF mutation types, the incidence of related co-mutations and TMB value, which is helpful to formulate targeted therapy strategies to adapt to different types of BRAF mutation functions according to their genomic and clinical characteristics.
Clinical • IO biomarker
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BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • STK11 (Serine/threonine kinase 11) • LRP1B (LDL Receptor Related Protein 1B) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • SPTA1 (Spectrin Alpha)
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TP53 mutation • BRAF V600E • BRAF mutation • BRAF V600 • STK11 mutation • BRAF K601E • BRAF D594G • BRAF G469A • BRAF L597R • BRAF G466A • SETD2 mutation • BRAF K601 • BRAF L597
over1year
Recognition of BRAF by CDC37 and Re-Evaluation of the Activation Mechanism for the Class 2 BRAF-L597R Mutant. (PubMed, Biomolecules)
We find an extended and conserved CDC37 motif, HPNID---SL--W, responsible for recognizing the C-lobe of BRAF kinase domain, while the c-terminal domain of CDC37 is responsible for the second of the bipartite interaction with BRAF. We show that dimerization of BRAF, independent of nucleotide binding, can act as a potent signal that prevents CDC37 recognition and discuss the implications of mutations in BRAF and the consequences on signaling in a clinical setting, particularly for class 2 BRAF mutations.
Journal
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BRAF (B-raf proto-oncogene) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1Heat Shock Protein 90 Alpha Family Class A Member 1)
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BRAF mutation • BRAF L597R • BRAF L597
almost2years
Evaluation of treatment patterns in patients with BRAF-mutant cutaneous melanoma in adjuvant setting in real practice. (ASCO 2022)
In our retrospective study we found that among stage III BRAF-mutant patients monotherapy with aPD1 was the most common adjuvant treatment regimen. In some patients with stage III disease IFN-alfa is still given. More studies are needed to define best adjuvant treatment for BRAF mutant stage III melanoma pts.
Clinical
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BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase)
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BRAF V600E • BRAF mutation • NRAS mutation • BRAF V600 • KIT mutation • BRAF V600K • BRAF wild-type • NRAS Q61K • NRAS Q61 • NRAS Q61R • BRAF K601E • NRAS G12D • NRAS Q61L • BRAF L597R • BRAF V600M • BRAF K601 • BRAF L597
almost2years
Evaluation of somatic and germline variants in patients with small bowel adenocarcinoma reveals clinically actionable targets. (ASCO 2022)
Of the entire cohort, we observed five activating PIK3CA mutations (R108H; G364R; E542K; E545K, n = 2) which may be sensitive to FDA-approved PIK3CA inhibitor alpelisib. Additionally, patients with loss-of-function mutation in NF1 (n = 2), STK11 (n = 1) and PTEN (n = 1) can be targeted with MEK inhibitor selumetinib and mTOR inhibitor everolimus, respectively. Except for one V600E mutation, all mutations in BRAF are either type 2 (L597R, n = 1) or type 3 (N581S, n = 1; D594N, n = 4) which were sensitive to MEK inhibitor trametinib...Interestingly, one IDH1 mutation (R132C) carrier in our cohort might benefit from ivosidenib... Through comprehensive genomic characterization of Chinese SBA patients, we identified actionable variants of multiple signaling pathways in plenty. NGS profiling results can guide physicians to enroll a significant portion of SBA patients in genomically-matched clinical trials.
Clinical • IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • PTEN (Phosphatase and tensin homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • STK11 (Serine/threonine kinase 11) • MAP2K1 (Mitogen-activated protein kinase kinase 1) • NF1 (Neurofibromin 1) • MDM2 (E3 ubiquitin protein ligase) • MLH1 (MutL homolog 1) • SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • KMT2C (Lysine Methyltransferase 2C) • FGF3 (Fibroblast growth factor 3) • ARID2 (AT-Rich Interaction Domain 2) • FAT3 (FAT Atypical Cadherin 3) • ERCC5 (ERCC Excision Repair 5 Endonuclease 2) • SOX9 (SRY-Box Transcription Factor 9) • SPTA1 (Spectrin Alpha)
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TP53 mutation • BRAF V600E • KRAS mutation • HER-2 amplification • PIK3CA mutation • BRAF V600 • IDH1 mutation • PTEN mutation • STK11 mutation • PIK3CA E545K • NF1 mutation • HER-2 S310F • HER-2 V777L • PIK3CA E542K • IDH1 R132C • PIK3CA E545 • BRAF L597R • HER-2 V842I • IDH1 R132 • PIK3CA E542 • BRAF D594N • MAP2K1 F53L • MAP2K1 K57E • MAP2K1 K57N • BRAF L597 • HER-2-H
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Onco PanScan™
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Mekinist (trametinib) • everolimus • Koselugo (selumetinib) • Piqray (alpelisib) • Tibsovo (ivosidenib)
3years
[VIRTUAL] Genomic profiling of small bowl adenocarcinoma reveals targetable mutations in multiple signaling pathways (AACR 2021)
We also found two MAP2K1 activating mutations (K57E and K57N) which can be targeted by trametinib...We also observed two activating PIK3CA mutations (R108H and G364R) which may be sensitive to PIK3CA inhibitor alpelisib... The mutational landscape of our SBA cohort provided compelling evidence that multiple signaling pathways play a role in the pathogenesis of SBA and many driver mutations in these pathways are targetable. Our findings indicated that SBA patients should participate in matched clinical trials for better management of this disease.
Tumor Mutational Burden
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • MAP2K1 (Mitogen-activated protein kinase kinase 1) • MLH1 (MutL homolog 1) • SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • KMT2C (Lysine Methyltransferase 2C) • FGF3 (Fibroblast growth factor 3) • ARID2 (AT-Rich Interaction Domain 2) • FAT3 (FAT Atypical Cadherin 3) • ERCC5 (ERCC Excision Repair 5 Endonuclease 2) • ZKSCAN1 (Zinc Finger With KRAB And SCAN Domains 1)
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TP53 mutation • BRAF V600E • KRAS mutation • HER-2 amplification • PIK3CA mutation • BRAF V600 • HER-2 V777L • BRAF L597R • HER-2 V842I • MET fusion • MAP2K1 K57E • MAP2K1 K57N • BRAF L597
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Mekinist (trametinib) • Piqray (alpelisib)
almost4years
Molecular landscape of BRAF-mutant NSCLC reveals an association between clonality and driver mutations and identifies targetable non-V600 driver mutations. (PubMed, J Thorac Oncol)
"In BRAF-mutant NSCLC, clonality is higher in known functional mutations and may allow identification of VUS more likely to be oncogenic drivers. Our data indicate certain non-V600 mutations are responsive to MEK and BRAF inhibitors. This integration of genomic profiling and drug sensitivity may guide treatment for BRAF-mutant NSCLC."
Journal
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BRAF (B-raf proto-oncogene)
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BRAF V600E • BRAF mutation • BRAF G469V • BRAF D594G • BRAF L597R • BRAF L597
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Guardant360® CDx
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Mekinist (trametinib) • Tafinlar (dabrafenib) • lifirafenib (BGB-283) • naporafenib (ERAS-254)