image: Figure 1:
(A) BRAF alteration frequencies, according to GENIE 15.1, among select solid organ tumors (glioma, 11%; thyroid cancer, 44%; non-small cell lung cancer, 6%; bladder cancer, 5%; prostate cancer, 3%; colorectal cancer, 12%; pancreatic cancer, 2%; and melanoma, 35%). (B) Relative proportions of distinct classifications of BRAF alterations across multiple cancer types (green = Class I, red = Class II, yellow = Class III, teal = structural rearrangement, and gray = unclassified).
Credit: 2024 Toye et al.
“Here we discuss the diverse forms of BRAF alterations found in human cancers and the strategies to inhibit them in patients harboring cancers of distinct origins.”
BUFFALO, NY- August 12, 2024 – A new research perspective was published in Oncotarget's Volume 15 on July 16, 2024, entitled, “Targeting the multifaceted BRAF in cancer: New directions.”
In cancer patients, BRAF-targeting precision therapeutics are effective against Class I BRAF alterations (p.V600 hotspot mutations) in tumors such as melanoma, thyroid cancer, and colorectal cancer. However, numerous non-Class I BRAF inhibitors are also in development and have been explored in various cancers.
Researchers Eamon Toye, Alexander Chehrazi-Raffle, Justin Hwang, and Emmanuel S. Antonarakis from the Masonic Cancer Center, University of Minnesota-Twin Cities, Department of Medicine, University of Minnesota-Twin Cities, Perelman School of Medicine, University of Pennsylvania, and the City of Hope Comprehensive Cancer Center in Duarte, California, discuss the diverse forms of BRAF alterations found in human cancers and the strategies used to inhibit them in patients with cancers of various origins.
As part of their conclusion, the researchers highlighted that Class I BRAF inhibitors represent a landmark achievement in precision oncology, as demonstrated by the recent tissue-agnostic FDA approval of dabrafenib/trametinib for patients with metastatic BRAF p.V600E-mutant solid tumors. Additionally, the accelerated approval of tovorafenib for patients with relapsed/refractory BRAF-altered pediatric low-grade glioma underscores the therapeutic potential of this and other next-generation strategies targeting aberrant MAPK signaling.
Continue reading: DOI: https://doi.org/10.18632/oncotarget.28612
Correspondence to: Emmanuel S. Antonarakis - anton401@umn.edu, and Justin Hwang - jhwang@umn.edu
Keywords: BRAF, MAPK, pan-cancer, precision oncology, genomics
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Journal
Oncotarget
Method of Research
News article
Subject of Research
Not applicable
Article Title
Targeting the multifaceted BRAF in cancer: New directions
Article Publication Date
16-Jul-2024
COI Statement
A.C.R. reports personal fees from Exelixis, Inc. and Aveo, Inc. outside the submitted work. JH consults for Tempus and is a co-founder of EMRGNSE. E.S.A. reports grants and personal fees from Janssen, Sanofi, Bayer, Bristol Myers Squibb, Curium, MacroGenics, Merck, Pfizer, AstraZeneca, and Clovis; personal fees from Aadi Bioscience, Aikido Pharma, Astellas, Amgen, Blue Earth, Corcept Therapeutics, Exact Sciences, Hookipa Pharma, Invitae, Eli Lilly, Foundation Medicine, Menarini-Silicon Biosystems, Tango Therapeutics, Tempus and Z-alpha; grants from Novartis, Celgene, and Orion; and has a patent for an AR-V7 biomarker technology that has been licensed to Qiagen.