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Molecular Pathways and Mechanisms of BRAF in Cancer Therapy
Open accessAbstract
With the identification of activating mutations in BRAF across a wide variety of malignancies, substantial effort was placed in designing safe and effective therapeutic strategies to target BRAF. These efforts have led to the development and regulatory approval of three BRAF inhibitors as well as five combinations of a BRAF inhibitor plus an additional agent(s) to manage cancer such as melanoma, non–small cell lung cancer, anaplastic thyroid cancer, and colorectal cancer. To date, each regimen is effective only in patients with tumors harboring BRAFV600 mutations and the duration of benefit is often short-lived. Further limitations preventing optimal management of BRAF-mutant malignancies are that treatments of non-V600 BRAF mutations have been less profound and combination therapy is likely necessary to overcome resistance mechanisms, but multi-drug regimens are often too toxic. With the emergence of a deeper understanding of how BRAF mutations signal through the RAS/MAPK pathway, newer RAF inhibitors are being developed that may be more effective and potentially safer and more rational combination therapies are being tested in the clinic. In this review, we identify the mechanics of RAF signaling through the RAS/MAPK pathway, present existing data on single-agent and combination RAF targeting efforts, describe emerging combinations, summarize the toxicity of the various agents in clinical testing, and speculate as to where the field may be headed.
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“BRAFV600E mutations are present in around 10% of advanced CRC patients and lead to constitutive activation of the MAPK pathway, drug resistance and a poor prognosis [1–4].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [4]
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Metadata
- Authors
- Poulikakos, P. I., Sullivan, R. J., & Yaeger, R.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Massachusetts General Hospital (US)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Poulikakos, Poulikos I.
- Sullivan, Ryan J.
- Yaeger, Rona
- Venue
- Clinical Cancer Research
- Published
- 2022-04-29
- Volume
- 28
- Issue
- 21
- Pages
- 4618-4628
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC9616966
- OpenAlex
- W4225136170
- Cited by
- 145
- References
- 125
- Citations by year
- 2026: 29 · 2025: 41 · 2024: 41 · 2023: 31 · 2022: 3
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (U54 CA224068, P30 CA008748, R01 C233736, R01 CA204314, R01 CA240362, R01CA238229, R01 CA193970, R01 CA229851, UM1 CA186709)
- Irma T. Hirschl Trust
- Melanoma Research Alliance
- Melanoma Research Foundation
- Breast Cancer Alliance
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- BRAF, BRAF inhibitors, BRAF V600 mutation, RAS/MAPK pathway, Raf signaling, combination therapy, melanoma, non-small cell lung cancer, anaplastic thyroid carcinoma, colorectal cancer, drug resistance, drug toxicity, targeted cancer therapy
- MeSH terms
- Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf
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