Table of ContentsView AllTable of ContentsHow BRAF Mutations WorkCancers That May Involve BRAF MutationsBRAF Mutation TestingTreatment ImplicationsFrequently Asked Questions
Table of ContentsView All
View All
Table of Contents
How BRAF Mutations Work
Cancers That May Involve BRAF Mutations
BRAF Mutation Testing
Treatment Implications
Frequently Asked Questions
BRAF mutations are DNA changes in some cancer cells that can be treated with newer targeted therapies.
BRAF mutations are found in roughly half of melanomas. Medications that target these mutations have significantly improved the survival rates of metastatic melanoma. BRAF mutations are also present in some non-small cell lung cancers, colon cancers, and other tumor types.
Verywell / Jessica Olah
Genomic testing of tumors can look for DNA alterations and determine if the cancer will respond to drugs targeting mutations.
This article looks at what a BRAF mutation is and its frequency in different types of cancer. It also looks at testing, treatment options, and recent advances.
Cancer begins when a series of gene mutations or other genomic alterations transforms a normal cell into acancer cell. Some of these mutations, referred to as “driver mutations,” code for proteins that drive the growth of the tumor.
Oncogenes and Tumor Suppressor Genes
Most often, cancer develops after a series of mutations in bothoncogenesandtumor suppressor genesoccurs.
Proto-oncogenes are normal genes that code for proteins important in stimulating cell growth and division. These genes are primarily active during fetal development in the uterus, and for short periods of time in adults to aid in tissue repair.
When mutated, proto-oncogenes become oncogenes. These genes can be thought of as an accelerator on a car that is stuck in the on position. BRAF is a proto-oncogene that becomes an oncogene when mutated—resulting in the continuous production of proteins that stimulate cell proliferation.
Tumor suppressor genes are genes that code for proteins that function to repair damaged DNA or eliminate cells that can’t be repaired. When these genes are damaged, they allow abnormal cells to continue to grow and reproduce. TheBRCA geneslinked to breast cancer are examples of tumor suppressor genes.
The BRAF Gene
The BRAF gene is a proto-oncogene found on chromosome 7, and becomes an oncogene when mutated. The gene codes for a protein (a serine-threonine kinase) that sends signals from outside of the cell to the nucleus that in turn drives the growth of a cell. Discovered in 2002, the oncogene is now known to be an important driver in more than one type of cancer.
While BRAF is an important “driver” of melanoma, a BRAF mutation alone is not responsible for the development of cancer. (At least one other mutation is needed for cancer to develop.) Alone, the mutation can lead to the development of benign moles.
Hereditary vs. Acquired Gene Mutations
It’s important to briefly discuss the difference between acquired (somatic) gene mutations (mutations that are acquired after birth in the process of a cell becoming a cancer cell), and hereditary (germline) mutations, mutations that are inherited from one’s parents.
BRAF mutations associated with cancer are almost always acquired mutations. Unlike the BRCA mutations that have received a lot of attention in recent years, these mutations are not inherited from a person’s parents andcannotbe passed down to children. They are present only in the cancer cells and not all of the cells in the body. Acquired mutations are much more common in oncology.
Hereditary (Germ-Line) vs. Acquired (Somatic) Gene Mutations
Types
There are more than 30 different types of mutations that may occur in the BRAF gene, and the most common types of mutations can vary with the type of cancer.
BRAF V600E and BRAF V600K
Non-V600 BRAF Mutations
With lung adenocarcinoma, around 50% to 80% of BRAF mutations are non-V600 variants. In colorectal cancer, 22% to 30% are non-V600 variants.
BRAF Mutations Classes
The science is in its infancy with regard to evaluating the different types of BRAF mutations with respect to treatment and prognosis.
A 2019 study looked at BRAF mutations in non-small cell lung cancer, separating these into three classes with different clinical characteristics. It could be that in the future, specific therapies will be designed to treat subsets of BRAF mutations rather than BRAF mutations in general.
How BRAF Mutations Drive the Growth of Cancer
The BRAF gene codes for (is a blueprint for) a protein called B-Raf. Mutations in the BRAF gene are referred to as “activating mutations” as the mutation results in continuous production of the protein. The continued presence of the B-Raf proteins, in turn, results in continuous signaling for the cell to divide and grow.
B-Raf proteins are part of a signaling pathway (RAF-MEK-ERK) that affects cell growth in several ways. This pathway:
This pathway is very important in the womb as the embryo develops. When continuously activated in an adult, it can result in uncontrolled growth of cells (cancer).
Part of the difficulty in treating cancer lies in the fact that cancer cells are not just a clone of cells that grows continuously. They have other characteristics, such as the ability to break free and spread, avoid cell death, and more. They are also continuously changing, developing new mutations that may allow them to escape our current treatments.
Cancer Cells vs. Normal Cells: How Are They Different?
At the current time, several different types of cancer have been found to harbor BRAF mutations. However, the frequency, as well as the response to BRAF inhibitors, varies.
BRAF mutations are an example of how cancer treatment is changing. In the past, cancers were usually treated according to type (such as breast cancer or colon cancer treatments). BRAF inhibitors, in contrast, are what are now considered “tumor agnostic” medications.
This means that the drugs may work fordifferent typesof cancer (for example, melanoma, lung cancer, and colon cancer). However, the cancer cells must have the same type of mutation responsible for driving the growth of the tumor.
Reading studies about BRAF mutations can be confusing. When the term “BRAF wild-type” or BRAF WT is used to describe a tumor, it refers to a cancer that doesnothave a BRAF mutation.
Melanoma
BRAF mutations are present in a large number of melanomas, and their discovery has led to treatments that have changed the outlook for some people with metastatic or locally advanced melanoma (stage IIIB or stage IIIC). Present in roughly 40% to 60% of melanomas, around 90% are BRAF V600E mutations, with most of the remaining being BRAF V600K.
BRAF mutations appear to be more common in some people and with some tumors, including:
Tumors that are BRAF mutated also appear to be more likely to spread to the brain.
Non-Small Cell Lung Cancer (Lung Adenocarcinoma)
BRAF mutations are present in a small number (roughly 3%) of people with the type ofnon-small cell lung cancercalledlung adenocarcinoma. This is the type of lung cancer that is most common in never smokers, women, and young people who develop the disease.
With lung adenocarcinoma, BRAF mutations may be present when the tumor is diagnosed, but are more often found as a resistance mutation. This is a mutation that develops in a cancer that has already been treated with another targeted therapy (such as anEGFR inhibitor).
Colorectal Cancer
BRAF mutations are common incolon cancer, but occur primarily in cancers that are “sporadic” (non-genetic). It is very uncommon for BRAF mutations to be present in hereditary colon cancers, such as those in people who haveLynch syndrome. In this way, the presence of the mutation may provide some information on whether the cancer has a genetic basis or not.
Colon tumors with BRAF mutations are more common:
While treatment addressing BRAF mutations in colon tumors was relatively ineffective in the past, newer triple therapy offers much more promise.
Hairy Cell Leukemia
BRAF mutations are relatively common withhairy cell leukemia. The presence of a BRAF mutation can help distinguish hairy cell leukemia from other B cell lymphomas or leukemias.
Thyroid Cancer
BRAF mutations are present in a large number ofanaplastic thyroid cancers(a very aggressive tumor that has been challenging to treat), and up to half ofpapillary thyroid cancers. BRAF mutations are not found in follicular thyroid cancer, medullary carcinomas, or benign tumors, so the presence of the mutation can help distinguish different types of thyroid cancer.
With papillary thyroid cancer, the presence of a BRAF mutation is associated with a higher risk of recurrence and spread to lymph nodes.
Serous Ovarian Cancer
BRAF mutations are relatively common in people who have serous ovarian cancer. The fact that BRAF inhibitors may be effective for treatment is yet another reason whyallwomen who have ovarian cancer should be tested for mutationsin addition toBRCA mutations.
Others
BRAF mutations have been found in a number of other cancers, although infrequently (usually less than 3%). It’s not yet known what the significance of the mutation might be with respect to treatment. Some of these include:
Other Conditions Related to BRAF Mutations
While BRAF mutations associated with cancer are almost always somatic (acquired mutations), both acquired and inherited mutations may be responsible for some non-cancer related conditions, such as cardiofaciocutaneous syndrome, Noonan syndrome, Erdheim Chester disease, and giant melanocytic nevus.
Testing for BRAF mutations is critical both for those who are found to have a BRAF mutation and those who are not. Those who have the mutation may be eligible for a treatment that has a significant chance of controlling the cancer for a period of time.
Testing is also important for those who do not have the mutation. For example, using BRAF inhibitors in melanomaswithouta BRAF mutation may actually lead to progression of a tumor.
Testing is recommended per guidelines for melanoma, non-small cell lung cancer, colon cancer, serous ovarian cancer, and others.
Verywell / Alison Czinkota
Methods
Several different methods of testing for BRAF are currently available. DNA sequencing (eg. next-generation sequencing) takes time but is the gold standard. It can detect different types of BRAF mutations, as well as many other alterations that may be treatable. A faster test (PCR) can be done, but only detects V600E mutations.
Tumor Testing vs. Liquid Biopsy
Historically, testing done on a sample of tissue obtained via a biopsy has been the gold standard. Unfortunately, tissue biopsies are invasive and may not always be possible.
In recent years, a simple blood test that looks for fragments of tumor DNA (cell-free DNA) in the blood has offered an additional option for genomic testing.Liquid biopsieshave been found to be comparable to tissue biopsies in some cases, though many oncologists believe that the ideal is to do genomic testing on both tissue and blood samples.
Discordance
The concept of discordance is an important one for people living with advanced cancer. Some people may be aware that breast cancer can change. For example, a tumor that was once estrogen receptor positive may become negative (and vice versa) when it progresses or spreads. The same is true with genomic alterations such as BRAF mutations.
For this reason, many oncologists recommendre-testinga tumor if it progresses or spreads (even ifnext-generation sequencing was done before). There can be discordance within a tumor as well, such that some parts of the tumor have a BRAF mutation and others do not.
A potential advantage of liquid biopsies is that they may detect mutations present in a tumor, but not seen in a specific area that is biopsied.
A common scenario is with lung adenocarcinoma that progresses. Since BRAF commonly develops as aresistance mutation, it maynotbe present on initial testing but may be present when a tumor progresses.
Cancers continually change and develop new mutations. With melanoma, metastases are more likely to be BRAF positive than a primary tumor.
How Cancer With BRAF Mutation Is Treated
There are several important treatment implications associated with the presence of BRAF mutations. This stresses the importance of testing.
For instance, BRAF-positive tumors are not only treated with targeted therapies, but those tumors may respond differently tootherforms of treatment, such aschemotherapyorimmunotherapy. The presence of BRAF mutations may also provide information about the prognosis of a tumor. Tumors that harbor BRAF mutations can behave differently clinically.
BRAF Inhibitors
BRAF inhibitors are medications that target the pathways cancer cells use to grow in tumors that harbor BRAF mutations.
Combined Therapy
BRAF inhibitors are most often used along with medications that inhibit the growth of a tumor at other points in the signaling pathway (such as MEK inhibitors). Interestingly, adding a MEK inhibitor to a BRAF inhibitor is actually associated withfewerside effects than using a BRAF inhibitor alone. The combination also appears to work for a longer period of time.
Triple Therapy
With both melanoma and colon cancer, combining a BRAF inhibitor and a MEK inhibitor with another medication has shown promise in clinical trials.
MEK Inhibitors
Metastatic Melanoma
With metastatic melanoma, using a combination of a BRAF inhibitor and MEK inhibitor has been a “game changer” for many people.
Among those treated, almost two-thirds of people with tumors found to be BRAF positive will respond. Newer combinations (such as the combination of Braftovi and Mektovi) may work even better or result in longer control.
Compared with the previous gold standard (the chemotherapy drug dacarbazine), these targeted therapies can increase both progression-free and overall survival.
Unfortunately, cancers almost always become resistant to these medications after a period of time; usually within a year.
Quandary
There is currently a quandary when it comes to choosing the best treatment for people with metastatic melanoma with BRAF mutations. Targeted therapy has a high chance of working, but only controls the disease for a while.
In contrast, immunotherapy is less likely to work, but in some cases can control the disease for a lengthy period of time. This is something referred to not as a cure, but a “durable response.”
Targeted therapy (BRAF plus MEK inhibitors) for metastatic melanoma has a high response rate but lasts, on average, only around a year. Immunotherapy has a lower response rate, but sometimes a much longer duration of action.
Clinical trials are in progress evaluating the combination of targeted therapy (BRAF and MEK inhibitors) with immunotherapy drugs known as checkpoint inhibitors (PD-1 and PD-L1 inhibitors).
These include a few promising studies published in June of 2019 that suggest that, for at least some people, the combination may result in a longer response:
Stage III Melanoma
A combination of a BRAF inhibitor and MEK inhibitor may also be used in people with locally advanced melanoma (such as stage IIIB and stage IIIC) to reduce the risk of recurrence (adjuvant therapy).
What Is Adjuvant Therapy?
Lung Cancer
A combination of the BRAF inhibitor Taflinar and the MEK inhibitor Mekinist is approved for treating non-small cell lung cancer with a BRAF V600E mutation, with a response rate of 64% in studies.
Guidelines also recommend avoiding immunotherapy (Keytruda) first-line in people with BRAF mutations, even if PD-L1 levels are high since people with BRAF mutations appear less likely to respond.
A large number of non-hereditary colon cancers have BRAF mutations, but studies using a combination of BRAF and MEK inhibitors showed a low response rate (roughly 5% with BRAF inhibition alone and 12% with the combination).
In the past, it was thought that the presence of a BRAF mutation might make a colon cancer unlikely to respond to an EGFR inhibitor, but this appears to depend on other genetic changes in the tumor. With colon cancer, tumors that have a BRAF mutation but not a KRAS mutation may not respond well to EGFR inhibitors such as cetuximab or panitumumab.
BRAF + MEK + EGFR Inhibitors
A 2019 study found that using triple therapy with the BRAF inhibitor Mektovi, the MEK inhibitor Braftovi, and the EGFR inhibitor Erbitux (cetuximab) resulted in a higher response rate and significantly longer survival among people with a BRAF V600E mutation.
Resistance
Unfortunately, most tumors become resistant to these targeted therapies in time. Research is in place evaluating the resistance mutations that develop with hope that further targets can be identified and treated when resistance occurs.
A Word From Verywell
The science surrounding BRAF mutations is young, though already approvals are present that can extend both length and quality of life for some people who have tumors with the mutations.
Not only does genomic testing allow more people to obtain effective treatments, but doing so is advancing our understanding of the natural history of cancer. That’s important as new therapies are developed to combat the disease.
Since the science is advancing so rapidly, however, it is hard for any physician to stay abreast of all of the changes with all cancers. Learning about your disease, getting a second (or third opinion), questioning potential clinical trials, and advocating for yourself are all important in receiving the best care possible for your cancer.
Yes. The BRAF gene, found on chromosome 7, is responsible for cell growth. However, not everyone has a mutation of the BRAF gene that contributes to cancer development.
“BRAF positive” means that your tumor has a mutation in the BRAF gene. This gene controls a protein that stimulates cell growth. When there’s a mutation, it causes the continuous production of this protein, which can lead to unchecked cell growth or cancer.
Knowing your status can help ensure that your healthcare provider is providing the right treatment. If you have a BRAF mutation, you may be eligible for certain targeted treatments, such as BRAF inhibitors, which may help improve survival rates.
It’s possible, but not likely. Usually, a BRAF mutation happens later in life from something in the environment or a mistake your body makes during cell division. In very rare cases, BRAF mutations can be inherited, causing serious health problems.
No, they can’t go away, but treatment may help with managing their effects. With a tumor related to a BRAF mutation, your oncologist can use targeted treatments that may temporarily stop the mechanism causing tumor growth.
11 SourcesVerywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Dankner M, Rose AAN, Raijkumar S, Siegel PM, Watson IR.Classifying BRAF alterations in cancer: new rational therapeutic strategies for actionable mutations.Oncogene.2018;37(24):3183-3199. doi:10.1038/s41388-018-0171-xDagogo-Jack I, Martinez P, Yeap BY, et al.Impact of BRAF mutation class on disease characteristics and clinical outcomes in BRAF-mutant lung cancer.Clin Cancer Res. 2019;25(1):158-165. doi:10.1158/1078-0432.CCR-18-2062Cheng L, Lopez-Beltran A, Massari F, MacLennan GT, Montironi R.Molecular testing forBRAFmutations to inform melanoma treatment decisions: a move toward precision medicine.Mod Pathol.2018;31:24-28. doi:10.1038.modpathol.2017.104Lee HM, Morris V, Napolitano S, Kopetz S.Evolving strategies for the management of BRAF-mutant metastatic colorectal cancer.Oncology (Williston Park).2019. 33(6):206-11.Ascierto PA, Ferrucci PF, Fisher R, et al.Dabrafenib, trametinib and pembrolizumab or placebo in BRAF-mutant melanoma.Nature Medicine.2019. 25(6):941-946. doi:10.1038/s41591-019-0448-9Sullivan RJ, Hamid O, Gonzalez R, et al.Atezolizumab plus cobimetinib and vemurafenib inBRAF-mutated melanoma patients.Nat Med. 2019;25(6):929-935. doi:10.1038/s41591-019-0474-7Tan I, Stinchcombe TE, Ready NE, et al.Therapeutic outcomes in non-small cell lung cancer withBRAFmutations: a single institution, retrospective cohort study.Translational Lung Cancer Research.2019;8(3):258-267. doi:10.21037/tlcr.2019.04.03Kopetz S, Grothey A, Yaeger R, et al.Encorafenib, binimetinib, and cetuximab inBRAFV600E–mutated colorectal cancer.N Engl J Med.2019;381:1632-1643. doi:10.1056/NEJMoa1908075Takeda H, Sunakawa Y.Management of BRAF gene alterations in metastatic colorectal cancer: From current therapeutic strategies to future perspectives.Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.602194MedlinePlus.BRAF genetic test.Johns Hopkins Medicine.BRAF mutation and cancer.Additional ReadingHauschild A, Dummer R, Schadendorf D, et al.Longer follow-up confirms relapse-free survival benefit with adjuvant dabrafenib plus trametinib in patients with resectedBRAFV600-mutant stage III melanoma.J Clin Oncol.2018; 36(35):3441-3449. doi:10.1200/jco.18.01219Kwak M, Farrow N, Salama A, et al.Updates in adjuvant systemic therapy for melanoma.J Surg Oncol.2019;119(2):222-231. doi:10.1002/jso.25298MedlinePlus.BRAF gene.Moujaber T, Etemadmoghadam D, Kennedy CJ, et al.BRAFmutations in low-grade serous ovarian cancer and response to BRAF inhibition.JCO Precision Oncology. 2018;(2):1-14. doi:10.1200/PO.17.00221My Cancer Genome.BRAF V600E.Ribas A, Lawrence D, Atkinson V, et al.Combined BRAF and MEK inhibition with PD-1 blockade immunotherapy inBRAF-mutant melanoma.Nat Med.2019;25(6):936-940. doi:10.1038/s41591-019-0476-5
11 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Dankner M, Rose AAN, Raijkumar S, Siegel PM, Watson IR.Classifying BRAF alterations in cancer: new rational therapeutic strategies for actionable mutations.Oncogene.2018;37(24):3183-3199. doi:10.1038/s41388-018-0171-xDagogo-Jack I, Martinez P, Yeap BY, et al.Impact of BRAF mutation class on disease characteristics and clinical outcomes in BRAF-mutant lung cancer.Clin Cancer Res. 2019;25(1):158-165. doi:10.1158/1078-0432.CCR-18-2062Cheng L, Lopez-Beltran A, Massari F, MacLennan GT, Montironi R.Molecular testing forBRAFmutations to inform melanoma treatment decisions: a move toward precision medicine.Mod Pathol.2018;31:24-28. doi:10.1038.modpathol.2017.104Lee HM, Morris V, Napolitano S, Kopetz S.Evolving strategies for the management of BRAF-mutant metastatic colorectal cancer.Oncology (Williston Park).2019. 33(6):206-11.Ascierto PA, Ferrucci PF, Fisher R, et al.Dabrafenib, trametinib and pembrolizumab or placebo in BRAF-mutant melanoma.Nature Medicine.2019. 25(6):941-946. doi:10.1038/s41591-019-0448-9Sullivan RJ, Hamid O, Gonzalez R, et al.Atezolizumab plus cobimetinib and vemurafenib inBRAF-mutated melanoma patients.Nat Med. 2019;25(6):929-935. doi:10.1038/s41591-019-0474-7Tan I, Stinchcombe TE, Ready NE, et al.Therapeutic outcomes in non-small cell lung cancer withBRAFmutations: a single institution, retrospective cohort study.Translational Lung Cancer Research.2019;8(3):258-267. doi:10.21037/tlcr.2019.04.03Kopetz S, Grothey A, Yaeger R, et al.Encorafenib, binimetinib, and cetuximab inBRAFV600E–mutated colorectal cancer.N Engl J Med.2019;381:1632-1643. doi:10.1056/NEJMoa1908075Takeda H, Sunakawa Y.Management of BRAF gene alterations in metastatic colorectal cancer: From current therapeutic strategies to future perspectives.Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.602194MedlinePlus.BRAF genetic test.Johns Hopkins Medicine.BRAF mutation and cancer.Additional ReadingHauschild A, Dummer R, Schadendorf D, et al.Longer follow-up confirms relapse-free survival benefit with adjuvant dabrafenib plus trametinib in patients with resectedBRAFV600-mutant stage III melanoma.J Clin Oncol.2018; 36(35):3441-3449. doi:10.1200/jco.18.01219Kwak M, Farrow N, Salama A, et al.Updates in adjuvant systemic therapy for melanoma.J Surg Oncol.2019;119(2):222-231. doi:10.1002/jso.25298MedlinePlus.BRAF gene.Moujaber T, Etemadmoghadam D, Kennedy CJ, et al.BRAFmutations in low-grade serous ovarian cancer and response to BRAF inhibition.JCO Precision Oncology. 2018;(2):1-14. doi:10.1200/PO.17.00221My Cancer Genome.BRAF V600E.Ribas A, Lawrence D, Atkinson V, et al.Combined BRAF and MEK inhibition with PD-1 blockade immunotherapy inBRAF-mutant melanoma.Nat Med.2019;25(6):936-940. doi:10.1038/s41591-019-0476-5
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Dankner M, Rose AAN, Raijkumar S, Siegel PM, Watson IR.Classifying BRAF alterations in cancer: new rational therapeutic strategies for actionable mutations.Oncogene.2018;37(24):3183-3199. doi:10.1038/s41388-018-0171-xDagogo-Jack I, Martinez P, Yeap BY, et al.Impact of BRAF mutation class on disease characteristics and clinical outcomes in BRAF-mutant lung cancer.Clin Cancer Res. 2019;25(1):158-165. doi:10.1158/1078-0432.CCR-18-2062Cheng L, Lopez-Beltran A, Massari F, MacLennan GT, Montironi R.Molecular testing forBRAFmutations to inform melanoma treatment decisions: a move toward precision medicine.Mod Pathol.2018;31:24-28. doi:10.1038.modpathol.2017.104Lee HM, Morris V, Napolitano S, Kopetz S.Evolving strategies for the management of BRAF-mutant metastatic colorectal cancer.Oncology (Williston Park).2019. 33(6):206-11.Ascierto PA, Ferrucci PF, Fisher R, et al.Dabrafenib, trametinib and pembrolizumab or placebo in BRAF-mutant melanoma.Nature Medicine.2019. 25(6):941-946. doi:10.1038/s41591-019-0448-9Sullivan RJ, Hamid O, Gonzalez R, et al.Atezolizumab plus cobimetinib and vemurafenib inBRAF-mutated melanoma patients.Nat Med. 2019;25(6):929-935. doi:10.1038/s41591-019-0474-7Tan I, Stinchcombe TE, Ready NE, et al.Therapeutic outcomes in non-small cell lung cancer withBRAFmutations: a single institution, retrospective cohort study.Translational Lung Cancer Research.2019;8(3):258-267. doi:10.21037/tlcr.2019.04.03Kopetz S, Grothey A, Yaeger R, et al.Encorafenib, binimetinib, and cetuximab inBRAFV600E–mutated colorectal cancer.N Engl J Med.2019;381:1632-1643. doi:10.1056/NEJMoa1908075Takeda H, Sunakawa Y.Management of BRAF gene alterations in metastatic colorectal cancer: From current therapeutic strategies to future perspectives.Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.602194MedlinePlus.BRAF genetic test.Johns Hopkins Medicine.BRAF mutation and cancer.
Dankner M, Rose AAN, Raijkumar S, Siegel PM, Watson IR.Classifying BRAF alterations in cancer: new rational therapeutic strategies for actionable mutations.Oncogene.2018;37(24):3183-3199. doi:10.1038/s41388-018-0171-x
Dagogo-Jack I, Martinez P, Yeap BY, et al.Impact of BRAF mutation class on disease characteristics and clinical outcomes in BRAF-mutant lung cancer.Clin Cancer Res. 2019;25(1):158-165. doi:10.1158/1078-0432.CCR-18-2062
Cheng L, Lopez-Beltran A, Massari F, MacLennan GT, Montironi R.Molecular testing forBRAFmutations to inform melanoma treatment decisions: a move toward precision medicine.Mod Pathol.2018;31:24-28. doi:10.1038.modpathol.2017.104
Lee HM, Morris V, Napolitano S, Kopetz S.Evolving strategies for the management of BRAF-mutant metastatic colorectal cancer.Oncology (Williston Park).2019. 33(6):206-11.
Ascierto PA, Ferrucci PF, Fisher R, et al.Dabrafenib, trametinib and pembrolizumab or placebo in BRAF-mutant melanoma.Nature Medicine.2019. 25(6):941-946. doi:10.1038/s41591-019-0448-9
Sullivan RJ, Hamid O, Gonzalez R, et al.Atezolizumab plus cobimetinib and vemurafenib inBRAF-mutated melanoma patients.Nat Med. 2019;25(6):929-935. doi:10.1038/s41591-019-0474-7
Tan I, Stinchcombe TE, Ready NE, et al.Therapeutic outcomes in non-small cell lung cancer withBRAFmutations: a single institution, retrospective cohort study.Translational Lung Cancer Research.2019;8(3):258-267. doi:10.21037/tlcr.2019.04.03
Kopetz S, Grothey A, Yaeger R, et al.Encorafenib, binimetinib, and cetuximab inBRAFV600E–mutated colorectal cancer.N Engl J Med.2019;381:1632-1643. doi:10.1056/NEJMoa1908075
Takeda H, Sunakawa Y.Management of BRAF gene alterations in metastatic colorectal cancer: From current therapeutic strategies to future perspectives.Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.602194
MedlinePlus.BRAF genetic test.
Johns Hopkins Medicine.BRAF mutation and cancer.
Hauschild A, Dummer R, Schadendorf D, et al.Longer follow-up confirms relapse-free survival benefit with adjuvant dabrafenib plus trametinib in patients with resectedBRAFV600-mutant stage III melanoma.J Clin Oncol.2018; 36(35):3441-3449. doi:10.1200/jco.18.01219Kwak M, Farrow N, Salama A, et al.Updates in adjuvant systemic therapy for melanoma.J Surg Oncol.2019;119(2):222-231. doi:10.1002/jso.25298MedlinePlus.BRAF gene.Moujaber T, Etemadmoghadam D, Kennedy CJ, et al.BRAFmutations in low-grade serous ovarian cancer and response to BRAF inhibition.JCO Precision Oncology. 2018;(2):1-14. doi:10.1200/PO.17.00221My Cancer Genome.BRAF V600E.Ribas A, Lawrence D, Atkinson V, et al.Combined BRAF and MEK inhibition with PD-1 blockade immunotherapy inBRAF-mutant melanoma.Nat Med.2019;25(6):936-940. doi:10.1038/s41591-019-0476-5
Hauschild A, Dummer R, Schadendorf D, et al.Longer follow-up confirms relapse-free survival benefit with adjuvant dabrafenib plus trametinib in patients with resectedBRAFV600-mutant stage III melanoma.J Clin Oncol.2018; 36(35):3441-3449. doi:10.1200/jco.18.01219
Kwak M, Farrow N, Salama A, et al.Updates in adjuvant systemic therapy for melanoma.J Surg Oncol.2019;119(2):222-231. doi:10.1002/jso.25298
MedlinePlus.BRAF gene.
Moujaber T, Etemadmoghadam D, Kennedy CJ, et al.BRAFmutations in low-grade serous ovarian cancer and response to BRAF inhibition.JCO Precision Oncology. 2018;(2):1-14. doi:10.1200/PO.17.00221
My Cancer Genome.BRAF V600E.
Ribas A, Lawrence D, Atkinson V, et al.Combined BRAF and MEK inhibition with PD-1 blockade immunotherapy inBRAF-mutant melanoma.Nat Med.2019;25(6):936-940. doi:10.1038/s41591-019-0476-5
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