Searching On:

Disease:

Gene:

BRAF, V600E (c.1799T>A)

View:
Expand Collapse No disease selected  - General Description
Mass General Hospital Cancer Center treats patients with many cancer types. To learn more about the different cancer types that can be treated at the Cancer Center, please visit the Cancer Center website at the following page: http://www.massgeneral.org/cancer/services/
Expand Collapse BRAF  - General Description The BRAF gene encodes a serine/threonine kinase that activates the growth-promoting MAP kinase signaling cascade. BRAF is commonly activated by somatic point mutations in human cancers, most frequently by mutations located within the kinase domain at amino acid positions G466, G469, L597 and V600. In regards to treatment, the Food and Drug Administration (FDA) approved the BRAF inhibitor, vemurafenib, for the treatment of unresectable or metastatic melanoma patients harboring specifically the BRAF V600E mutation, as detected by an FDA-approved test. In addition, there are a growing number of targeted agents that are being evaluated for the treatment of various BRAF-mutant advanced cancers, including other RAF kinase inhibitors and/or MEK inhibitors. Recently, the combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib was approved by FDA for the treatment of patients with BRAF V600E or V600K mutations. Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of BRAF mutations in thyroid cancer (30-40%), melanoma (20-30%) and colon cancer (10-15%). To read more about the various BRAF based trials ongoing at the MGH Cancer Center, click on the "disease-gene-mutation" tab on the web page, and select relevant information. Current trials will appear as a ist under the posted information. Source: Genetics Home Reference The BRAF gene encodes a serine/threonine kinase that activates the growth-promoting MAP kinase signaling cascade. BRAF is commonly activated by somatic point mutations in human cancers, most frequently by mutations located within the kinase domain at amino acid positions G466, G469, L597 and V600. In regards to treatment, the Food and Drug Administration (FDA) approved the BRAF inhibitor, vemurafenib, for the treatment of unresectable or metastatic melanoma patients harboring specifically the BRAF V600E mutation, as detected by an FDA-approved test. In addition, there are a growing number of targeted agents that are being evaluated for the treatment of various BRAF-mutant advanced cancers, including other RAF kinase inhibitors and/or MEK inhibitors. Recently, the combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib was approved by FDA for the treatment of patients with BRAF V600E or V600K mutations. Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of BRAF mutations in thyroid cancer (30-40%), melanoma (20-30%) and colon cancer (10-15%). To read more about the various BRAF based trials ongoing at the MGH Cancer Center, click on the "disease-gene-mutation" tab on the web page, and select relevant information. Current trials will appear as a ist under the posted information. Source: Genetics Home Reference
CLICK IMAGE FOR MORE INFORMATION
The BRAF gene encodes a serine/threonine kinase that activates the growth-promoting MAP kinase signaling cascade. BRAF is commonly activated by somatic point mutations in human cancers, most frequently by mutations located within the kinase domain at amino acid positions G466, G469, L597 and V600.

In regards to treatment, the Food and Drug Administration (FDA) approved the BRAF inhibitor, vemurafenib, for the treatment of unresectable or metastatic melanoma patients harboring specifically the BRAF V600E mutation, as detected by an FDA-approved test. In addition, there are a growing number of targeted agents that are being evaluated for the treatment of various BRAF-mutant advanced cancers, including other RAF kinase inhibitors and/or MEK inhibitors. Recently, the combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib was approved by FDA for the treatment of patients with BRAF V600E or V600K mutations.

Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of BRAF mutations in thyroid cancer (30-40%), melanoma (20-30%) and colon cancer (10-15%).

To read more about the various BRAF based trials ongoing at the MGH Cancer Center, click on the "disease-gene-mutation" tab on the web page, and select relevant information. Current trials will appear as a ist under the posted information.


Source: Genetics Home Reference
The BRAF gene encodes a serine/threonine kinase that activates the growth-promoting MAP kinase signaling cascade. BRAF is commonly activated by somatic point mutations in human cancers, most frequently by mutations located within the kinase domain at amino acid positions G466, G469, L597 and V600.

In regards to treatment, the Food and Drug Administration (FDA) approved the BRAF inhibitor, vemurafenib, for the treatment of unresectable or metastatic melanoma patients harboring specifically the BRAF V600E mutation, as detected by an FDA-approved test. In addition, there are a growing number of targeted agents that are being evaluated for the treatment of various BRAF-mutant advanced cancers, including other RAF kinase inhibitors and/or MEK inhibitors. Recently, the combination of the BRAF inhibitor dabrafenib with the MEK inhibitor trametinib was approved by FDA for the treatment of patients with BRAF V600E or V600K mutations.

Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of BRAF mutations in thyroid cancer (30-40%), melanoma (20-30%) and colon cancer (10-15%).

To read more about the various BRAF based trials ongoing at the MGH Cancer Center, click on the "disease-gene-mutation" tab on the web page, and select relevant information. Current trials will appear as a ist under the posted information.

Source: Genetics Home Reference
PubMed ID's
12068308, 15947100, 20401974, 20425073, 21606968
Expand Collapse V600E (c.1799T>A)  in BRAF
The BRAF V600E mutation arises from a single nucleotide change (c.1799T>A) and results in an amino acid substitution of the valine (V) at position 600 by a glutamic acid (E).
The BRAF V600E mutation arises from a single nucleotide change (c.1799T>A) and results in an amino acid substitution of the valine (V) at position 600 by a glutamic acid (E).

Share with your Physican

Print information for your Physician.

Print information

Your Matched Clinical Trials

Trial Matches: (G) - Gene, (M) - Mutation
Trial Status: Showing Results: 1-10 of 19 Per Page:
12Next »
Protocol # Title Location Status Match
NCT02327169 A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies MGH Open GM
NCT02110355 A Phase 1b/2a Study Evaluating AMG 232 in Metastatic Melanoma A Phase 1b/2a Study Evaluating AMG 232 in Metastatic Melanoma MGH Open GM
NCT02428712 A Study of PLX8394 as a Single Agent in Patients With Advanced Unresectable Solid Tumors A Study of PLX8394 as a Single Agent in Patients With Advanced Unresectable Solid Tumors MGH Open GM
NCT01989585 Dabrafenib, Trametinib, and Navitoclax in Treating Patients With BRAF Mutant Melanoma or Solid Tumors That Are Metastatic or Cannot Be Removed by Surgery Dabrafenib, Trametinib, and Navitoclax in Treating Patients With BRAF Mutant Melanoma or Solid Tumors That Are Metastatic or Cannot Be Removed by Surgery MGH Open GM
NCT02034110 Efficacy and Safety of the Combination Therapy of Dabrafenib and Trametinib in Subjects With BRAF V600E- Mutated Rare Cancers Efficacy and Safety of the Combination Therapy of Dabrafenib and Trametinib in Subjects With BRAF V600E- Mutated Rare Cancers MGH Open GM
NCT02097225 Onalespib, Dabrafenib, and Trametinib in Treating Patients With BRAF-Mutant Melanoma or Solid Tumors That Are Metastatic or Cannot Be Removed by Surgery Onalespib, Dabrafenib, and Trametinib in Treating Patients With BRAF-Mutant Melanoma or Solid Tumors That Are Metastatic or Cannot Be Removed by Surgery MGH Open GM
NCT02961283 Study of ASN003 in Subjects With Advanced Solid Tumors Study of ASN003 in Subjects With Advanced Solid Tumors MGH Open GM
NCT02974725 Study of LXH254 and LTT462 in NSCLC Study of LXH254 and LTT462 in NSCLC MGH Open GM
NCT02723006 Study to Evaluate the Safety, Tolerability, and Pharmacodynamics of Investigational Treatments in Combination With Standard of Care Immune Checkpoint Inhibitors in Participants With Advanced Melanoma Study to Evaluate the Safety, Tolerability, and Pharmacodynamics of Investigational Treatments in Combination With Standard of Care Immune Checkpoint Inhibitors in Participants With Advanced Melanoma MGH Open GM
NCT03224767 Vemurafenib and Cobimetinib in Treating Patients With BRAF V600E Mutation Positive Craniopharyngioma Vemurafenib and Cobimetinib in Treating Patients With BRAF V600E Mutation Positive Craniopharyngioma MGH Open GM
Trial Status: Showing Results: 1-10 of 19 Per Page:
12Next »

Share with your Physican

Print information for your Physician.

Print information