Indication
Malignant melanoma with BRAF V600E mutation
Malignant melanoma with BRAF V600E mutation is an aggressive neoplasm of the integumentary system arising from the malignant transformation of pigment-producing melanocytes. Read more about Malignant melanoma with BRAF V600E mutation
11 drugs 6 manufacturers
Drugs that treat it
Common Malignant melanoma with BRAF V600E mutation therapies.
MEKINIST (trametinib dimethyl sulfoxide)
COTELLIC (cobimetinib fumarate)
MEKINIST (trametinib dimethyl sulfoxide)
TAFINLAR (dabrafenib mesylate)
BRAFTOVI (encorafenib)
MEKTOVI (binimetinib)
BRAFTOVI (encorafenib)
MEKTOVI (binimetinib)
News & literature
Coming soonRelated codes
Coming soonRelated conditions & guidelines
Coming soonMalignant melanoma with BRAF V600E mutation is an aggressive neoplasm of the integumentary system arising from the malignant transformation of pigment-producing melanocytes.
The defining molecular feature is a specific somatic missense mutation in the *BRAF* proto-oncogene where valine is substituted by glutamic acid at codon 600, leading to constitutive, ligand-independent activation of the downstream MAPK/ERK kinase pathway.
This unconstrained signaling accelerates cellular proliferation, survival, and metastatic potential, most frequently manifesting in cutaneous lesions associated with intermittent ultraviolet radiation exposure.
Identification of this actionable biomarker delineates a distinct therapeutic subset responsive to targeted kinase inhibition, notably within advanced, unresectable, or metastatic disease stages.
- nih.gov
Malignant melanoma with BRAF V600E mutation is an aggressive neoplasm of the integumentary system arising from the malignant transformation of pigment-producing melanocytes The defining molecular feature is a specific somatic missense mutation in the *BRAF* proto-oncogene where valine is substituted by glutamic acid at codon 600, leading to constitutive, ligand-independent activation of the downstream MAPK/ERK kinase pathway This unconstrained signaling accelerates cellular proliferation, surviv...
- nih.gov
The defining molecular feature is a specific somatic missense mutation in the *BRAF* proto-oncogene where valine is substituted by glutamic acid at codon 600, leading to constitutive, ligand-independent activation of the downstream MAPK/ERK kinase pathway This unconstrained signaling accelerates cellular proliferation, survival, and metastatic potential, most frequently manifesting in cutaneous lesions associated with intermittent ultraviolet radiation exposure
- nih.gov
The defining molecular feature is a specific somatic missense mutation in the *BRAF* proto-oncogene where valine is substituted by glutamic acid at codon 600, leading to constitutive, ligand-independent activation of the downstream MAPK/ERK kinase pathway
- nih.gov
This unconstrained signaling accelerates cellular proliferation, survival, and metastatic potential, most frequently manifesting in cutaneous lesions associated with intermittent ultraviolet radiation exposure
- nih.gov
Identification of this actionable biomarker delineates a distinct therapeutic subset responsive to targeted kinase inhibition, notably within advanced, unresectable, or metastatic disease stages
- nih.gov
Identification of this actionable biomarker delineates a distinct therapeutic subset responsive to targeted kinase inhibition, notably within advanced, unresectable, or metastatic disease stages
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