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BRAF V600E and metastatic colorectal cancer

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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BRAF V600E and metastatic colorectal cancer

BRAF is a serine-threonine kinase playing a key role as downstream RAS effector in the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signal transduction cascade

BRAF V600E mutation accounts for 8-10% of metastatic colorectal cancer (mCRC) patients and it is an established prognostic factor (1,2)

  • is recognized as a poor prognostic factor with a median overall survival inferior to 20 months (1)

  • BRAF V600E mutant mCRCs are frequently characterized by hypermethylation, microsatellite instability (MSI) and consensus molecular subtype 1 (CMS1)

  • BRAF mutations account for 8-10% of mCRCs and more than 90% are missense mutations occurring in codon 600, leading to an aminoacidic substitution of a valine for a glutamic acid (V600E)

  • BRAF mutations different from V600E (BRAFnon-V600E) account for about 2% of mCRCs and they have been associated with specific clinicopathological features and a better clinical outcome

  • MSI mCRCs harboring BRAFV600E mutation are always sporadic and do not arise in the context of Lynch Syndrome

  • BRAFV600E mutation is also a target of treatment in various types of malignancies such as melanoma, non-small cell lung cancer (NSCLC), and hairy-cell leukemia
    • BRAF inhibitors in monotherapy do not have the same clinical activity for colorectal cancer relative to other solid tumors harboring an oncogenic BRAF V600E mutation, combination approaches targeting BRAF + MEK +EGFR hold promise for patients BRAF V600E colorectal cancer (3)

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