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Trying for a BRAF Slam Dunk

Antoni Ribas1, Roger S Lo1

  • 1Jonsson Comprehensive Cancer Center at the University of California, Los Angeles, Los Angeles, California. aribas@mednet.ucla.edu rlo@mednet.ucla.edu.

Cancer Discovery
|May 3, 2020
PubMed

Insights

Vemurafenib showed activity in 13 cancers with BRAF V600 mutations. However, response rates varied, indicating different cancer types rely differently on the BRAF oncogene.

Area of Science:

  • Oncology
  • Molecular Biology
  • Clinical Trials

Background:

  • The BRAF V600 mutation is a key driver oncogene in various cancers.
  • Targeted therapies like vemurafenib have shown promise against BRAF-mutated cancers.
  • Basket trials are designed to test a single drug in multiple cancer types harboring a specific mutation.

Purpose of the Study:

  • To evaluate the activity of the BRAF inhibitor vemurafenib across multiple cancer types with BRAF V600 mutations.
  • To investigate the variability in response rates to vemurafenib among different cancer histologies.

Main Methods:

  • A first-in-human basket clinical trial design.
  • Administration of the BRAF inhibitor vemurafenib.
  • Assessment of drug activity and response rates in patients with 13 distinct cancer types harboring BRAF V600 mutations.

Main Results:

  • Vemurafenib demonstrated clinical activity in all 13 tested cancer types with BRAF V600 mutations.
  • Significant variability in response rates was observed across the different cancer histologies.
  • This suggests differential reliance on the BRAF-driven oncogenic pathway based on cancer type.

Conclusions:

  • The BRAF inhibitor vemurafenib exhibits activity across a spectrum of BRAF V600-mutated cancers.
  • Cancer histology significantly influences the degree of oncogenic pathway addiction, impacting treatment response.
  • These findings highlight the complexity of targeted therapy efficacy and the need for histology-specific considerations.

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