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Rationale for targeting the Ras/MAPK pathway in triple-negative breast cancer.

Authors
  • 1
  • 2
  • 1 Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN 37232, USA.
  • 2 Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA.
Type
Published Article
Journal
Discovery medicine
1944-7930
Publication Date
Volume
17
Issue
95
Pages
275–283
Identifiers
PMID: 24882719
Source
Medline
License
Unknown

Abstract

"Triple negative" breast cancer (TNBC) is the most aggressive and least common clinical subtype of breast cancer. As its nomenclature implies, TNBC lacks specific biomarker expression marking response to an effective targeted therapy. The incidence of TNBC is higher in young minority women who suffer from high rates of early recurrence and death from their disease. Mounting preclinical evidence supports targeting the Ras/MAPK cell signaling pathway in the TNBC subtype, despite large genomic surveys such as The Cancer Genome Atlas demonstrating infrequent canonical mutations in this pathway. Due to the early spread of TNBC, targeted treatment in the neoadjuvant setting may offer the effective therapeutic punch needed to eliminate micro-metastatic disease and reduce mortality. Herein, we will review the evidence supporting clinical trials of targeted inhibitors of the Ras/MAPK pathway in TNBC, and discuss the obstacles and opportunities of this approach.

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