RB in breast cancer: At the crossroads of tumorigenesis and treatment

Emily E. Bosco, Erik S. Knudsen

Research output: Contribution to journalReview articlepeer-review

82 Scopus citations


Cancer is a highly heterogeneous disease, wherein specific determinants modulate disease severity and therapeutic outcomes. In breast cancer, significant effort has been channeled into defining critical genetic effectors of disease behavior. One key molecular determinant is the retinoblastoma tumor suppressor (RB), which is functionally inactivated in the majority of human cancers, and aberrant in nearly half of breast cancers. Deficiency in RB function compromises cell cycle checkpoints, contributes to aggressive tumor proliferation, and is associated with advanced disease. Recent investigation indicates that RB-deficiency has dramatic and disparate effects on the response to therapeutic modalities utilized in the treatment of breast cancer. Loss of RB function promotes inappropriate cell cycle progression during therapeutic challenge. In the context of cytotoxic therapies, this lack of checkpoint function leads to increased sensitivity to the agent. However, RB-deficiency efficiently bypasses the anti-mitogenic function of hormonal therapies and is associated with early disease recurrence following tamoxifen therapy. Thus, RB-pathway status has powerful effects on both tumorigenic proliferation and therapeutic response, and may represent a critical basis for informing breast cancer therapy.

Original languageEnglish (US)
Pages (from-to)667-671
Number of pages5
JournalCell Cycle
Issue number6
StatePublished - Mar 15 2007


  • Breast cancer
  • DNA damage
  • E2F
  • RB
  • Tamoxifen

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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