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Herceptin: mechanisms of action and resistance

Rita Nahta1, Francisco J Esteva

  • 1Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030-4009, USA.

Cancer Letters
|February 7, 2006
PubMed

Insights

Human Epidermal Growth Factor Receptor 2 (HER-2) overexpression in breast cancer indicates aggressive disease. This review covers how HER-2 targeted therapy like Herceptin works and why resistance develops.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • HER-2 overexpression occurs in 20-25% of invasive breast cancers, correlating with aggressive phenotypes and poorer survival.
  • HER-2 status is crucial for predicting response to HER-2-targeted therapies, such as the antibody Herceptin.
  • Accurate HER-2 assessment is vital for patient selection for HER-2-targeted treatment.

Purpose of the Study:

  • To review the mechanisms of Herceptin's anti-cancer effects in HER-2 overexpressing breast cancers.
  • To explore the potential mechanisms underlying the development of resistance to Herceptin therapy.

Main Methods:

  • Literature review of studies on HER-2 expression, Herceptin efficacy, and resistance mechanisms in breast cancer.
  • Analysis of preclinical and clinical data regarding HER-2 targeted therapy.

Main Results:

  • Herceptin, in combination with chemotherapy, improves response rates, delays disease progression, and enhances survival in HER-2 positive breast cancer.
  • Despite initial efficacy, most HER-2 positive breast cancers develop resistance to Herceptin within a year.

Conclusions:

  • Understanding HER-2 biology and Herceptin's action is key to optimizing breast cancer treatment.
  • Further research into resistance mechanisms is necessary to overcome treatment limitations and improve long-term outcomes for patients with HER-2 positive breast cancer.

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