Neoadjuvant treatment for HER-2-positive and triple-negative breast cancers

Ann Oncol. 2012 Sep:23 Suppl 10:x237-42. doi: 10.1093/annonc/mds348.

Abstract

Neoadjuvant therapy (NT) has become a valuable research tool for the incorporation of alternative cytotoxic agents, as well as new biological therapies, into anthracycline and taxane chemotherapy-based regimens. Her-2-positive disease is predictive of higher pathological complete response (pCR) to neoadjuvant chemotherapy and trastuzumab. Benefits were also seen for the combination of trastuzumab with lapatinib or pertuzumab, suggesting that dual blockage of the HER-2 will probably emerge as the new standard. Triple-negative phenotype is also predictive of high pCR to NT, but the prognosis of patients whose tumours do not achieve a pCR after neoadjuvant chemotherapy with anthracyclines and taxanes is dismal. Currently, it is recommended to use the same chemotherapy regimens as in non-triple-negative disease. The suggested benefit of neoadjuvant platinum, mainly in BRCA1-related cancers, needs to be confirmed in large randomized trials. Bevacizumab combined with neoadjuvant chemotherapy yields increased pCR compared with non-bevacizumab treatment, in large randomized data recently published. One study suggested higher benefit in triple-negative tumours. Long-term follow-up of these trials is needed to understand the role of bevacizumab treatment in BC and its important to find predictive biomarkers of response to this drug.

Publication types

  • Congress
  • Overall

MeSH terms

  • Anthracyclines / therapeutic use
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Antineoplastic Agents / therapeutic use
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology
  • Female
  • Humans
  • Lapatinib
  • Neoadjuvant Therapy*
  • Quinazolines / therapeutic use
  • Receptor, ErbB-2* / genetics
  • Receptor, ErbB-2* / metabolism
  • Receptors, Estrogen* / genetics
  • Receptors, Estrogen* / metabolism
  • Taxoids / therapeutic use
  • Trastuzumab

Substances

  • Anthracyclines
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents
  • Quinazolines
  • Receptors, Estrogen
  • Taxoids
  • Lapatinib
  • ERBB2 protein, human
  • Receptor, ErbB-2
  • pertuzumab
  • Trastuzumab