Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

Br J Cancer. 1999 Mar;79(7-8):1220-6. doi: 10.1038/sj.bjc.6690196.

Abstract

The present study investigated the interaction between c-erbB2 overexpression and the response to first-line endocrine therapy in patients with advanced breast cancer. The primary tumours of 241 patients who were treated at first relapse with endocrine therapy were assessed for overexpression of c-erbB2 by immunohistochemistry. c-erbB2 was overexpressed in 76 (32%) of primary breast cancers and did not correlate with any other prognostic factor. The overall response to treatment and time to progression were significantly lower in patients with c-erbB2-positive tumours compared to those that were c-erbB2-negative (38% vs 56%, P = 0.02; and 4.1 months vs 8.7 months, P < 0.001, respectively). In multivariate analysis, c-erbB2 status was the most significant predictive factor for a short time to progression (P = 0.0009). In patients with ER-positive primary tumours treated at relapse with tamoxifen (n = 170), overexpression of c-erbB2 was associated with a significantly shorter time to progression (5.5 months vs 11.2 months, P < 0.001). In conclusion, overexpression of c-erbB2 in the primary tumour is an independent marker of relative resistance to first-line endocrine therapy in patients with advanced breast cancer. In patients with ER-positive primary tumours, the overexpression of c-erbB2 defines a subgroup less likely to respond to endocrine therapy.

MeSH terms

  • Adult
  • Aged
  • Analysis of Variance
  • Antineoplastic Agents, Hormonal / therapeutic use
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Breast Neoplasms / therapy*
  • Disease Progression
  • Female
  • Humans
  • Immunohistochemistry
  • Middle Aged
  • Receptor, ErbB-2 / metabolism*
  • Receptors, Estrogen / metabolism
  • Tamoxifen / therapeutic use

Substances

  • Antineoplastic Agents, Hormonal
  • Receptors, Estrogen
  • Tamoxifen
  • Receptor, ErbB-2