Epidermal growth factor receptor (ErbB1) expression in prostate cancer progression: correlation with androgen independence

Prostate. 2006 Sep 15;66(13):1437-44. doi: 10.1002/pros.20460.

Abstract

Background: The role of the epidermal growth factor receptor (ErbB1) in the progression of prostate cancer is incompletely understood.

Methods: Tissue microarrays from hormone-naive and advanced androgen-independent tumors were used to investigate the role of ErbB1 in prostate cancer progression.

Results: ErbB1 expression in tumor tissues was strongly associated with hormone-refractory status (odds ratio = 6.67, 95% CI = (2.6, 17.4), P = 0.0001). However, ErbB1 overexpression was not a statistically significant covariate in a multivariate proportional hazards model for biochemical failure of hormone-naïve prostate cancer. Moreover, ErbB1 overexpression was not associated with tumor differentiation (P = 0.44), positive margins (P = 0.53), seminal vesicle invasion (P = 0.69), extraprostatic extension (P = 0.10), or preoperative PSA (P = 0.18) in the hormone-naïve group.

Conclusions: These findings are consistent with a model in which ErbB1 expression increases during the development of the androgen-independent state, and suggest that drugs targeted toward ErbB signaling could be of therapeutic relevance in the management of advanced prostatic carcinoma.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Androgens / physiology*
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / pathology
  • Disease Progression
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Middle Aged
  • Multivariate Analysis
  • Neoplasm Metastasis / genetics
  • Neoplasm Metastasis / pathology
  • Neoplasm Staging
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology*
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism

Substances

  • Androgens
  • Receptors, Androgen
  • ErbB Receptors