Tamoxifen may prevent both ER+ and ER- breast cancers and select for ER- carcinogenesis: an alternative hypothesis

Breast Cancer Res. 2005;7(6):R1153-8. doi: 10.1186/bcr1342. Epub 2005 Nov 21.

Abstract

Introduction: Breast Cancer Prevention Trial (BCPT) and Multiple Outcomes of Raloxifene (MORE) data have been interpreted to indicate that tamoxifen reduces the risk of ER+ but not ER- breast carcinogenesis. We explored whether these data also support an alternative hypothesis, that tamoxifen influences the natural history of both ER+ and ER- cancers, that it may be equally effective in abrogating or delaying ER- and ER+ carcinogenesis, and place selection pressure, in some cases, for the outgrowth of ER- cancers.

Methods: BCPT and MORE data were used to investigate whether: first, tamoxifen could reduce equally the emergence of ER- and ER+ tumors; and second, tamoxifen could select a fraction of emerging ER+ cancers and promote their transformation to ER- cancers. Assuming that some proportion, Z, of ER+ tumors becomes ER- after tamoxifen exposure and that the risk reduction for both ER- and ER+ tumors is equal, we solved for both the transformation rate and the risk reduction rate.

Results: If tamoxifen equally reduces the incidence of ER+ and ER- tumors by 60%, the BCPT results are achieved with a transformation of approximately Z = 20% of ER+ to ER- tumors. Validation with MORE data using an equal risk reduction of 60% associated with tamoxifen produces an almost identical transformation rate Z of 23%.

Conclusion: Data support an alternative hypothesis that tamoxifen may promote ER- carcinogenesis from a precursor lesion that would otherwise have developed as ER+ without tamoxifen selection.

MeSH terms

  • Adult
  • Aged
  • Antineoplastic Agents, Hormonal / pharmacology*
  • Breast Neoplasms / epidemiology
  • Breast Neoplasms / genetics
  • Breast Neoplasms / physiopathology
  • Breast Neoplasms / prevention & control*
  • Cell Transformation, Neoplastic / drug effects*
  • Chemoprevention
  • Female
  • Genes, BRCA1
  • Genes, BRCA2
  • Genetic Predisposition to Disease
  • Humans
  • Incidence
  • Middle Aged
  • Neoplasms, Second Primary / chemically induced
  • Neoplasms, Second Primary / physiopathology
  • Ovariectomy
  • Receptors, Estrogen / antagonists & inhibitors
  • Receptors, Estrogen / physiology*
  • Risk Factors
  • Tamoxifen / pharmacology*

Substances

  • Antineoplastic Agents, Hormonal
  • Receptors, Estrogen
  • Tamoxifen