Breast Cancer Research and Treatment

, Volume 26, Issue 3, pp 237–246

Measurement of steroid hormone receptors in breast cancer patients on tamoxifen

Authors

  • Carlos A. Encarnación
    • Department of Medicine, Division of Medical OncologyUniversity of Texas Health Science Center at San Antionio
  • Daniel R. Ciocca
    • Laboratorio de Reproducción y Lactancia (LARLAC)
  • William L. McGuire
    • Department of Medicine, Division of Medical OncologyUniversity of Texas Health Science Center at San Antionio
  • Gary M. Clark
    • Department of Medicine, Division of Medical OncologyUniversity of Texas Health Science Center at San Antionio
  • Suzanne A. W. Fuqua
    • Department of Medicine, Division of Medical OncologyUniversity of Texas Health Science Center at San Antionio
  • C. Kent Osborne
    • Department of Medicine, Division of Medical OncologyUniversity of Texas Health Science Center at San Antionio
Report

DOI: 10.1007/BF00665801

Cite this article as:
Encarnación, C.A., Ciocca, D.R., McGuire, W.L. et al. Breast Cancer Res Tr (1993) 26: 237. doi:10.1007/BF00665801

Summary

Estrogen (ER) and progesterone receptor (PgR) positive breast tumors often respond to tamoxifen, but ultimately progress as they become tamoxifen resistant. An accurate assessment of receptor status in specimens from tamoxifen-resistant patients could help to understand potential mechanisms of resistance and to predict response to second line hormonal therapies. However, since tamoxifen itself can affect ER and PgR determinations, assay results can be misleading. We measured ER and PgR by both ligand binding (LBA) and immunohistochemical (IHC) assays in 34 tumors from patients on tamoxifen, 30 of whom were displaying resistance to the drug. These tumors were classified into several receptor phenotypes. Eleven patients, 8 of whom were clearly progressing, expressed both receptors while on tamoxifen. ER was significantly less often negative when measured by IHC, suggesting that ER status by LBA was falsely negative in this group due to receptor occupancy by tamoxifen. Six patients had no detectable ER by LBA or IHC but still expressed PgR. The presence of PgR suggests that ER could still be functional, though undetectable, in these tumors, or that PgR is constitutively expressed by them. Finally, 12 patients were ER and PgR-negative by both assays, suggesting hormonal independence as the mechanism for resistance in this group. In a subset of patients with receptor assays both prior to tamoxifen and at the time of progression while taking the drug, we found that most ER-positive tumors converted to an apparent ER-negative status when assayed by LBA, while PgR status frequently remained unchanged. The continued expression of ER and/or PgR in many patients with tumor progression on tamoxifen indicates that mechanisms for resistance other than receptor loss are common in breast cancer.

Key words

tamoxifenestrogen receptorprogesterone receptorligand binding assayimmunohistochemical assaydrug resistance

Copyright information

© Kluwer Academic Publishers 1993