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The molecular mechanism underlying the acquisition of the antiestrogen-resistant phenotype in breast cancer

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Abstract

Breast cancer is thought to develope as an estrogen-dependent tumor. Approximately 30% of breast cancers can be treated by agents that block estrogen. However, all breast cancers have been known to acquire the hormone therapy-resistant phenotype with ultimate fatal results. Recent progress in breast cancer research has provided the important clues for elucidating the molecular mechanism of this conversion. The presence of the cross-talk between estrogen signaling and other mitogen-dependent signaling has been clarified at the estrogen receptor level. In addition, an estrogen-dependent transcriptional control mechanism has been characterized in detail. These breakthrough and the development of a pure antiestrogen would make it possible to consider the more sophisticated hormone therapy. In this review article, I summarized the current findings which seem to be essential in the treatment of breast cancer.

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Abbreviations

E2:

Estradiol-1 7ß

ER:

Estrogen receptor

CBP:

CREB binding protein

ERE:

Estrogen responsive element

TAM:

Tamoxifen

TGF:

Transforming growth factor

EGF:

Epidermal growth factor

FGF:

Fibroblast growth factor

IGF 1:

Insulin-like growth factor 1

CDK:

Cyclin-dependent kinase

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Author information

Correspondence to Bunzo Sato.

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Sato, B. The molecular mechanism underlying the acquisition of the antiestrogen-resistant phenotype in breast cancer. Breast Cancer 5, 25 (1998). https://doi.org/10.1007/BF02967412

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Keywords

  • Estrogen action
  • Cyclin D1
  • Growth factors
  • Antiestrogen
  • Hormone resistance