Cited by 82Estrogen and related hormone effectsProstate Cancer Treatment and ResearchBreast Cancer Treatment Studies

Human breast cancer: androgen action mediated by estrogen receptor.

Zava, David T., McGuire, William L.·1978·Science

Abstract

Growth of the human breast cancer cell line MCF-7 is enhanced by androgens, but only at pharmacological concentrations. Although physiological concentrations of androgens translocate the androgen receptor into the nucleus, no mitogenic effects are observed. By contrast, pharmacological androgens translocate not only the androgen receptor but also the estrogen receptor, and at these high doses significantly increase both DNA and estrogen-dependent protein synthesis. We therefore propose that androgens stimulate MCF-7 cell growth not through the androgen receptor but rather through the estrogen receptor.

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Crossref · 10.1126/science.622569

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7 of 7 references verified0 citation errors · 0 not checkable

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Authors
Zava, D. T., & McGuire, W. L.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Venue
Science
Published
1978-02-17
Volume
199
Issue
4330
Pages
787-788
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2075739846
Cited by
82
References
7
Citations by year
2018: 2 · 2016: 1 · 2014: 1 · 2013: 1 · 2012: 1
FWCI
7.17
Type
journal article
Language
en
Open access
closed
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
Keywords
breast cancer, androgen action, estrogen receptor, androgen receptor, MCF-7 cells, cell growth, mitogen response, receptor translocation, DNA synthesis, protein synthesis
MeSH terms
Androgens, Breast Neoplasms, Cell Line, Cell Nucleus, Cytoplasm, Humans, Receptors, Androgen, Receptors, Estrogen, Receptors, Glucocorticoid, Receptors, Progesterone, Dihydrotestosterone, Stimulation, Chemical, Translocation, Genetic

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