rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1990-8-13
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pubmed:abstractText |
The effects induced by the antiandrogen Cyproterone Acetate (CPA) on the proliferation of EVSA-T human breast cancer cells endowed with androgen receptors were studied. Kinetic analyses were carried out by two autoradiographic techniques measuring the percentage of cells in S-phase and the growth fraction (GF). The exposure of the cultures to CPA for 24 h caused a marked inhibition on S-phase cells without significantly affecting the CF. The accumulation of cells in G1-phase, confirmed by cytometric analysis, was rescued to the S compartment by replacing the culture medium 24 h after CPA administration. Exposure of EVSA-T to Doxorubicin or Methotrexate after CPA and medium change at the time of maximal proliferative recruitment, led to an enhancement of cytotoxicity as demonstrated by colony survival assay.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Androgen Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cyproterone,
http://linkedlifedata.com/resource/pubmed/chemical/Cyproterone Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Doxorubicin,
http://linkedlifedata.com/resource/pubmed/chemical/Methotrexate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Androgen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Progesterone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Steroid
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pubmed:status |
MEDLINE
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pubmed:issn |
0250-7005
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
853-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2142397-Androgen Antagonists,
pubmed-meshheading:2142397-Antineoplastic Agents,
pubmed-meshheading:2142397-Breast Neoplasms,
pubmed-meshheading:2142397-Cell Cycle,
pubmed-meshheading:2142397-Cell Division,
pubmed-meshheading:2142397-Cell Line,
pubmed-meshheading:2142397-Cell Nucleus,
pubmed-meshheading:2142397-Cyproterone,
pubmed-meshheading:2142397-Cyproterone Acetate,
pubmed-meshheading:2142397-Cytosol,
pubmed-meshheading:2142397-DNA, Neoplasm,
pubmed-meshheading:2142397-Doxorubicin,
pubmed-meshheading:2142397-Drug Synergism,
pubmed-meshheading:2142397-Female,
pubmed-meshheading:2142397-Humans,
pubmed-meshheading:2142397-Methotrexate,
pubmed-meshheading:2142397-Receptors, Androgen,
pubmed-meshheading:2142397-Receptors, Estrogen,
pubmed-meshheading:2142397-Receptors, Progesterone,
pubmed-meshheading:2142397-Receptors, Steroid,
pubmed-meshheading:2142397-Tumor Cells, Cultured
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pubmed:articleTitle |
Manipulation of the growth rate of human breast cancer cells by antiandrogen followed by chemotherapy.
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pubmed:affiliation |
Department of Pharmacology, Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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