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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1980-6-25
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pubmed:abstractText |
The growth and regression patterns of estrogen (E)-sensitive mammary tumors (SNMU) and autonomous mammary tumors (ANMU) were studied in normal, castrated, and alpha-fetoprotein (AFP)-secreting and nonsecreting hepatoma-bearing female BUF rats. Both SNMU and ANMU tumors had comparable amounts of E receptor. SNMU tumors grew faster in female hosts than in male hosts. The latency period of SNMU tumors was lengthened when the tumor was inoculated into newborn hosts. These E-sensitive tumors regressed after castration of the adult hosts. Tumor regression was also observed in SNMU-bearing rats inoculated with AFP-secreting hepatomas. The growth pattern of the ANMU tumor was not affected by the sex or age of the host. Castration and inoculation of hepatomas to ANMU tumor-bearing rats did not result in regression of the ANMU tumors. We suggest that AFP inhibited the growth of E-sensitive cells in newborn and hepatoma 7777-bearing hosts. This inhibitory effect of AFP could not be attributed to a "functional castration" resulting from the trapping of 17 beta-estradiol (E2) by AFP, because the plasma levels of E2 in these animals affect levels of gonadotropins. Moreover, castration of hepatoma 7777-bearing rats resulted in increased plasma follicle-stimulating hormone and luteinizing hormones levels. The results strongly suggested that a) the malignant properties of E2-sensitive cells in adult hosts can be controlled by AFP, and b) the mechanism by which AFP inhibits the growth of E2-sensitive cells is independent of the E2 "trapping" phenomenon. An ontogenetic approach to the mechanism of action of estrogens may account for available results.
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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/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Follicle Stimulating Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Luteinizing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/alpha-Fetoproteins
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0027-8874
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
64
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1147-52
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:6154169-Animals,
pubmed-meshheading:6154169-Animals, Newborn,
pubmed-meshheading:6154169-Castration,
pubmed-meshheading:6154169-Estradiol,
pubmed-meshheading:6154169-Female,
pubmed-meshheading:6154169-Follicle Stimulating Hormone,
pubmed-meshheading:6154169-Liver Neoplasms, Experimental,
pubmed-meshheading:6154169-Luteinizing Hormone,
pubmed-meshheading:6154169-Male,
pubmed-meshheading:6154169-Mammary Neoplasms, Experimental,
pubmed-meshheading:6154169-Neoplasm Transplantation,
pubmed-meshheading:6154169-Rats,
pubmed-meshheading:6154169-Rats, Inbred BUF,
pubmed-meshheading:6154169-Receptors, Estrogen,
pubmed-meshheading:6154169-Time Factors,
pubmed-meshheading:6154169-Transplantation, Homologous,
pubmed-meshheading:6154169-alpha-Fetoproteins
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pubmed:year |
1980
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pubmed:articleTitle |
Growth inhibition of estrogen-sensitive rat mammary tumors. Effect of an alpha-fetoprotein-secreting hepatoma.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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