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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1995-4-12
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pubmed:abstractText |
To investigate possible relationships between genetic alterations and hormonal deregulation during breast cancer development and/or progression, we examined 616 primary breast cancers for loss of heterozygosity (LOH) at chromosomal regions 16q24, 17p13.3 and 17q21, and for amplifications of the ERBB2 and c-MYC loci. A comparison of oestrogen receptor (ER) and progesterone receptor (PgR) status in tumour cells with data concerning these genetic alterations revealed that LOH at 17q21 was significantly correlated with absence of oestrogen receptors (ER) (P < 0.0003) or progesterone receptors (PgR) (P < 0.0001), and with the absence of both (P < 0.0001). Similarly, a significant association was observed between amplification of ERBB2 and the absence of either ER or PgR. LOH at 17p13.3 was associated with the absence of PgR (P < 0.01). These data suggest a possible relationship between specific genetic changes on chromosome 17 and hormonal deregulation in the progression of breast cancer.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1350457,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1354643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1671531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1672082,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1682035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-1977515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2137009,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2685334,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2825969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2878870,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2892166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2892175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-2902581,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-3003577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-3029872,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-3798106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-6329026,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-8104866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-8104920,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-8219249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-8381331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7880720-8437862
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0007-0920
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
71
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pubmed:geneSymbol |
ERBB2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
N
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pubmed:pagination |
438-41
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7880720-Breast Neoplasms,
pubmed-meshheading:7880720-Chromosomes, Human, Pair 16,
pubmed-meshheading:7880720-Chromosomes, Human, Pair 17,
pubmed-meshheading:7880720-DNA, Neoplasm,
pubmed-meshheading:7880720-Gene Amplification,
pubmed-meshheading:7880720-Gene Deletion,
pubmed-meshheading:7880720-Genes, erbB-2,
pubmed-meshheading:7880720-Genes, myc,
pubmed-meshheading:7880720-Heterozygote,
pubmed-meshheading:7880720-Humans,
pubmed-meshheading:7880720-Neoplasms, Hormone-Dependent,
pubmed-meshheading:7880720-Receptors, Estrogen,
pubmed-meshheading:7880720-Receptors, Progesterone
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pubmed:year |
1995
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pubmed:articleTitle |
Association of genetic alterations on chromosome 17 and loss of hormone receptors in breast cancer.
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pubmed:affiliation |
Department of Biochemistry, Cancer Institute, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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