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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
15
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pubmed:dateCreated |
1998-11-6
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pubmed:abstractText |
Deletion of the q23-24 region of human chromosome 10 is one of the most frequent genetic alterations in prostate cancer, suggesting that inactivation of a tumor suppressor gene in this region is involved in the development or progression of this carcinoma. A candidate gene, PTEN/MMAC1, has been identified from this chromosomal region; mutations of this gene have been found in various advanced tumors and cell lines including those of prostate cancer. To further define the role of PTEN/MMAC1 in the development of prostate cancer and its spectrum of genetic alterations, we analysed 40 pT2 or pT3 prostate tumors for allelic loss, mutations, and homozygous deletions using PCR-based methods. Six tumors showed loss of heterozygosity for one of the ten markers analysed, while one tumor showed loss of two markers. None of the markers within PTEN/MMAC1 was lost. Direct sequencing of PCR amplified exons and intron/exon junctions of all 40 tumors revealed three sequence variants, one of which was a point mutation in exon 9, while the other two were polymorphisms. Using multiplex PCR, no homozygous deletions were detected in any of the neoplasms. Our results showing a low frequency of alterations of PTEN/MMAC1 in pT2 and pT3 prostate cancers suggest that this gene plays an insignificant role in the development of most low stage carcinomas of the prostate.
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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/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN Phosphohydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoric Monoester Hydrolases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1979-82
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:9788441-Adult,
pubmed-meshheading:9788441-Aged,
pubmed-meshheading:9788441-Base Sequence,
pubmed-meshheading:9788441-DNA Primers,
pubmed-meshheading:9788441-Genes, Tumor Suppressor,
pubmed-meshheading:9788441-Homozygote,
pubmed-meshheading:9788441-Humans,
pubmed-meshheading:9788441-Loss of Heterozygosity,
pubmed-meshheading:9788441-Male,
pubmed-meshheading:9788441-Middle Aged,
pubmed-meshheading:9788441-Mutation,
pubmed-meshheading:9788441-PTEN Phosphohydrolase,
pubmed-meshheading:9788441-Phosphoric Monoester Hydrolases,
pubmed-meshheading:9788441-Prostatic Neoplasms,
pubmed-meshheading:9788441-Protein Tyrosine Phosphatases,
pubmed-meshheading:9788441-Sequence Deletion,
pubmed-meshheading:9788441-Tumor Suppressor Proteins
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pubmed:year |
1998
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pubmed:articleTitle |
PTEN/MMAC1 is infrequently mutated in pT2 and pT3 carcinomas of the prostate.
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pubmed:affiliation |
Department of Pathology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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