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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-10-24
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pubmed:databankReference | |
pubmed:abstractText |
To discern the structural features of cellular loci that are disrupted by type 16 human papillomavirus (HPV-16) integration in cervical cancer, a polymerase chain reaction (PCR)-based strategy was employed for direct amplification and sequence analysis of four such cellular loci in cancer biopsy samples. One of the HPV-16-disrupted loci was found to be the microtubule-associated protein (MAP-2) gene and the other three loci were uncharacterized and were designated PID-1 to -3 (for papillomavirus integration-disrupted). The junctional sequences of the viral integration sites in the four loci analyzed are bracketed by long tracts of homogeneous purine or pyrimidine or alternating purine-pyrimidine which are known to destabilize the B-form conformation of the DNA structure. Using a panel of human/hamster hybrid cell DNAs and PCR analysis, the four loci were assigned to chromosomes 2 (MAP-2), 9 (PID-1), 1 (PID-2) and 8 (PID-3), respectively. These chromosomes carry numerous other previously determined viral integration and chromosomal fragile sites and the myc oncogenes. The PID-1 locus was further found in Southern analysis to be rearranged and amplified in another cervical cancer biopsy and a cervical carcinoma cell line (CaSki). On Northern analysis, the PID-1 and -3 probes detected a 3.0- and a 3.6-kb transcript, respectively, in normal cervical cells and in cervical cancer cell lines. The findings suggest that HPV-16 genome integrates frequently into topologically destabilized and transcriptionally active chromosomal sites. It remains to be elucidated whether the MAP-2 and the PID loci contribute to the pathogenesis of cervical cancer.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0146-6615
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
15-22
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8732866-Base Sequence,
pubmed-meshheading:8732866-Blotting, Northern,
pubmed-meshheading:8732866-Blotting, Southern,
pubmed-meshheading:8732866-Chromosome Mapping,
pubmed-meshheading:8732866-DNA, Viral,
pubmed-meshheading:8732866-Female,
pubmed-meshheading:8732866-Humans,
pubmed-meshheading:8732866-Molecular Sequence Data,
pubmed-meshheading:8732866-Papillomaviridae,
pubmed-meshheading:8732866-Papillomavirus Infections,
pubmed-meshheading:8732866-Tumor Cells, Cultured,
pubmed-meshheading:8732866-Tumor Virus Infections,
pubmed-meshheading:8732866-Uterine Cervical Neoplasms,
pubmed-meshheading:8732866-Virus Integration
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pubmed:year |
1996
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pubmed:articleTitle |
Molecular analysis of cellular loci disrupted by papillomavirus 16 integration in cervical cancer: frequent viral integration in topologically destabilized and transcriptionally active chromosomal regions.
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pubmed:affiliation |
Department of Medical Research and Education, Veterans General Hospital, Taipei, Taiwan, Republic of China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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