Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3–q27 are associated with development of esophageal adenocarcinoma
dc.contributor.author | Lin, Lin | en_US |
dc.contributor.author | Wang, Zhuwen | en_US |
dc.contributor.author | Prescott, Michael S. | en_US |
dc.contributor.author | van Dekken, Herman | en_US |
dc.contributor.author | Thomas, Dafydd G. | en_US |
dc.contributor.author | Giordano, Thomas J. | en_US |
dc.contributor.author | Chang, Andrew C. | en_US |
dc.contributor.author | Orringer, Mark B. | en_US |
dc.contributor.author | Gruber, Stephen B. | en_US |
dc.contributor.author | Moran, John V. | en_US |
dc.contributor.author | Glover, Thomas W. | en_US |
dc.contributor.author | Beer, David G. | en_US |
dc.date.accessioned | 2007-05-01T19:29:11Z | |
dc.date.available | 2007-05-01T19:29:11Z | |
dc.date.issued | 2006-04 | en_US |
dc.identifier.citation | Lin, Lin; Wang, Zhuwen; Prescott, Michael S.; van Dekken, Herman; Thomas, Dafydd G.; Giordano, Thomas J.; Chang, Andrew C.; Orringer, Mark B.; Gruber, Stephen B.; Moran, John V.; Glover, Thomas W.; Beer, David G. (2006). "Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3–q27 are associated with development of esophageal adenocarcinoma." Genes, Chromosomes and Cancer 45(4): 319-331. <http://hdl.handle.net/2027.42/50630> | en_US |
dc.identifier.issn | 1045-2257 | en_US |
dc.identifier.issn | 1098-2264 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/50630 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16320248&dopt=citation | en_US |
dc.description.abstract | Gene amplification is one of the mechanisms to activate oncogenes in many cancers, including esophageal adenocarcinoma (EA). In the present study, we used two-dimensional restriction landmark genome scanning to clone a Not I/ Dpn II fragment that showed increased genomic dosage in 1 of 44 EAs analyzed. This fragment maps to 3q26.3–q27, and subsequent experiments identified two intrachromosomal amplicons within a 10-Mb DNA segment in 7 of 75 (9%) EAs. The distal amplified-core region maps centromeric to the PIK3CA locus, and a microsatellite ( D3S1754 ) within this region exhibited significant instability (MSI), in stark contrast to the genomewide microsatellite stability found in EA. D3S1754-MSI arises in premalignant Barrett's dysplastic cells and preceded amplification of the nascent MSI allele in the corresponding EA. Seven ESTs within the amplified-core were overexpressed in amplicon-containing EAs. One of these, EST AW513672 , represents a chimeric transcript that initiated from an antisense promoter sequence in the 5′UTR of a full-length LINE-1 element (L1-5′ASP). Similar chimeric transcripts encoding portions of the MET oncogene and the BCAS3 gene also were overexpressed in EAs, suggesting that L1-5′ASP activation may occur at a broad level in primary EAs. Thus, the fine dissection of a 2-Mb amplified DNA segment in 3q26.3–q27 in EA revealed multiple genetic alterations that had occurred sequentially and/or concurrently during EA development. This article has supplementary material, available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat . © 2005 Wiley-Liss, Inc. | en_US |
dc.format.extent | 830486 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cancer Research, Oncology and Pathology | en_US |
dc.title | Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3–q27 are associated with development of esophageal adenocarcinoma | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Genetics | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan ; Department of Surgery Thoracic Section, University of Michigan Medical School, B560 MSRB2, Box 0686, Ann Arbor, MI 48109 | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Human Genetics, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Human Genetics, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Surgery, University of Michigan, Ann Arbor, Michigan ; Department of Surgery Thoracic Section, University of Michigan Medical School, B560 MSRB2, Box 0686, Ann Arbor, MI 48109 | en_US |
dc.contributor.affiliationother | Department of Pathology, Erasmus Medical Center, University Medical Center Rotterdam, The Netherlands | en_US |
dc.identifier.pmid | 16320248 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/50630/1/20293_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/gcc.20293 | en_US |
dc.identifier.source | Genes, Chromosomes and Cancer | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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