| Cell proliferation, cell cycle abnormalities, and cancer outcome in patients with Barrett's esophagus: a long-term prospective study. | |
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MedLine Citation:
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PMID: 18980994 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Elevated cellular proliferation and cell cycle abnormalities, which have been associated with premalignant lesions, may be caused by inactivation of tumor suppressor genes. We measured proliferative and cell cycle fractions of biopsies from a cohort of patients with Barrett's esophagus to better understand the role of proliferation in early neoplastic progression and the association between cell cycle dysregulation and tumor suppressor gene inactivation. EXPERIMENTAL DESIGN: Cell proliferative fractions (determined by Ki67/DNA multiparameter flow cytometry) and cell cycle fractions (DNA content flow cytometry) were measured in 853 diploid biopsies from 362 patients with Barrett's esophagus. The inactivation status of CDKN2A and TP53 was assessed in a subset of these biopsies in a cross-sectional study. A prospective study followed 276 of the patients without detectable aneuploidy for an average of 6.3 years with esophageal adenocarcinoma as an end point. RESULTS: Diploid S and 4N (G(2)/tetraploid) fractions were significantly higher in biopsies with TP53 mutation and loss of heterozygosity. CDKN2A inactivation was not associated with higher Ki67-positive, diploid S, G(1), or 4N fractions. High Ki67-positive and G(1)-phase fractions were not associated with the future development of esophageal adenocarcinoma (P=0.13 and P=0.15, respectively), whereas high diploid S-phase and 4N fractions were (P=0.03 and P<0.0001, respectively). CONCLUSIONS: High Ki67-positive proliferative fractions were not associated with inactivation of CDKN2A and TP53 or future development of cancer in our cohort of patients with Barrett's esophagus. Biallelic inactivation of TP53 was associated with elevated 4N fractions, which have been associated with the future development of esophageal adenocarcinoma. |
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Authors:
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Dennis L Chao; Carissa A Sanchez; Patricia C Galipeau; Patricia L Blount; Thomas G Paulson; David S Cowan; Kamran Ayub; Robert D Odze; Peter S Rabinovitch; Brian J Reid |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Clinical cancer research : an official journal of the American Association for Cancer Research Volume: 14 ISSN: 1078-0432 ISO Abbreviation: Clin. Cancer Res. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-11-04 Completed Date: 2008-12-19 Revised Date: 2010-12-17 |
Medline Journal Info:
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Nlm Unique ID: 9502500 Medline TA: Clin Cancer Res Country: United States |
Other Details:
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Languages: eng Pagination: 6988-95 Citation Subset: IM |
Affiliation:
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Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. dchao@fhcrc.org |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenocarcinoma
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diagnosis,
pathology* Adult Aged Barrett Esophagus / complications*, pathology* Cell Cycle* Cell Division* Cohort Studies Esophageal Neoplasms / etiology, pathology* Female Genes, p16 Genes, p53 Humans Ki-67 Antigen / metabolism Longitudinal Studies Loss of Heterozygosity Male Middle Aged Mutation Prospective Studies |
| Grant Support | |
ID/Acronym/Agency:
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K07 CA089147/CA/NCI NIH HHS; K07 CA089147-05/CA/NCI NIH HHS; P01 CA091955-06/CA/NCI NIH HHS; P01 CA91955/CA/NCI NIH HHS; R01 CA061202-08/CA/NCI NIH HHS; R01 CA61202/CA/NCI NIH HHS; T32 CA080416-10/CA/NCI NIH HHS; T32 CA80416/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Ki-67 Antigen |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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