Genetic analysis of long-term Barrett's esophagus epithelial cultures exhibiting cytogenetic and ploidy abnormalities
Identifieur interne : 003C17 ( Main/Merge ); précédent : 003C16; suivant : 003C18Genetic analysis of long-term Barrett's esophagus epithelial cultures exhibiting cytogenetic and ploidy abnormalities
Auteurs : M. Corinna Palanca-Wessels ; Michael T. Barrett [États-Unis] ; Patricia C. Galipeau [États-Unis] ; Katherine L. Rohrer ; Brian J. Reid [États-Unis] ; Peter S. RabinovitchSource :
- Gastroenterology [ 0016-5085 ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Abnormality, Adenocarcinoma, Allelic losses, Becton dickinson, Biopsy, Biopsy specimens, Cell cultures, Cell cycle, Cell cycle arrest, Cell line, Cell lines, Cell population, Cells explanting, Chromosome, Chromosome arms, Chromosome numbers, Clonal, Culture medium, Cultured cells, Cytogenetic, Cytoplasmic enlargement, Deletion, Dicentric chromosomes, Diploid, Diploid cells, Dysplasia, Early passage, Endoscopic, Endoscopic biopsy specimens, Enzymatic method, Epithelial, Epithelial cell cultures, Epithelial cells, Epithelial cultures, Epithelium, Esophageal, Esophageal adenocarcinoma, Esophagus, Etiologic factors, Explant method, Fibroblast overgrowth, Fitc igg2a, Flow cytometry, Galipeau, Gastroenterology, Genetic abnormalities, Genetic analysis, Genetic intermediates, Growth medium, Haggitt, Inactivation, Late passage, Levine, Missense mutation, Mitotic, Mitotic cells, Mutation, Neoplastic, Neoplastic progression, Other patients, Ploidy abnormalities, Polymerase chain reaction, Polymorphic markers, Premalignant, Primary culture, Primary cultures, Proc natl acad, Progression, Rabinovitch, Reid, Sanchez, Sequencing, Sigma, Sigma chemical, Subsequent development, Tetraploid, Tetraploid cells, Tissue culture, Unpublished data, Unsuccessful cultures, Vivo, Vivo biopsy specimens, Vivo samples, Whole genome amplification.
Abstract
Abstract: Background & Aims: Progression to cancer in Barrett's esophagus occurs through an accumulation of cell cycle and genetic abnormalities that have been documented in vivo. To better study neoplastic evolution in Barrett's esophagus, the aim of this study was to establish in vitro cultures from preneoplastic tissues. Methods: Mechanical and enzymatic dissociation methods were used to initiate Barrett's epithelial cultures from endoscopic biopsy specimens, and the cells were characterized using flow-cytometric, cytogenetic, and molecular genetic analyses. Results: Four long-term cultures were established from 39 attempts. All cultures contain cytogenetic abnormalities and elevated flow-cytometric 4N DNA content fractions. Molecular genetic abnormalities detected include the following: 9p and/or CDKN2/p16 abnormalities in 4 of 4 cultures, 17p loss of heterozygosity and p53 mutation in 3 of 4 cultures, and 5q loss of heterozygosity in 1 of 4 cultures. Inactivation of p53 was statistically associated with successful long-term culture. Conclusions: These cultures contain cell cycle and molecular genetic abnormalities that closely parallel those previously documented to occur early in cancer development in Barrett's esophagus in vivo. These alterations also appear to be associated with successful growth in vitro. The cultures may provide a premalignant in vitro system in which to test potential therapies for Barrett's esophagus as well as to examine etiologic factors and genetic intermediates important in neoplastic progression. GASTROENTEROLOGY 1998;114:295-304
Url:
DOI: 10.1016/S0016-5085(98)70480-9
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<front><div type="abstract" xml:lang="en">Abstract: Background & Aims: Progression to cancer in Barrett's esophagus occurs through an accumulation of cell cycle and genetic abnormalities that have been documented in vivo. To better study neoplastic evolution in Barrett's esophagus, the aim of this study was to establish in vitro cultures from preneoplastic tissues. Methods: Mechanical and enzymatic dissociation methods were used to initiate Barrett's epithelial cultures from endoscopic biopsy specimens, and the cells were characterized using flow-cytometric, cytogenetic, and molecular genetic analyses. Results: Four long-term cultures were established from 39 attempts. All cultures contain cytogenetic abnormalities and elevated flow-cytometric 4N DNA content fractions. Molecular genetic abnormalities detected include the following: 9p and/or CDKN2/p16 abnormalities in 4 of 4 cultures, 17p loss of heterozygosity and p53 mutation in 3 of 4 cultures, and 5q loss of heterozygosity in 1 of 4 cultures. Inactivation of p53 was statistically associated with successful long-term culture. Conclusions: These cultures contain cell cycle and molecular genetic abnormalities that closely parallel those previously documented to occur early in cancer development in Barrett's esophagus in vivo. These alterations also appear to be associated with successful growth in vitro. The cultures may provide a premalignant in vitro system in which to test potential therapies for Barrett's esophagus as well as to examine etiologic factors and genetic intermediates important in neoplastic progression. GASTROENTEROLOGY 1998;114:295-304</div>
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