17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus. - Wikidata - wikimedia - TriplyDB

17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus.

17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus.

http://www.wikidata.org/entity/Q37487038

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Defining the sister rat mammary tumor cell lines HH-16 cl.2/1 and HH-16.cl.4 as an in vitro cell model for Erbb2 NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma FLJ25439, a novel cytokinesis-associated protein, induces tetraploidization and maintains chromosomal stability via enhancing expression of endoplasmic reticulum stress chaperones Evolution of neoplastic cell lineages in Barrett oesophagus Genome management and mismanagement--cell-level opportunities and challenges of whole-genome duplication Early events during neoplastic progression in Barrett's esophagus Progressive telomere dysfunction causes cytokinesis failure and leads to the accumulation of polyploid cells Molecular changes in the progression of Barrett's oesophagus Inactivation of p16, RUNX3, and HPP1 occurs early in Barrett's-associated neoplastic progression and predicts progression risk Novel roles for p53 in the genesis and targeting of tetraploid cancer cells Transcriptome analysis of tetraploid cells identifies cyclin D2 as a facilitator of adaptation to genome doubling in the presence of p53 Vascular smooth muscle polyploidization as a biomarker for aging and its impact on differential gene expression Lats2/Kpm is required for embryonic development, proliferation control and genomic integrity The causes and consequences of genetic heterogeneity in cancer evolution Molecular biology of Barrett's adenocarcinoma.Persistent telomere damage induces bypass of mitosis and tetraploidy.Cytokinesis failure due to derailed integrin traffic induces aneuploidy and oncogenic transformation in vitro and in vivo.Transcriptional regulation by normal epithelium of premalignant to malignant progression in Barrett's esophagus Her-2/neu gene amplification, elevated mRNA expression, and protein overexpression in the metaplasia-dysplasia-adenocarcinoma sequence of Barrett's esophagus.p16 mutation spectrum in the premalignant condition Barrett's esophagus.Interrelationship between TP53 gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma.Integrins promote cytokinesis through the RSK signaling axis.Cyclin D mediates tolerance of genome-doubling in cancers with functional p53.Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus High-throughput screens in diploid cells identify factors that contribute to the acquisition of chromosomal instability Single nucleotide polymorphism-based genome-wide chromosome copy change, loss of heterozygosity, and aneuploidy in Barrett's esophagus neoplastic progression.Barrett's esophagus: progression to adenocarcinoma and markers.p53 dependent centrosome clustering prevents multipolar mitosis in tetraploid cells The SET domain protein, Set3p, promotes the reliable execution of cytokinesis in Schizosaccharomyces pombe.Absolute quantification of somatic DNA alterations in human cancer Formation of bipolar spindles with two centrosomes in tetraploid cells established from normal human fibroblasts.Review article: a conceptual approach to understanding the molecular mechanisms of cancer development in Barrett's oesophagus.Abnormal DNA content in oral epithelial dysplasia is associated with increased risk of progression to carcinoma.Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis.Integrative post-genome-wide association analysis of CDKN2A and TP53 SNPs and risk of esophageal adenocarcinoma.Elucidation of proliferative capability of mononuclear tetraploid cells, emerging spontaneously from diploid cells, using image cytometry and fluorescence in situ hybridization.Quantitative characterization of preneoplastic progression using single-cell computed tomography and three-dimensional karyometry Surveillance in Barrett's oesophagus: a personal view Tolerance of whole-genome doubling propagates chromosomal instability and accelerates cancer genome evolution.Progressive silencing of p14ARF in oesophageal adenocarcinoma.

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17p (p53) allelic losses, 4N (G2/tetraploid) populations, and progression to aneuploidy in Barrett's esophagus.

http://www.wikidata.org/entity/Q37487038

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bilimsel makale

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scientific article published on July 1996

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PNAS.93.14.7081

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Proceedings of the National Academy of Sciences of the United States of America

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17p (p53) allelic losses, 4N ( ...... ploidy in Barrett's esophagus.

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B J Reid

http://www.w3.org/2001/XMLSchema#string

C A Sanchez

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D S Cowan

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D S Levine

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M J Emond

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M T Barrett

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P C Galipeau

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P S Rabinovitch

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P2860

Checkpoints: controls that ensure the order of cell cycle events

The clonal evolution of tumor cell populations

Genetic alterations during colorectal-tumor development

p53 mutations in human cancers

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae

Participation of p53 protein in the cellular response to DNA damage

Differential sensitivity of p53(-) and p53(+) cells to caffeine-induced radiosensitization and override of G2 delay.

Clonal ordering of 17p and 5q allelic losses in Barrett dysplasia and adenocarcinoma.

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7081-7084

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8692948

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38939

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