Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells
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Home > Medicine & Health Science textbooks > Medicine: general issues > Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells
Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells

Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells


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About the Book

This dissertation, "Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells" by Hao, Zhang, 張浩, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Cytogenetic and Molecular Alterations in Immortalization of Normal Esophageal Epithelial Cells Submitted by Zhang Hao for the degree of Master of Philosophy at The University of Hong Kong in October, 2005 Esophageal carcinoma is common worldwide especially in China. The high-risk human papillomavirus type 16 E6/E7 (HPV16E6/E7) infection might play an important pathogenetic role in esophageal squamous cell carcinoma (SCC) in the Chinese population, whereas progressive up-regulation of telomerase is associated with the development of adenocarcinoma common in Western countries. Multiple genetic alterations have been identified in esophageal carcinoma, but the early genetic events required for pathogenesis of cancer remain unknown. In this study, esophageal epithelial cells were immortalized by the transfection of HPV16E6/E7 or human telomerase reverse transcriptase (hTERT), to define the cytogenetic and molecular alterations necessary for cell immortalization and early stage of carcinogenesis, and to compare these alterations with those of esophageal cancer cells. Two HPV16E6/E7 transfected (NE083/E6E7 and NE108/E6E7) and one hTERT transfected (NE083/hTERT) esophageal cell lines were immortalized successfully. During crisis leading to immortalization, the frequency of negative telomere termini and chromosomal instability events, including mitotically unstable chromosomes and anaphase bridges, were high in NE108/E6E7 cells, corresponding with the predominance of nonclonal chromosomal changes in this stage, suggesting that telomere dysfunction and the consequent chromosomal instability contributed to the formation of chromosomal aberrations essential for cell immortalization. Analysis of chromosomal abnormalities in immortalized cells (including two previously immortalized NE3/E6E7 and NECA6/E6E7 esophageal cells) showed that gain of chromosome 20q material was consistently observed in HPVE6/E7 immortalized cells, whereas gain of chromosome 5q material was preferentially found in hTERT immortalized cells. Chromosomal rearrangements in some immortalized NE cells, such as deletion of 3p and unbalanced structural rearrangements involving centromeric regions of chromosome 8, 13, 14, and 21 were similar to that of esophageal cancer. These alterations might play important roles in cellular immortalization and the early stages of carcinogenesis. HPVE6/E7 immortalized esophageal cells showed suppression of RB and p53 INK4A WAF1 and over-expression of p16 and p21 . They failed to up-regulate p53 in response to mitomycin C. On the other hand, hTERT immortalized esophageal cells INK4A WAF1 showed unaffected RB and p53 and down-regulated p16 and p21 . Treatment with mitomycin C resulted in the up-regulation of p53. Interestingly, the expression of Aurora-A was up-regulated in both HPVE6/E7 and hTERT immortalized cells. Over-expression of Aurora-A disrupted the DNA-damage- INK4A induced G2 checkpoint. The multiple alterations in p16 /RB and p53 pathways, and checkpoint defects caused by Aurora-A over-expression might further induce chromosomal instability and contribute to esophageal cell immortalization and carcinogenesis. DOI: 10.5353/th_b3204701 Subjects: Epithelial cells Continuous cell lines Papillomaviruses Cell transformation Esophagus - Cancer - Genetic aspects Cytogenetics


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Product Details
  • ISBN-13: 9781361397022
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 164
  • Weight: 395 gr
  • ISBN-10: 1361397020
  • Publisher Date: 27 Jan 2017
  • Binding: Paperback
  • Language: English
  • Spine Width: 9 mm
  • Width: 216 mm


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