Cytogenetic aberrations in immortalization of esophageal epithelial cells
(2006) In Cancer Genetics and Cytogenetics 165(1). p.25-35- Abstract
- To define the early cytogenetic events important in esophageal carcinogenesis, we immortalized normal esophageal epithelial cells by overexpression of human papillomavirus type 16 E6/E7 (HPV16E6/E7) and human telomerase reverse transcriptase (hTERT), and characterized the chromosomal abnormalities serially before and after Cellular immortalizaiton. During crisis. most cells had simple nonclonal karyotypic changes with cytogenetic divergence. Mitotically unstable chromosomes (i.e., telomere association and dicentric chromosomes) were the most common aberrations. After crisis, the karyotypic patterns were more convergent with nonrandom clonal changes. A few clones dominated the culture. Gain of chromosome 20q was consistently observed in... (More)
- To define the early cytogenetic events important in esophageal carcinogenesis, we immortalized normal esophageal epithelial cells by overexpression of human papillomavirus type 16 E6/E7 (HPV16E6/E7) and human telomerase reverse transcriptase (hTERT), and characterized the chromosomal abnormalities serially before and after Cellular immortalizaiton. During crisis. most cells had simple nonclonal karyotypic changes with cytogenetic divergence. Mitotically unstable chromosomes (i.e., telomere association and dicentric chromosomes) were the most common aberrations. After crisis, the karyotypic patterns were more convergent with nonrandom clonal changes. A few clones dominated the culture. Gain of chromosome 20q was consistently observed in four HPVE6/E7 immortalized esophageal lines, whereas amplification of chromosome 5q was preferentially found in hTERT immortalized cells. In addition, chromosomal aberrations of immortalized cells, including del(3p) and centromere rearrangements, were similar to those observed in esophageal cancer. Furthermore, in E6/E7-expressing cells, the frequency of negative telomere termini and anaphase bridges were high during crisis and low after crisis. These findings suggested that telomere dysfunction might be an important cause of cellular crisis, and the resultant chromosomal aberrations, mainly amplification of chromosome 20q or 5q, might be early genetic events required in esophageal cell immortalization. These alterations might be valuable models for further study of molecular mechanisms contributing to esophageal carcinogenesis. (c) 2006 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/415800
- author
- Zhang, H ; Jin, Yuesheng LU ; Chen, XH ; Jin, Charlotte LU ; Law, S ; Tsao, SW and Kwong, YL
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Cancer Genetics and Cytogenetics
- volume
- 165
- issue
- 1
- pages
- 25 - 35
- publisher
- Elsevier
- external identifiers
-
- wos:000236133000004
- pmid:16490594
- scopus:32844475447
- ISSN
- 0165-4608
- DOI
- 10.1016/j.cancergencyto.2005.07.016
- language
- English
- LU publication?
- yes
- id
- ce27cc1f-8389-411a-9962-5e40ea091b4c (old id 415800)
- date added to LUP
- 2016-04-01 15:58:22
- date last changed
- 2022-01-28 08:22:31
@article{ce27cc1f-8389-411a-9962-5e40ea091b4c,
abstract = {{To define the early cytogenetic events important in esophageal carcinogenesis, we immortalized normal esophageal epithelial cells by overexpression of human papillomavirus type 16 E6/E7 (HPV16E6/E7) and human telomerase reverse transcriptase (hTERT), and characterized the chromosomal abnormalities serially before and after Cellular immortalizaiton. During crisis. most cells had simple nonclonal karyotypic changes with cytogenetic divergence. Mitotically unstable chromosomes (i.e., telomere association and dicentric chromosomes) were the most common aberrations. After crisis, the karyotypic patterns were more convergent with nonrandom clonal changes. A few clones dominated the culture. Gain of chromosome 20q was consistently observed in four HPVE6/E7 immortalized esophageal lines, whereas amplification of chromosome 5q was preferentially found in hTERT immortalized cells. In addition, chromosomal aberrations of immortalized cells, including del(3p) and centromere rearrangements, were similar to those observed in esophageal cancer. Furthermore, in E6/E7-expressing cells, the frequency of negative telomere termini and anaphase bridges were high during crisis and low after crisis. These findings suggested that telomere dysfunction might be an important cause of cellular crisis, and the resultant chromosomal aberrations, mainly amplification of chromosome 20q or 5q, might be early genetic events required in esophageal cell immortalization. These alterations might be valuable models for further study of molecular mechanisms contributing to esophageal carcinogenesis. (c) 2006 Elsevier Inc. All rights reserved.}},
author = {{Zhang, H and Jin, Yuesheng and Chen, XH and Jin, Charlotte and Law, S and Tsao, SW and Kwong, YL}},
issn = {{0165-4608}},
language = {{eng}},
number = {{1}},
pages = {{25--35}},
publisher = {{Elsevier}},
series = {{Cancer Genetics and Cytogenetics}},
title = {{Cytogenetic aberrations in immortalization of esophageal epithelial cells}},
url = {{http://dx.doi.org/10.1016/j.cancergencyto.2005.07.016}},
doi = {{10.1016/j.cancergencyto.2005.07.016}},
volume = {{165}},
year = {{2006}},
}