Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20
(2004) In Gynecologic Oncology 92(1). p.183-191- Abstract
- Objectives. This study aimed at identifying the genetic events involved in immortalization of ovarian epithelial cells, which might be important steps in ovarian carcinogenesis. Methods. The genetic profiles of five human ovarian surface epithelial (HOSE) cell lines immortalized by retroviral transfection of the human papillomavirus (HPV) E6/E7 genes were thoroughly characterized by chromosome banding and fluorescence in situ hybridization (FISH), at various passages pre- and post-crisis. Results. In pre-crisis, most cells had simple, non-clonal karyotypic changes. Telomere association was the commonest aberration, suggesting that tolermase dysfunction might be an important genetic event leading to cellular crisis. After immortalization... (More)
- Objectives. This study aimed at identifying the genetic events involved in immortalization of ovarian epithelial cells, which might be important steps in ovarian carcinogenesis. Methods. The genetic profiles of five human ovarian surface epithelial (HOSE) cell lines immortalized by retroviral transfection of the human papillomavirus (HPV) E6/E7 genes were thoroughly characterized by chromosome banding and fluorescence in situ hybridization (FISH), at various passages pre- and post-crisis. Results. In pre-crisis, most cells had simple, non-clonal karyotypic changes. Telomere association was the commonest aberration, suggesting that tolermase dysfunction might be an important genetic event leading to cellular crisis. After immortalization post-crisis, however, the karyotypic patterns were non-random. Loss of genetic materials was a characteristic feature. The commonest numerical aberrations were -13, -14, -16, -17, -18, and +5. Among them, loss of chromosome 13 was common change observed in all lines. The only recurrent structural aberration was homogeneously staining regions (hsr) observed in three lines. FISH and combined binary ratio labeling (COBRA)-FISH showed in two cases that the lists were derived from chromosome 20. Clonal evolution was observed in four of the lines. In one line, hsr was the only change shared by all subclones, suggesting that it might be a primary event in cell immortalization. Conclusion. The results of the present study suggested that loss of chromosome 13 and the amplification of chromosome 20 might be early genetic events involved in ovarian cell immortalization, and might be useful targets for the study of genomic aberrations in ovarian carcinogenesis. (C) 2003 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/286449
- author
- Jin, Yuesheng LU ; Zhang, H ; Tsao, SW ; Jin, Charlotte LU ; Lv, M ; Strömbeck, Bodil LU ; Wiegant, J ; Wan, TSK ; Yuen, PW and Kwong, YL
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- chromosome aberrations, Hsr, immortalized ovarian cell lines
- in
- Gynecologic Oncology
- volume
- 92
- issue
- 1
- pages
- 183 - 191
- publisher
- Academic Press
- external identifiers
-
- pmid:14751156
- wos:000189159600028
- scopus:9144230586
- ISSN
- 1095-6859
- DOI
- 10.1016/j.ygyno.2003.09.007
- language
- English
- LU publication?
- yes
- id
- 192a79d4-00c5-49cc-ba95-1be0f961067f (old id 286449)
- date added to LUP
- 2016-04-01 11:38:24
- date last changed
- 2022-01-26 08:00:00
@article{192a79d4-00c5-49cc-ba95-1be0f961067f,
abstract = {{Objectives. This study aimed at identifying the genetic events involved in immortalization of ovarian epithelial cells, which might be important steps in ovarian carcinogenesis. Methods. The genetic profiles of five human ovarian surface epithelial (HOSE) cell lines immortalized by retroviral transfection of the human papillomavirus (HPV) E6/E7 genes were thoroughly characterized by chromosome banding and fluorescence in situ hybridization (FISH), at various passages pre- and post-crisis. Results. In pre-crisis, most cells had simple, non-clonal karyotypic changes. Telomere association was the commonest aberration, suggesting that tolermase dysfunction might be an important genetic event leading to cellular crisis. After immortalization post-crisis, however, the karyotypic patterns were non-random. Loss of genetic materials was a characteristic feature. The commonest numerical aberrations were -13, -14, -16, -17, -18, and +5. Among them, loss of chromosome 13 was common change observed in all lines. The only recurrent structural aberration was homogeneously staining regions (hsr) observed in three lines. FISH and combined binary ratio labeling (COBRA)-FISH showed in two cases that the lists were derived from chromosome 20. Clonal evolution was observed in four of the lines. In one line, hsr was the only change shared by all subclones, suggesting that it might be a primary event in cell immortalization. Conclusion. The results of the present study suggested that loss of chromosome 13 and the amplification of chromosome 20 might be early genetic events involved in ovarian cell immortalization, and might be useful targets for the study of genomic aberrations in ovarian carcinogenesis. (C) 2003 Elsevier Inc. All rights reserved.}},
author = {{Jin, Yuesheng and Zhang, H and Tsao, SW and Jin, Charlotte and Lv, M and Strömbeck, Bodil and Wiegant, J and Wan, TSK and Yuen, PW and Kwong, YL}},
issn = {{1095-6859}},
keywords = {{chromosome aberrations; Hsr; immortalized ovarian cell lines}},
language = {{eng}},
number = {{1}},
pages = {{183--191}},
publisher = {{Academic Press}},
series = {{Gynecologic Oncology}},
title = {{Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20}},
url = {{http://dx.doi.org/10.1016/j.ygyno.2003.09.007}},
doi = {{10.1016/j.ygyno.2003.09.007}},
volume = {{92}},
year = {{2004}},
}