PMID- 14751156
OWN - NLM
STAT- MEDLINE
DCOM- 20040316
LR  - 20190827
IS  - 0090-8258 (Print)
IS  - 0090-8258 (Linking)
VI  - 92
IP  - 1
DP  - 2004 Jan
TI  - Cytogenetic and molecular genetic characterization of immortalized human ovarian 
      surface epithelial cell lines: consistent loss of chromosome 13 and amplification 
      of chromosome 20.
PG  - 183-91
AB  - 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 hsrs 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.
FAU - Jin, Yuesheng
AU  - Jin Y
AD  - Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, 
      China.
FAU - Zhang, Hao
AU  - Zhang H
FAU - Tsao, Sai Wah
AU  - Tsao SW
FAU - Jin, Charlotte
AU  - Jin C
FAU - Lv, Mei
AU  - Lv M
FAU - Strombeck, Bodil
AU  - Strombeck B
FAU - Wiegant, Joop
AU  - Wiegant J
FAU - Wan, Thomas Shek Kong
AU  - Wan TS
FAU - Yuen, Po Wing
AU  - Yuen PW
FAU - Kwong, Yok-Lam
AU  - Kwong YL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Gynecol Oncol
JT  - Gynecologic oncology
JID - 0365304
SB  - IM
MH  - *Cell Line, Transformed
MH  - Cell Transformation, Neoplastic/genetics
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 13/*genetics
MH  - Chromosomes, Human, Pair 20/*genetics
MH  - Epithelial Cells/cytology/physiology
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Ovarian Neoplasms/*genetics
MH  - Ovary/cytology/physiology/*ultrastructure
EDAT- 2004/01/31 05:00
MHDA- 2004/03/18 05:00
CRDT- 2004/01/31 05:00
PHST- 2004/01/31 05:00 [pubmed]
PHST- 2004/03/18 05:00 [medline]
PHST- 2004/01/31 05:00 [entrez]
AID - S009082580300619X [pii]
AID - 10.1016/j.ygyno.2003.09.007 [doi]
PST - ppublish
SO  - Gynecol Oncol. 2004 Jan;92(1):183-91. doi: 10.1016/j.ygyno.2003.09.007.