SwePub
Sök i LIBRIS databas

  Extended search

onr:"swepub:oai:lup.lub.lu.se:192a79d4-00c5-49cc-ba95-1be0f961067f"
 

Search: onr:"swepub:oai:lup.lub.lu.se:192a79d4-00c5-49cc-ba95-1be0f961067f" > Cytogenetic and mol...

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist
  • Jin, YueshengLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine (author)

Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20

  • Article/chapterEnglish2004

Publisher, publication year, extent ...

  • Elsevier BV,2004

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:192a79d4-00c5-49cc-ba95-1be0f961067f
  • https://lup.lub.lu.se/record/286449URI
  • https://doi.org/10.1016/j.ygyno.2003.09.007DOI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • 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.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Zhang, H (author)
  • Tsao, SW (author)
  • Jin, CharlotteLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kgen-cji (author)
  • Lv, M (author)
  • Strömbeck, BodilLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kgen-bst (author)
  • Wiegant, J (author)
  • Wan, TSK (author)
  • Yuen, PW (author)
  • Kwong, YL (author)
  • Avdelningen för klinisk genetikInstitutionen för laboratoriemedicin (creator_code:org_t)

Related titles

  • In:Gynecologic Oncology: Elsevier BV92:1, s. 183-1911095-68590090-8258

Internet link

Find in a library

To the university's database

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist

Search outside SwePub

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view