Literature DB >> 9317174

Identification of allelic losses in benign, borderline, and invasive epithelial ovarian tumors and correlation with clinical outcome.

G Saretzki1, U Hoffmann, P Röhlke, R Psille, T Gaigal, G Keller, H Höfler, T Löning, I Petersen, M Dietel.   

Abstract

BACKGROUND: The somatogenetic alterations that lead to the development of benign adenomas, borderline tumors, and invasive ovarian carcinomas are not well understood. This study investigated allelic losses in these three types of ovarian tumors.
METHODS: Twelve genetic regions on chromosomes 2q, 5q, 6p, 6q, 9p, 11q, 17p, 17q, 18q, and 22q were analyzed by polymerase chain reaction for loss of heterozygosity (LOH). The study was performed on formalin fixed, paraffin embedded tissue samples from 72 invasive ovarian carcinomas, 35 ovarian tumors of borderline malignancy, and 25 benign ovarian adenomas.
RESULTS: LOH was found in only 8% of the analyzed adenomas (at 2q21 and 17p13) and 11% of the borderline tumors (at 2q21, 5q21, 6p21, 17p13, and 17q21). Allelic losses were noted for 77.7% of all of the invasive carcinomas analyzed. The frequency of LOH was 56% at a locus near 17p13 (TP53) and 40.5% at 17q21 (BRCA1). LOH was observed in 30.4% of informative cases at 5q21 and in 21.4% at chromosome 18q21. The chromosomal regions 2q21-22 and 9p21 had deletions at frequencies of 32.4% and 25%, respectively. International Federation of Gynecology and Obstetrics stage and the presence of LOH correlated significantly with survival but were not independent predictors of survival. Serous subtypes of invasive carcinoma were significantly more prone to deletions than nonserous tumors.
CONCLUSIONS: The results of this study suggest that LOH occurs only occasionally in adenomas and borderline tumors, whereas it is frequently observed in invasive ovarian carcinomas. Therefore, other genetic events seem to be involved in early ovarian tumor development. However, the presence of multiple allelic losses is an indicator of higher stages of invasive carcinoma.

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Year:  1997        PMID: 9317174     DOI: 10.1002/(sici)1097-0142(19971001)80:7<1241::aid-cncr7>3.0.co;2-n

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  8 in total

1.  Localization of a susceptibility gene for familial nonmedullary thyroid carcinoma to chromosome 2q21.

Authors:  J D McKay; F Lesueur; L Jonard; A Pastore; J Williamson; L Hoffman; J Burgess; A Duffield; M Papotti; M Stark; H Sobol; B Maes; A Murat; H Kääriäinen; M Bertholon-Grégoire; M Zini; M A Rossing; M E Toubert; F Bonichon; M Cavarec; A M Bernard; A Boneu; F Leprat; O Haas; C Lasset; M Schlumberger; F Canzian; D E Goldgar; G Romeo
Journal:  Am J Hum Genet       Date:  2001-07-02       Impact factor: 11.025

2.  Somatic mutations of the PPP2R1B candidate tumor suppressor gene at chromosome 11q23 are infrequent in ovarian carcinomas.

Authors:  R Wu; D C Connolly; X Ren; E R Fearon; K R Cho
Journal:  Neoplasia       Date:  1999-10       Impact factor: 5.715

3.  Genomic aberrations in borderline ovarian tumors.

Authors:  Francesca Micci; Lisbeth Haugom; Terje Ahlquist; Hege K Andersen; Vera M Abeler; Ben Davidson; Claes G Trope; Ragnhild A Lothe; Sverre Heim
Journal:  J Transl Med       Date:  2010-02-26       Impact factor: 5.531

4.  Multiple chromosomal underrepresentations detected by interphase cytogenetics - possible prognostic markers in head and neck tumors?

Authors:  B Kleist; A Bankau; G Lorenz; M Poetsch
Journal:  Pathol Oncol Res       Date:  2001       Impact factor: 3.201

Review 5.  Peritoneal carcinoma in women with genetic susceptibility: implications for Jewish populations.

Authors:  Murray Joseph Casey; Chhanda Bewtra
Journal:  Fam Cancer       Date:  2004       Impact factor: 2.375

6.  P53, bcl-2, ki-67 li (labeling index) status in benign, proliferative, and malignant ovarian surface epithelial neoplasms.

Authors:  Nesrin Gursan; Sare Sipal; Muhammed Calik; Cemal Gundogdu
Journal:  Eurasian J Med       Date:  2009-04

7.  Molecular genetic evidence for monoclonal origin of bilateral ovarian serous borderline tumors.

Authors:  Nathalie L G Sieben; Sandra M Kolkman-Uljee; Adrienne M Flanagan; Saskia le Cessie; Anne-Marie Cleton-Jansen; Cees J Cornelisse; Gert Jan Fleuren
Journal:  Am J Pathol       Date:  2003-04       Impact factor: 4.307

8.  Tumor spreading to the contralateral ovary in bilateral ovarian carcinoma is a late event in clonal evolution.

Authors:  Francesca Micci; Lisbeth Haugom; Terje Ahlquist; Vera M Abeler; Claes G Trope; Ragnhild A Lothe; Sverre Heim
Journal:  J Oncol       Date:  2009-09-15       Impact factor: 4.375

  8 in total

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