Higher frequency of chromosomal aberrations in ovarian endometriosis compared to extragonadal endometriosis: A possible link to endometrioid adenocarcinoma

Körner, Meike; Burckhardt, Elisabeth; Mazzucchelli, Luca (2006). Higher frequency of chromosomal aberrations in ovarian endometriosis compared to extragonadal endometriosis: A possible link to endometrioid adenocarcinoma. Modern pathology, 19(12), pp. 1615-23. London: Nature Publishing Group 10.1038/modpathol.3800699

Full text not available from this repository. (Request a copy)

Endometriosis may progress to invasive endometrioid adenocarcinoma, particularly in the ovary. Up to now, little is known of the molecular mechanisms possibly involved in the malignant transformation of endometriosis. Therefore, in this study, extragonadal endometriosis (n = 10), ovarian endometriosis without malignancy (n = 10), ovarian endometriosis with direct transition into endometrioid adenocarcinoma (n = 8), and normal endometrium (n = 12) were investigated for numerical chromosomal aberrations by fluorescence in situ hybridization using centromere enumeration probes. The proportions of cells with aneusomies were semiquantitatively assessed. Trisomies 1 and 7, and monosomies 9 and 17 were found in endometriosis, ovarian endometrioid adenocarcinoma, and normal endometrium. The proportions of aneusomic cells were significantly higher in ovarian endometrioid carcinoma compared with ovarian endometriosis (P < 0.001), and in ovarian endometriosis compared with extragonadal endometriosis and normal endometrium (P < 0.001). The data provide new evidence of a common lineage of endometriosis and ovarian endometrioid carcinoma. The higher frequency of chromosomal aberrations in endometrioid carcinoma than in endometriosis may reflect an expansion of aberrant cell clones already present in endometriosis during the progression to cancer. The higher frequency of chromosomal aberrations in ovarian endometriosis than in extragonadal endometriosis suggests a role of the ovarian stromal milieu in the induction of genetic changes, which may eventually lead to invasive cancer.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute of Pathology

UniBE Contributor:

Körner Jachertz, Meike, Burckhardt, Elisabeth, Mazzucchelli, Luca

ISSN:

0893-3952

ISBN:

16980942

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:48

Last Modified:

05 Dec 2022 14:15

Publisher DOI:

10.1038/modpathol.3800699

PubMed ID:

16980942

Web of Science ID:

000242237700012

URI:

https://boris.unibe.ch/id/eprint/20305 (FactScience: 3561)

Actions (login required)

Edit item Edit item
Provide Feedback