NDLI: Detection of chromosomal aneuploidy in endometriosis by multi-color fluorescence in situ hybridization (FISH)

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Human Genetics : Volume 100, Issue 2, July 1997

Human Genetics : Volume 100, Issue 1, June 1997

Human Genetics : Volume 99

Detection of chromosomal aneuploidy in endometriosis by multi-color fluorescence in situ hybridization (FISH)

Content Provider	Springer Nature Link
Author	Shin, Jong Chul Ross, Helen L. Elias, Sherman Nguyen, Dianne D. Mitchell Leef, Dorothy Simpson, Joe Leigh Bischoff, F. Z.
Copyright Year	1997
Abstract	Endometriosis affects 10–15% of women of reproductive age and is a common cause of infertility and pelvic pain. Although endometriosis is characterized by abnormal growth or turn-over of cells, the genetic changes involved remain unclear. We employed a multi-color fluorescence in situ hybridization (FISH) strategy to determine the incidence of somatic chromosomal numeric alterations in severe/late stage endometriosis. Using alpha-satellite sequence-specific DNA probes for chromosomes 7, 8, 11, 12, 16, 17, and 18, simultaneous two- and three-color FISH were performed to evaluate the frequency of monosomic, disomic, and trisomic cells in normal control and endometriotic tissue specimens. In one of four endometriosis samples studied, a significantly higher frequency of monosomy for chromosome 17 (14.8%, χ2 4 = 53.3, P < 0.0001) and 16 (8.8%, χ2 4 = 11.4, P < 0.05) was observed. An increased number of cells with chromosome 11 trisomy (14.8%, χ2 4 = 96.2, P < 0.0001) were detected in a second case. In a third case, a distinct colony of nuclei with chromosome 16 monosomy (14.1%, χ2 4 = 21.39, P < 0.005) was detected. Acquired chromosome-specific aneuploidy may be involved in endometriosis, reflecting clonal expansion of chromosomally abnormal cells. That candidate tumor suppressor genes and oncogenes have been mapped to chromosomes 11, 16, and 17 suggests that chromosomal loss or gain plays a role in the development and/or progression of endometriosis.
Starting Page	401
Ending Page	406
Page Count	6
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	100
Issue Number	3-4
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	1997-08-04
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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