Comparative genomic hybridization analysis of chromosomal alterations in patients with long-standing ulcerative colitis

Kupka, Susan; Schröder, Kristina; Porschen, Rainer; Borchard, F; Gregor, Michael; Blin, Nikolaus; Holzmann, Karlheinz

doi:10.3892/ijo.19.3.489

Cited by 1 publication

(3 citation statements)

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“…Metaphase-comparative genomic hybridization also necessitates considerable cytogenetic expertise for the morphologic evaluation of hybridization signals along physical chromosomes rather than the automated signal detection of known chromosomal sites spotted onto systematic arrays. Regardless of the differences in these technologies, it is encouraging that a few differential chromosomal sites identified by earlier metaphase-comparative genomic hybridization were also observed in our array results, specifically chromosomal losses on 15, 5q, and 18q ( 26 - 28 ).…”

Section: Discussionsupporting

confidence: 56%

“…Discoveries in the last several years have advanced our understanding of the molecular biology of ulcerative colitis. Widespread genomic alterations have been demonstrated in ulcerative colitis progressors with neoplasia, but not nonprogressors, using assays of telomere shortening and anaphase bridge development ( 2 ), DNA-fingerprinting by arbitrarily primed PCR ( 13 - 15 ), preclonal chromosomal gains and losses by fluorescence in situ hybridization (FISH) ( 1 , 2 , 28 ), metaphase-comparative genomic hybridization ( 26 - 28 ), and estrogen receptor gene promoter hypermethylation ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

“…Array technology permits high resolution genomic scanning for chromosomal losses and gains over many thousands of genomic targets. The much higher resolution afforded by array technology is a major advance over earlier comparative genomic hybridization technology using metaphase chromosomes ( 26 - 28 ). The higher density 4,298 feature BAC array used in this study has a mean intermarker spacing of 675 kilobase in comparison to the approximate five megabase resolution of metaphase chromosomes.…”

Section: Discussionmentioning

confidence: 99%

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Array-based comparative genomic hybridization in ulcerative colitis neoplasia: single non-dysplastic biopsies distinguish progressors from non-progressors

Bronner

Skacel²,

Crispin

et al. 2010

Modern Pathology

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Approximately 10% of ulcerative colitis patients develop colorectal neoplasia. At present, identification of this subset is markedly limited and necessitates lifelong colonoscopic surveillance for the entire ulcerative colitis population. Better risk markers are needed to focus surveillance onto the patients most likely to benefit. Using array-based comparative genomic hybridization, we analyzed single, non-dysplastic biopsies from three patient groups: ulcerative colitis progressors (n=9) with cancer or high-grade dysplasia at a mean distance of 18 cm from the analyzed site; ulcerative colitis nonprogressors (n=8) without dysplasia during long-term surveillance; and non-ulcerative colitis normal controls (n=2). Genomic DNA from fresh colonic epithelium purified from stroma was hybridized to 287 (low-density) and 4,342 (higher-density) feature bacterial artificial chromosome arrays. Sample-to-reference fluorescence ratios were calculated for individual chromosomal targets and globally across the genome. The low-density arrays yielded pronounced genomic gains and losses in 3 of 9 (33%) ulcerative colitis progressors but in none of the 10 control patients. Identical DNA samples analyzed on the higher density arrays, using a combination of global and individual high variance assessments, distinguished all 9 progressors from all 10 controls. These data confirm that genomic alterations in ulcerative colitis progressors are widespread, even involving single non-dysplastic biopsies far distant from neoplasia. They therefore show promise toward eliminating full colonoscopic surveillance with extensive biopsy sampling in the majority of ulcerative colitis patients.

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Section: Discussionsupporting

confidence: 56%