Literature DB >> 12749233

3p21, 5q21, 9p21 and 17p13.1 allelic deletions are potential markers of individuals with a high risk of developing adenocarcinoma in Barrett's epithelium without dysplasia.

Julian Sanz-Ortega1, Susana Hernández, Maria C Saez, Elena Sierra, Gonzalo Sanz-Ortega, Antonio Torres, Jose L Balibrea, Julian Sanz-Esponera, Maria J Merino.   

Abstract

BACKGROUND/AIMS: A common genetic abnormality detected in Barrett's adenocarcinoma is LOH (loss of heterozygosity) at the sites of known or putative tumor suppressor genes. Thus, some deletions have also been determined in peritumoral Barrett's epithelium. These findings suggest that a tissue field of somatic genetic alterations precede the histopathological phenotypic changes of carcinoma. We investigated 32 cases of Barrett's esophagus with no evidence of dysplasia for LOH at 5q21 (APC), 3p21, 9p21 (p16) and 17p13.1 (p53) chromosomal regions.
METHODOLOGY: Two groups were randomly selected and compared: 16 cases of Barrett's epithelium adjacent to adenocarcinoma and 16 cases of Barrett's epithelium with no evidence of malignant transformation in a 5-10 years follow-up period. In three adenocarcinomas cases several previous endoscopic biopsies of Barrett's esophagus were available.
RESULTS: We determined frequent allelic losses in adenocarcinomas at p53 (54%), p16 (50%), 3p21 (40%) and 5q21 (33%). Identical LOH was present in most cases in the Barrett's epithelium adjacent to adenocarcinoma. LOH at these loci was unusual in Barrett's epithelium with no evidence of malignant transformation. However, in cases where sequential endoscopic biopsies were performed in advance to the adenocarcinoma diagnosis LOH was already present in the Barrett's epithelium.
CONCLUSIONS: We suggest that LOH at these loci may be present before the onset of the malignant growth and LOH studies may supplement the histopathological evaluation of Barrett's epithelium. LOH at 3p21, 5q21, 9p21 and 17p13 chromosomal regions in cells of Barrett's epithelium without dysplasia may have a role as a potential marker for individuals with a high risk of developing adenocarcinoma.

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Year:  2003        PMID: 12749233

Source DB:  PubMed          Journal:  Hepatogastroenterology        ISSN: 0172-6390


  11 in total

1.  A Multicenter Study of a Fluorescence In Situ Hybridization Probe Set for Diagnosing High-Grade Dysplasia and Adenocarcinoma in Barrett's Esophagus.

Authors:  John M Poneros; Adam S Faye; Emily G Barr Fritcher; Ananda Sen; Sharmila Anandasabapathy; Robert S Bresalier; Norman Marcon; D Kim Turgeon; Henry Appelman; Daniel Normolle; Larry E Morrison; Dean E Brenner; Kevin C Halling
Journal:  Dig Dis Sci       Date:  2017-03-06       Impact factor: 3.199

2.  TP53 gene mutations are rare in nondysplastic Barrett's esophagus.

Authors:  Kamila Novotna; Marie Trkova; Alexandr Pazdro; Milan Smejkal; Alzbeta Soukupova; Daniela Kodetova; Premysl Smejkal; Zdenek Sedlacek
Journal:  Dig Dis Sci       Date:  2006-01       Impact factor: 3.199

Review 3.  Clinical implications of molecular changes in pediatric Barrett's esophagus.

Authors:  Licia Pensabene; Marta C Cohen; Michael Thomson
Journal:  Curr Gastroenterol Rep       Date:  2012-06

4.  Molecular cytogenetic characterization of esophageal cancer detected by comparative genomic hybridization.

Authors:  Yuli C Chang; Kun-Tu Yeh; Ta-Chih Liu; Jan-Gowth Chang
Journal:  J Clin Lab Anal       Date:  2010       Impact factor: 2.352

5.  The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus.

Authors:  Shannon M Brankley; Kenneth K Wang; Aaron R Harwood; Dylan V Miller; Mona S Legator; Lori S Lutzke; Benjamin R Kipp; Larry E Morrison; Kevin C Halling
Journal:  J Mol Diagn       Date:  2006-05       Impact factor: 5.568

6.  Validation of a biomarker panel in Barrett's esophagus to predict progression to esophageal adenocarcinoma.

Authors:  S Eluri; E Klaver; L C Duits; S A Jackson; J J Bergman; N J Shaheen
Journal:  Dis Esophagus       Date:  2018-11-01       Impact factor: 3.429

7.  Targeting chemokine pathways in esophageal adenocarcinoma.

Authors:  Makardhwaj S Shrivastava; Zulfiqar Hussain; Orsolya Giricz; Niraj Shenoy; Rahul Polineni; Anirban Maitra; Amit Verma
Journal:  Cell Cycle       Date:  2014       Impact factor: 4.534

8.  Correlation of the presence and extent of loss of heterozygosity mutations with histological classifications of Barrett's esophagus.

Authors:  Eric Ellsworth; Sara A Jackson; Shyam J Thakkar; Dennis M Smith; Sydney Finkelstein
Journal:  BMC Gastroenterol       Date:  2012-12-27       Impact factor: 3.067

9.  The Presence of Genetic Mutations at Key Loci Predicts Progression to Esophageal Adenocarcinoma in Barrett's Esophagus.

Authors:  Swathi Eluri; William R Brugge; Ebubekir S Daglilar; Sara A Jackson; Mindi A Styn; Keith M Callenberg; Derek C Welch; Todd M Barr; Lucas C Duits; Jacques J Bergman; Nicholas J Shaheen
Journal:  Am J Gastroenterol       Date:  2015-05-26       Impact factor: 10.864

10.  Recurring Translocations in Barrett's Esophageal Adenocarcinoma.

Authors:  Manisha Bajpai; Anshuman Panda; Kristen Birudaraju; James Van Gurp; Amitabh Chak; Kiron M Das; Parisa Javidian; Hana Aviv
Journal:  Front Genet       Date:  2021-06-09       Impact factor: 4.599

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