Subscribe to RSS
DOI: 10.1055/s-2005-870456
Barrett’s Esophagus, Colorectal Adenomas and Carcinomas - What’s the Connection? Reply to Vieth & Stolte
Publication History
Publication Date:
05 December 2005 (online)
![](https://www.thieme-connect.de/media/endoscopy/200512/lookinside/thumbnails/10.1055-s-2005-870456-1.jpg)
I thank Drs Vieth and Stolte for their report of another patient with Barrett’s disease and an adenomatous colorectal polyposis syndrome. I suspect many investigators around the world are also looking for a connection between the dysplasia-carcinoma sequences of Barrett’s esophagus and colorectal adenomas [1]. Such a connection may be related to cytogenetic abnormalities, such as the loss of heterozygosity at tumor suppressor genes (DCC, APC, TP16 and TP53) found in both diseases [2]. Other investigators have studied clinical factors, such as the decreased use of aspirin or cyclooxygenase-2 inhibitors in patients with esophageal and colonic neoplasms [3] [4] [5] [6] [7]. Perhaps of most concern are the pleiomorphic changes observed in Barrett’s glandular mucosa induced by hypergastrinemia in patients treated chronically with acid suppressive drugs [8] [9] [10] [11] [12]. Investigations into the association of Barrett’s disease with adenomatous colon polyposis syndromes, including genomic studies, may yield important clues regarding germ-line and somatic cell abnormalities and the variability in genotype-phenotype correlations, the effect of modifying genes, and the contribution of environmental influences [13] [14].
References
- 1 Wong R S, Temes R T, Follis F M. et al . Multiple polyposis and adenocarcinoma arising in Barrett’s esophagus. Ann Thorac Surg. 1996; 61 216-218
- 2 Dolan K, Garde J, Walker S J. et al . LOH at the sites of the DCC, APC, and TP53 tumor suppressor genes occurs in Barrett’s metaplasia and dysplasia adjacent to adenocarcinoma of the esophagus. Hum Pathol. 1999; 30 1508-1514
- 3 Reddy B S, Rao C V, Seibert K. Evaluation of cyclooxygenase-2 inhibitor for potential chemopreventive properties in colon carcinogenesis. Cancer Res. 1996; 56 4566-4569
- 4 Kawamori T, Rao C V, Seibert K. et al . Chemopreventive activity of celecoxib, a specific cyclooxygenase-2 inhibitor, against colon carcinogenesis. Cancer Res. 1998; 58 409-412
- 5 Funkhouser E M, Sharp G B. Aspirin and reduced risk of esophageal carcinoma. Cancer. 1995; 76 1116-1119
- 6 Schreinemachers D M, Everson R B. Aspirin use and lung, colon, and breast cancer incidence in a prospective study. Epidemiology. 1994; 5 138-146
- 7 Zimmermann K C, Sarbia M, Weber A A. et al . Cyclooxygenase-2 expression in human esophageal carcinoma. Cancer Res. 1999; 59 198-204
- 8 Atherfold P, Obszynska A, Jankowski J. Gastrin, the Janus peptide, induces pleiomorphic changes associated with Barrett’s metaplasia [abstract]. Gastroenterology. 2005; 128 A232
- 9 Singh P, Velasco M, Given R. et al . Progastrin expression predisposes mice to colon carcinomas and adenomas in response to a chemical carcinogen. Gastroenterology. 2000; 119 162-171
- 10 Watson S A, Smith A M. Hypergastrinemia promotes adenoma progression in the APC (Min-/+) mouse model of familial adenomatous polyposis. Cancer Res. 2001; 61 625-631
- 11 Watson S A, Morris T M, McWilliams D F. et al . Potential role of endocrine gastrin in the colonic adenoma carcinoma sequence. Br J Cancer. 2002; 87 567-573
- 12 Ottewell P D, Watson A J, Wang T C. et al . Progastrin stimulates murine colonic epithelial mitosis after DNA damage. Gastroenterology. 2003; 124 1348-1357
- 13 Fitzgerald R C. Complex diseases in gastroenterology and hepatology: GERD, Barrett’s, and esophageal adenocarcinoma. Clin Gastroenterol Hepatol. 2005; 3 529-537
- 14 Hall I P. Expression profiling: fishing and chips. Gut. 2004; 53 917-918
H. C. Wolfsen, M. D.
Division of Gastroenterology and HepatologyMayo Clinic
4500 San Pablo RoadJacksonvilleFlorida 32224 USA
Fax: +1-904-953-7260
Email: pdt@mayo.edu