Barrett's esophagus

Current Opinion in Gastroenterology

Volumn 15, Issue 4, 1999, Pages 352-358

  Spechler, Stuart Jon ^a,b  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

^b VA NORTH TEXAS HEALTH CARE SYSTEM   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA CATENIN; AMINOLEVULINIC ACID; BETA CATENIN; CELL ADHESION MOLECULE; CYCLIN DEPENDENT KINASE; CYCLINE; CYCLOOXYGENASE 2; NITRIC OXIDE SYNTHASE; PHOTOFRIN; PHOTOSENSITIZING AGENT; PROTON PUMP INHIBITOR; UVOMORULIN; VILLIN;

ARTICLE; BARRETT ESOPHAGUS; CELL CULTURE; ENZYME ACTIVITY; ESOPHAGUS CARCINOMA; ESOPHAGUS MUCOSA; GASTROESOPHAGEAL REFLUX; GRAM NEGATIVE INFECTION; HELICOBACTER PYLORI; HUMAN; INTESTINE METAPLASIA; LOWER ESOPHAGUS SPHINCTER; PHOTODYNAMIC THERAPY; STOMACH FUNDOPLICATION; TUMOR SUPPRESSOR GENE;

EID: 0032770559     PISSN: 02671379     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001574-199907000-00014     Document Type: Article

References (34)

1. + exchanger, an ion transporter found in the membranes of most mammalian cells, mediates the hyperproliferation of cells in Barrett's esophagus induced by brief exposure to acid.
2. 2 Washington K, Chiappori A, Hamilton K, Shyr Y, Blanke C, Johnson D, et al: Expression of β-catenin, α-catenin, and E-cadherin in Barrett's esophagus and esophageal adenocarcinomas. Mod Pathol 1998, 11:805-813. Decreased expression of β-catenin was found in 11 of 17 cases of low-grade dysplasia, in 14 of 16 cases of high-grade dysplasia, and in all of 7 cases of intramucosal carcinoma in Barrett's esophagus.
3. 3 Bailey T, Biddlestone L, Shepherd N, Barr H, Warner P, Jankowski J: Altered cadherin and catenin complexes in the Barrett's esophagus-dysplasia-adenocarcinoma sequence: correlation with disease progression and dedifferentiation. Am J Pathol 1998, 152:135-144. Using immunohistochemical techniques and Western blotting to study cadherins and catenins in tissue specimens, these investigators found a significant correlation between abnormal expression of adhesion molecules and the stage of neoplasia in Barrett's esophagus.
4. 4 Wu TT, Watanabe T, Heitmiller R, Zahurak M, Forastiere AA, Hamilton SR: Genetic alterations in Barrett esophagus and adenocarcinomas of the esophagus and esophagogastric junction region. Ann J Pathol 1998, 153:287-294. Allelic deletions of chromosomes known to harbor important tumor-suppressor genes were studied in surgical resection specimens from patients who had esophagectomies for adenocarcinoma or dysplasia in Barrett's esophagus. The findings suggest that deletions of chromosomes 17p and 18q occur early and often in the carcinogenetic sequence in Barrett's esophagus, whereas loss of chromosome 5q is a later event.
5. 5 Khan S, Do KA, Kuhnert P, Pillay SP, Papadimos D, Conrad R, Jass JR: Diagnostic value of p53 immunohistochemistry in Barrett's esophagus: an endoscopic study. Pathology 1998, 30:136-140. Strong immunohistochemical staining for p53 staining was found in 0 of 79 cases of nondysplastic intestinal metaplasia, 5 of 15 cases (33%) of low-grade dysplasia, and 7 of 8 cases (87%) of high-grade dysplasia in Barret's esophagus.
6. 6 Gimenez A, Minguela A, Parrilla P, Bermejo J, Perez D, Molina J, et al: Flow cytometric DNA analysis and p53 protein expression show a good correlation with histologic findings in patients with Barrett's esophagus. Cancer 1998, 15:83:641-651. Immunostaining for p53 was found to correlate well with the histologic grade of dysplasia in biopsy specimens from 55 patients with Barrett's esophagus.
7. 7 Cawley HM, Meltzer SJ, De Benedetti VMG, Hollstein MC, Muehlbauer KR, Liang L, et al: Anti-p53 antibodies in patients with Barrett's esophagus or esophageal carcinoma can predate cancer diagnosis. Gastroenterology 1998, 115:19-27. Antibodies to p53 protein were found in the plasma in 3 of 36 patients with benign Barrett's esophagus, 8 of 23 patients with esophageal squamous cell cancers, 3 of 10 patients with esophageal adenocarcinoma, and 1 of 19 control subjects. In two patients with esophageal cancer, the finding of circulating antibodies to p53 predated the diagnosis of malignancy.
8. 8 Singh SP, Lipman J, Goldman H, Ellis FH Jr, Aizenman Lcangi MF, Signoretti S, et al: Loss or altered subcellular localization of p27 in Barrett's associated adenocarcinoma. Cancer Res 1998, 58:1730-1735. In surgical resection specimens from 58 patients with adenocarcinomas in Barrett's esophagus, abnormally increased expression of p27 protein was observed in all of the high-grade dysplastic tissue adjacent to the tumors, whereas the tumors themselves usually exhibited low levels of p27 protein. The latter finding correlated with higher histologic grade, greater depth of invasion, the presence of lymph node metastases, and poorer survival.
9. 9 Klump B, Hsieh CJ, Holzmann K, Gregor M, Porschen R: Hypermethylation of the CDKN2/p16 promoter during neoplastic progression in Barrett's esophagus. Gastroenterology 1998, 115:1381-1386. This study suggests that promoter hypermethylation may be a common mechanism for p16 gene inactivation during neoplastic progression in Barrett's esophagus.
10. 10 Wilson KT, Fu S, Ramanujam KS, Meltzer SJ: Increased expression of inducible nitric oxide synthase and cyclooxygenase-2 in Barrett's esophagus and associated adenocarcinoma. Cancer Res 1998, 58:2929-2934. Elevated levels of COX-2 and iNOS mRNA were found in biopsy specimens of intestinal metaplasia from 17 and 16 of 21 patients with Barrett's esophagus. All five patients with adenocarcinoma in Barrett's esophagus exhibited elevated levels of COX-2 mRNA, whereas elevated iNOS mRNA levels were found in four patients.
11. 11 Regalado SP, Nambu Y, Iannettoni MD, Orringer MB, Beer DG: Abundant expression of the intestinal protein villin in Barrett's metaplasia and esophageal adenocarcinomas. Mol Carcinog 1998, 22:182-189. Expression of the intestinal protein villin was observed in intestinal metaplasia in Barrett's esophagus in all of 21 cases, in adenocarcinomas in Barrett's esophagus in 28 of 30 cases (93%), and in 13 of 16 cases (81%) of adenocarcinoma of the gastric cardia.
12. 12 Palanca-Wessels MC, Barrett MT, Galipeau PC, Rohrer KL, Reid BJ, Rabinovitch PS: Genetic analysis of long-term Barrett's esophagus epithelial cultures exhibiting cytogenetic and ploidy abnormalities. Gastroenterology 1998, 114:295-304. These investigators describe the successful establishment of cultures of epithelial cells isolated from biopsy specimens of Barrett's esophagus that have survived for 12 to 17 months and that exhibit a number of molecular genetic abnormalities.
13. 13 Ǒberg S, Peters JH, DeMeester TR, Chandrasoma P, Hagen JA, Ireland AP, et al: Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg 1997, 226:522-532.
14. 14 Csendes A, Smok G, Burdiles P, Sagastume H, Rojas J, Puente G, et al: "Carditis": an objective histological marker for pathologic gastroesophageal reflux disease. Dis Esophagus 1998, 11:101-105. Carditis was found in biopsy specimens obtained just distal to the squamocolumnar junction in 47% of patients with GERD but in only 8% of control subjects without GERD. The Investigators concluded that carditis is an objective marker for GERD.
15. 15 Goldblum JR, Vicari JJ, Falk GW, Rice TW, Peek RM, Easley K, Richter JE: Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology 1998, 114:633-639. Biopsy specimens were taken from the gastric cardia in 58 patients with GERD and in 27 control subjects. Carditis was not found to be associated with GERD, but H. pylori infection was found in all 11 control subjects and in 22 of the 23 patients who had carditis. Eight patients had intestinal metaplasia in the cardia, all eight of whom had carditis. The authors concluded that carditis is associated with H. pylori infection, not with GERD, and that intestinal metaplasia in the cardia is merely a manifestation of the generalized atrophic gastritis caused by H. pylori infection elsewhere in the stomach.
16. 16 Chen YY, Antonioli DA, Spechler SJ, Zeroogian JM, Goyal RK, Wang HH: Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. Mod Pathol 1998, 11:950-956. Cardiac epithelium was found of the squamocolumnar junction in 116 (75%) of 155 unselected patients in a general endoscopy unit, and carditis was found in 107 (92%) of those 116 patients. A strong correlation was found between the severity of carditis and the frequency of H. pylori infection. Neither the severity of carditis nor the presence of H. pylori infection correlated with the finding of intestinal metaplasia at the squamocolumnar junction.
17. 17 Hackelsberger A, Günther T, Schultze V, Manes G, Dominguez-Muñoz JE, Roessner A, Malfertheiner P: Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease? Gut 1998, 43:17-21. This study suggests that there may be substantial differences in the pathogenesis of intestinal metaplasia in the gastric cardia and in the esophagus.
18. 18 Dias Pereira A, Suspiro A, Chaves P, Sraiva A, Gloria L, Mendes de Almeida JC, et al: Short segments of Barrett's epithelium and intestinal metaplasia in normal appearing oesophagogastric junctions: the same or two different entities? Gut 1998, 42:659-662. A greater frequency of intestinal metaplasia and male predominance was found in patients whose squamocolumnar junction was abnormal in appearance, location, or both.
19. 19 Chow WH, Blaser MJ, Blot WJ, Gammon MD, Vaughan TL, Risch HA, et al: An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res 1998, 58:588-590. In a study of 129 patients with adenocarcinomas of the esophagus and gastric cardia and 224 population controls, infection with cagA-positive H. pylori was found to be associated with a significantly reduced risk for these cancers.
20. 20 Vicari JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, Schnell J, et al: The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998, 115:50-57. cagA-Positive H. pylori infections were found in 11 of 26 control subjects (42%) but in none of 7 patients with dysplasia or adenocarcinoma in Barrett's esophagus.
21. 21 Graham DY, Yamaoka Y: H. pylori and cagA: relationships with gastric cancer, duodenal ulcer, and reflux esophagitis and its complications. Helicobacter 1998, 3:145-150. These authors propose that H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD.
22. 22 Devesa SS, Blot WJ, Fraumeni JF Jr: Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 1998, 83:2049-2053. This analysis of data from the SEER program of the National Cancer Institute indicates that the incidence of adenocarcinoma of the esophagus among white men in the United States has more than tripled since the mid-1970s.
23. 23 Sharma P, Morales TG, Bhattacharyya A, Garewal HS, Sampliner RE: Squamous islands in Barrett's esophagus: what lies underneath? Am J Gastroenterol 1998, 93:332-335. Biopsy specimens were taken from squamous islands in 22 patients with Barrett's esophagus, and intestinal metaplasia underlying squamous epithelium was found in 15 of 39 specimens (39%).
24. 24 Byrne JP, Armstrong GR, Attwood SEA: Restoration of the normal squamous lining in Barrett's esophagus by argon beam plasma coagulation. Am J Gastroenterol 1998, 93:1810-1815.
25. 25 Salo JA, Salminen JT, Kiviluoto TA, Nemlander AT, Rǎmǒ OJ, Fǎrkkilä MA, et al: Treatment of Barrett's esophagus by endoscopic laser ablation and antireflux surgery. Ann Surg 1998, 227:40-44.
26. 26 Bremner RM, Mason RJ, Bremner CG, DeMeester TR, Chandrasoma P, Peters JH, et al: Ultrasonic epithelial ablation of the lower esophagus without stricture formation. Surg Endosc 1998, 12:342-347. A new, experimental technique for epithelial ablation using ultrasonic energy generated by a Cavitron Ultrasonic Surgical Aspirator is described.
27. 27 Biddlestone LR, Barham CP, Wilkinson SP, Barr H, Shepherd NA: The histopathology of treated Barrett's esophagus: squamous reepithelialization after acid suppression and laser and photodynamic therapy. Am J Surg Pathol 1998, 22:239-245. Thermal and photochemical ablative therapies for Barrett's esophagus often result in the burying of intestinal metaplasia under a superficial layer of squamous epithelium.
28. 28 Nishioka NS: Drug, light, and oxygen: a dynamic combination in the clinic. Gastroenterology 1998, 114:604-606.
29. 29 Gossner L, Stolte M, Sroka R, Rick K, May A, Hahn EG, Ell C: Photodynamic ablation of high-grade dysplasia and early cancer in Barrett's esophagus by means of 5-aminolevulinic acid. Gastroenterology 1998, 114:448-455. Photodynamic therapy with 5-ALA was used to treat 22 patients with superficial cancers and 10 patients with high-grade dysplasia in Barrett's esophagus. During a mean follow-up period of 9.9 months, no residual cancer was found in 17 of 22 patients (77%), and high-grade dysplasia appeared to have been eradicated in all 10 cases. Cancers with a thickness of greater than 2 mm were not eliminated by PDT with ALA.
30. 30 Sampliner RE, and The Practice Parameters Committee of the American College of Gastroenterology: Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus. Am J Gastroenterol 1998, 93:1028-1032. Specific management recommendations for patients with Barrett's esophagus are provided.
31. 31 Falk GW, Richter JE: Reflux disease and Barrett's esophagus. Endoscopy 1998, 30:61-72.
32. 32 Cameron AJ. Management of Barrett's esophagus. Mayo Clin Proc 1998, 73:457-461.
33. 33 Fitzgerald RC, Triadafilopoulos G: Recent developments in the molecular characterization of Barrett's esophagus. Dig Dis 1998, 16:63-80.
34. 34 Sharma P, Morales TG, Sampliner RE: Short segment Barrett's esophagus - the need for standardization of the definition and of endoscopic criteria. Am J Gastroenterol 1998, 93:1033-1036.