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• W2092341500 abstract "Background & Aims: Eradication of Helicobacter pylori appears to reduce gastric cancer incidence. We examined the effect of successful H pylori therapy on histology, phenotype of gastric intestinal metaplasia (GIM) (complete vs incomplete), and expression of several biomarkers related to carcinogenesis. Methods: Ninety-six H pylori–positive patients from Japan were treated successfully and followed up prospectively over 4 years with yearly endoscopy and were classified into 3 groups: group CG, chronic gastritis without GIM (n = 36); group IM, chronic gastritis with GIM (n = 33); group DYS, and GIM with dysplasia/cancer in a different location of the stomach (n = 27). A total of 288 endoscopic procedures were performed. Histology, mucin-histochemistry, and immunoperoxidase assays using monoclonal antibodies (mAbs) for cell phenotype (monoclonal antibody Das-1/colonic) and for neoplasia (TC22 and p53) were performed. Results: The GIM histologic score was higher in group DYS than in group IM (P < .05) and group CG (P < .0001). The GIM scores did not change in groups IM and DYS over 4 years. mAb Das-1 reactivity was higher in group DYS (63%) than in group IM (39%) and group GC (0%). After eradication of H pylori, mAb Das-1 reactivity disappeared in 40% of patients (P < .0001) despite the unchanged GIM scores, and regression of TC22-4 was noted in the same patients. Conclusions:H pylori eradication does not reduce the histologic GIM score, but changes the cellular phenotype of GIM. This change of phenotype may be an important factor in the reduction of cancer incidence after eradication of H pylori. Background & Aims: Eradication of Helicobacter pylori appears to reduce gastric cancer incidence. We examined the effect of successful H pylori therapy on histology, phenotype of gastric intestinal metaplasia (GIM) (complete vs incomplete), and expression of several biomarkers related to carcinogenesis. Methods: Ninety-six H pylori–positive patients from Japan were treated successfully and followed up prospectively over 4 years with yearly endoscopy and were classified into 3 groups: group CG, chronic gastritis without GIM (n = 36); group IM, chronic gastritis with GIM (n = 33); group DYS, and GIM with dysplasia/cancer in a different location of the stomach (n = 27). A total of 288 endoscopic procedures were performed. Histology, mucin-histochemistry, and immunoperoxidase assays using monoclonal antibodies (mAbs) for cell phenotype (monoclonal antibody Das-1/colonic) and for neoplasia (TC22 and p53) were performed. Results: The GIM histologic score was higher in group DYS than in group IM (P < .05) and group CG (P < .0001). The GIM scores did not change in groups IM and DYS over 4 years. mAb Das-1 reactivity was higher in group DYS (63%) than in group IM (39%) and group GC (0%). After eradication of H pylori, mAb Das-1 reactivity disappeared in 40% of patients (P < .0001) despite the unchanged GIM scores, and regression of TC22-4 was noted in the same patients. Conclusions:H pylori eradication does not reduce the histologic GIM score, but changes the cellular phenotype of GIM. This change of phenotype may be an important factor in the reduction of cancer incidence after eradication of H pylori. See de Vries AC et al on page 945 for companion article in the April 2008 issue of Gastroenterology.Gastric cancer remains the second most common cause of cancer deaths in the world.1Parkin D.M. Pisani P. Ferlay J. Estimates of the worldwide incidence of eighteen major cancers in 1985.Int J Cancer. 1993; 54: 594-606Crossref PubMed Scopus (1584) Google Scholar Since the discovery of Helicobacterpylori in 1983,2Warren J.R. Marshall B.J. Unidentified curved bacilli on gastric epithelium in active chronic gastritis.Lancet. 1983; 1: 1273-1275PubMed Google Scholar its infection is well-known to be associated with the development of chronic gastritis, gastric atrophy, gastric intestinal metaplasia (GIM), and cancer.3Correa P. Helicobacter pylori and gastric carcinogenesis.Am J Surg Pathol. 1995; 19: S37-S43Crossref PubMed Scopus (21) Google Scholar, 4Huang J.Q. Sridhar S. Chen Y. et al.Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer.Gastroenterology. 1998; 114: 1169-1179Abstract Full Text Full Text PDF PubMed Scopus (816) Google Scholar, 5Danesh J. Helicobacter pylori infection and gastric cancer: systematic review of the epidemiological studies.Aliment Pharmacol Ther. 1999; 13: 851-856Crossref PubMed Scopus (221) Google Scholar, 6You W.C. Zhang L. Gail M.H. et al.Gastric dysplasia and gastric cancer: Helicobacter pylori, serum vitamin C, and other risk factors.J Natl Cancer Inst. 2000; 92: 1607-1612Crossref PubMed Scopus (238) Google Scholar, 7Uemura N. Okamoto S. Yamamoto S. et al.Helicobacter pylori infection and the development of gastric cancer.N Engl J Med. 2001; 345: 784-789Crossref PubMed Scopus (3612) Google Scholar, 8Take S. Mizuno M. Ishiki K. et al.The effect of eradicating Helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease.Am J Gastroenterol. 2005; 100: 1037-1042Crossref PubMed Scopus (187) Google Scholar Based on these reports, it is believed that eradication of H pylori may prevent the development of gastric cancer. More recently, a prospective, randomized, placebo-controlled, population-based study reported that eradication of H pylori significantly decreased the development of gastric cancer.9Wong B.C. Lam S.K. Wong W.M. et al.Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial.JAMA. 2004; 291: 187-194Crossref PubMed Scopus (1224) Google Scholar GIM is believed to be a preneoplastic lesion of the stomach.3Correa P. Helicobacter pylori and gastric carcinogenesis.Am J Surg Pathol. 1995; 19: S37-S43Crossref PubMed Scopus (21) Google Scholar, 10Correa P. Shiao Y.H. Phenotypic and genotypic events in gastric carcinogenesis.Cancer Res. 1994; 54: 1941s-1943sPubMed Google Scholar, 11Filipe M.I. Munoz N. Matko I. et al.Intestinal metaplasia types and the risk of gastric cancer: a cohort study in Slovenia.Int J Cancer. 1994; 57: 324-329Crossref PubMed Scopus (389) Google Scholar Whether eradication of H pylori influences gastric cancer incidence, the results are conflicting (Table 1). Some studies reported that the histologic grade of GIM had improved after eradication,12Genta R.M. Lew GM Graham D.Y. Changes in the gastric mucosa following eradication of Helicobacter pylori.Mod Pathol. 1993; 6: 281-289PubMed Google Scholar, 13Uemura N. Mukai T. Okamoto S. et al.Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer.Cancer Epidemiol Biomarkers Prev. 1997; 6: 639-642PubMed Google Scholar, 14Nardone G. Staibano S. Rocco A. et al.Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.Gut. 1999; 44: 789-799Crossref PubMed Scopus (135) Google Scholar, 15Sung J.J. Lin S.R. Ching J.Y. et al.Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study.Gastroenterology. 2000; 119: 7-14Abstract Full Text Full Text PDF PubMed Scopus (324) Google Scholar, 16Ohkusa T. Fujiki K. Takashimizu I. et al.Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated.Ann Intern Med. 2001; 134: 380-386Crossref PubMed Scopus (198) Google Scholar, 17Kokkola A. Sipponen P. Rautelin H. et al.The effect of Helicobacter pylori eradication on the natural course of atrophic gastritis with dysplasia.Aliment Pharmacol Ther. 2002; 16: 515-520Crossref PubMed Scopus (104) Google Scholar, 18Correa P. Fontham E.T.H. Bravo J.C. et al.Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-Helicobacter pylori therapy.J Natl Cancer Inst. 2000; 92: 1881-1888Crossref PubMed Scopus (602) Google Scholar, 19Ley C. Mohar A. Guarner J. et al.Helicobacter pylori eradication and gastric preneoplastic conditions: a randomized, double-blind, placebo-controlled trial.Cancer Epidemiol Biomarkers Prev. 2004; 13: 4-10Crossref PubMed Scopus (117) Google Scholar, 20Mera R. Fontham E.T. Bravo L.E. et al.Long term follow up of patients treated for Helicobacter pylori infection.Gut. 2005; 54: 1536-1540Crossref PubMed Scopus (272) Google Scholar, 21You W.C. Brown L.M. Zhang L. et al.Randomized double-blind factorial of three treatments to reduce the precancerous gastric lesion.J Natl Cancer Inst. 2006; 98: 974-983Crossref PubMed Scopus (359) Google Scholar but other studies did not find any change.22Witteman E.M. Mravunac M. Becx M.J. et al.Improvement of gastric inflammation and resolution of epithelial damage one year after eradication of Helicobacter pylori.J Clin Pathol. 1995; 48: 250-256Crossref PubMed Scopus (93) Google Scholar, 23Forbes G.M. Warren J.R. Glaser M.E. et al.Long-term follow-up of gastric histology after Helicobacter pylori eradication.J Gastroenterol Hepatol. 1996; 11: 670-673Crossref PubMed Scopus (109) Google Scholar, 24van der Hulst R.W. van der Ende A. Dekker F.W. et al.Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study.Gastroenterology. 1997; 113: 25-30Abstract Full Text PDF PubMed Scopus (193) Google Scholar, 25Hibi K. Mitomi H. Koizumi W. et al.Enhanced cellular proliferation and p53 accumulation in gastric mucosa chronically infected with Helicobacter pylori.Am J Clin Pathol. 1997; 108: 26-34PubMed Google Scholar, 26Satoh K. Kimura K. Takimoto T. et al.A follow-up study of atrophic gastritis and intestinal metaplasia after eradication of Helicobacter pylori.Helicobacter. 1998; 3: 236-240PubMed Google Scholar, 27Tucci A. Poli L. Tosetti C. et al.Reversal of fundic atrophy after eradication of Helicobacter pylori.Am J Gastroenterol. 1998; 93: 1425-1431Crossref PubMed Scopus (105) Google Scholar, 28Tepes B. Kavcic B. Zaletel L.K. et al.Two- to four-year histological follow-up of gastric mucosa after Helicobacter pylori eradication.J Pathol. 1999; 188: 24-29Crossref PubMed Scopus (84) Google Scholar, 29El-Omar E.M. Oien K. Murray L.S. et al.Increased prevalence of precancerous changes in relatives of gastric cancer patients: critical role of H. pylori.Gastroenterology. 2000; 118: 22-30Abstract Full Text Full Text PDF PubMed Scopus (269) Google Scholar, 30Kim N. Lim S.H. Lee K.H. et al.Long-term effects of Helicobacter pylori eradication on intestinal metaplasia in patients with duodenal and benign gastric ulcers.Dig Dis Sci. 2000; 45: 1754-1762Crossref PubMed Scopus (33) Google Scholar, 31Kuipers E.J. Nelis G.F. Klinkenberg-Knol E.C. et al.Cure of Helicobacter pylori infection in patients with reflux oesophagitis treated with long term omeprazole reverses gastritis without exacerbation of reflux disease: results of a randomised controlled trial.Gut. 2004; 53: 12-20Crossref PubMed Scopus (187) Google Scholar, 32Tanaka A. Watari J. Tanabe H. et al.Effect of eradication of Helicobacter pylori on genetic instabilities in gastric intestinal metaplasia.Aliment Pharmacol Ther. 2006; 24: 194-202Google Scholar Some of the reasons for these discrepancies may be ethnic variations, completeness of eradication, stage of the disease when treatment was initiated, and the short follow-up period (in most studies the follow-up period did not exceed 1 year).17Kokkola A. Sipponen P. Rautelin H. et al.The effect of Helicobacter pylori eradication on the natural course of atrophic gastritis with dysplasia.Aliment Pharmacol Ther. 2002; 16: 515-520Crossref PubMed Scopus (104) Google Scholar, 23Forbes G.M. Warren J.R. Glaser M.E. et al.Long-term follow-up of gastric histology after Helicobacter pylori eradication.J Gastroenterol Hepatol. 1996; 11: 670-673Crossref PubMed Scopus (109) Google Scholar, 27Tucci A. Poli L. Tosetti C. et al.Reversal of fundic atrophy after eradication of Helicobacter pylori.Am J Gastroenterol. 1998; 93: 1425-1431Crossref PubMed Scopus (105) Google Scholar, 28Tepes B. Kavcic B. Zaletel L.K. et al.Two- to four-year histological follow-up of gastric mucosa after Helicobacter pylori eradication.J Pathol. 1999; 188: 24-29Crossref PubMed Scopus (84) Google Scholar, 30Kim N. Lim S.H. Lee K.H. et al.Long-term effects of Helicobacter pylori eradication on intestinal metaplasia in patients with duodenal and benign gastric ulcers.Dig Dis Sci. 2000; 45: 1754-1762Crossref PubMed Scopus (33) Google Scholar, 32Tanaka A. Watari J. Tanabe H. et al.Effect of eradication of Helicobacter pylori on genetic instabilities in gastric intestinal metaplasia.Aliment Pharmacol Ther. 2006; 24: 194-202Google ScholarTable 1Summary of Studies on Changes of GIM Scores After Successful H pylori EradicationStudyMaterialsFollow-up periodImprovement Genta et al12Genta R.M. Lew GM Graham D.Y. Changes in the gastric mucosa following eradication of Helicobacter pylori.Mod Pathol. 1993; 6: 281-289PubMed Google ScholarPeptic ulcer (n = 8) and others (n = 3)1 y Uemura et al13Uemura N. Mukai T. Okamoto S. et al.Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer.Cancer Epidemiol Biomarkers Prev. 1997; 6: 639-642PubMed Google ScholarGastric cancer (n = 65)6 mo Nardone et al14Nardone G. Staibano S. Rocco A. et al.Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.Gut. 1999; 44: 789-799Crossref PubMed Scopus (135) Google ScholarDyspepsia (n = 45)1 y Sung et al15Sung J.J. Lin S.R. Ching J.Y. et al.Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study.Gastroenterology. 2000; 119: 7-14Abstract Full Text Full Text PDF PubMed Scopus (324) Google ScholarVolunteer (n = 226)1 y Ohkusa et al16Ohkusa T. Fujiki K. Takashimizu I. et al.Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated.Ann Intern Med. 2001; 134: 380-386Crossref PubMed Scopus (198) Google ScholarDyspepsia (n = 115)12–15 mo Kokkola et al17Kokkola A. Sipponen P. Rautelin H. et al.The effect of Helicobacter pylori eradication on the natural course of atrophic gastritis with dysplasia.Aliment Pharmacol Ther. 2002; 16: 515-520Crossref PubMed Scopus (104) Google ScholarAtrophic corpus gastritis (n = 22)2.5 y Correa et al18Correa P. Fontham E.T.H. Bravo J.C. et al.Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-Helicobacter pylori therapy.J Natl Cancer Inst. 2000; 92: 1881-1888Crossref PubMed Scopus (602) Google ScholarVolunteer (n = 226)72 mo Ley et al19Ley C. Mohar A. Guarner J. et al.Helicobacter pylori eradication and gastric preneoplastic conditions: a randomized, double-blind, placebo-controlled trial.Cancer Epidemiol Biomarkers Prev. 2004; 13: 4-10Crossref PubMed Scopus (117) Google ScholarVolunteer (n = 248)1 y Mera et al20Mera R. Fontham E.T. Bravo L.E. et al.Long term follow up of patients treated for Helicobacter pylori infection.Gut. 2005; 54: 1536-1540Crossref PubMed Scopus (272) Google ScholarVolunteer (n = 394)12 y You et al21You W.C. Brown L.M. Zhang L. et al.Randomized double-blind factorial of three treatments to reduce the precancerous gastric lesion.J Natl Cancer Inst. 2006; 98: 974-983Crossref PubMed Scopus (359) Google ScholarVolunteer (n = 3365)7 yUnchanged Witteman et al22Witteman E.M. Mravunac M. Becx M.J. et al.Improvement of gastric inflammation and resolution of epithelial damage one year after eradication of Helicobacter pylori.J Clin Pathol. 1995; 48: 250-256Crossref PubMed Scopus (93) Google ScholarDyspepsia (n = 23)1 y Forbes et al23Forbes G.M. Warren J.R. Glaser M.E. et al.Long-term follow-up of gastric histology after Helicobacter pylori eradication.J Gastroenterol Hepatol. 1996; 11: 670-673Crossref PubMed Scopus (109) Google ScholarDuodenal ulcer (n = 32)85 mo van der Hulst et al24van der Hulst R.W. van der Ende A. Dekker F.W. et al.Effect of Helicobacter pylori eradication on gastritis in relation to cagA: a prospective 1-year follow-up study.Gastroenterology. 1997; 113: 25-30Abstract Full Text PDF PubMed Scopus (193) Google ScholarDyspepsia and peptic ulcer (n = 106)1 y Hibi et al25Hibi K. Mitomi H. Koizumi W. et al.Enhanced cellular proliferation and p53 accumulation in gastric mucosa chronically infected with Helicobacter pylori.Am J Clin Pathol. 1997; 108: 26-34PubMed Google ScholarGastric ulcer (n = 16)6 moDuodenal ulcer (n = 9) Satoh et al26Satoh K. Kimura K. Takimoto T. et al.A follow-up study of atrophic gastritis and intestinal metaplasia after eradication of Helicobacter pylori.Helicobacter. 1998; 3: 236-240PubMed Google ScholarAtrophic gastritis (n = 20)12–33 mo Tucci et al27Tucci A. Poli L. Tosetti C. et al.Reversal of fundic atrophy after eradication of Helicobacter pylori.Am J Gastroenterol. 1998; 93: 1425-1431Crossref PubMed Scopus (105) Google ScholarFundic atrophic gastritis (n = 20)3 y Tepes et al28Tepes B. Kavcic B. Zaletel L.K. et al.Two- to four-year histological follow-up of gastric mucosa after Helicobacter pylori eradication.J Pathol. 1999; 188: 24-29Crossref PubMed Scopus (84) Google ScholarDuodenal ulcer (n = 63)4 y El-Omar et al29El-Omar E.M. Oien K. Murray L.S. et al.Increased prevalence of precancerous changes in relatives of gastric cancer patients: critical role of H. pylori.Gastroenterology. 2000; 118: 22-30Abstract Full Text Full Text PDF PubMed Scopus (269) Google ScholarCancer patients’ relatives (n = 40)1 y Kim et al30Kim N. Lim S.H. Lee K.H. et al.Long-term effects of Helicobacter pylori eradication on intestinal metaplasia in patients with duodenal and benign gastric ulcers.Dig Dis Sci. 2000; 45: 1754-1762Crossref PubMed Scopus (33) Google ScholarGastric ulcer (n = 41)2 yDuodenal ulcer (n = 72) Kuipers et al31Kuipers E.J. Nelis G.F. Klinkenberg-Knol E.C. et al.Cure of Helicobacter pylori infection in patients with reflux oesophagitis treated with long term omeprazole reverses gastritis without exacerbation of reflux disease: results of a randomised controlled trial.Gut. 2004; 53: 12-20Crossref PubMed Scopus (187) Google ScholarReflux esophagitis (n = 231)2 y Tanaka et al32Tanaka A. Watari J. Tanabe H. et al.Effect of eradication of Helicobacter pylori on genetic instabilities in gastric intestinal metaplasia.Aliment Pharmacol Ther. 2006; 24: 194-202Google ScholarAtrophic gastritis (n = 39)1 y Open table in a new tab We developed a monoclonal antibody (mAb), Das-1 (formerly known as 7E12H12, immunoglobulin [Ig]M isotype), that specifically reacts with colonic epithelium33Das K.M. Sakamaki S. Vecchi M. et al.The production and characterization of monoclonal antibodies to a human colonic antigen associated with ulcerative colitis: cellular localization of the antigen by using the monoclonal antibody.J Immunol. 1987; 139: 77-84PubMed Google Scholar (both goblet and nongoblet absorptive cells), but not with enterocytes (including goblet cells) from jejunum or ileum and normal epithelium from the stomach and esophagus.33Das K.M. Sakamaki S. Vecchi M. et al.The production and characterization of monoclonal antibodies to a human colonic antigen associated with ulcerative colitis: cellular localization of the antigen by using the monoclonal antibody.J Immunol. 1987; 139: 77-84PubMed Google Scholar, 34Halstensen T.S. Das K.M. Brandtzaeg P. Epithelial deposits of immunoglobulin G1 and activated complement colocalise with the M(r) 40 kD putative autoantigen in ulcerative colitis.Gut. 1993; 34: 650-657Crossref PubMed Scopus (108) Google Scholar However, mAb Das-1 reacts sensitively (95%) and specifically (100%) to Barrett’s epithelium, a preneoplastic condition of the esophagus, and adenocarcinoma of the esophagus.35Das K.M. Prasad I. Garla S. et al.Detection of a shared colon epithelial epitope on Barrett epithelium by a novel monoclonal antibody.Ann Intern Med. 1994; 120: 753-756Crossref PubMed Scopus (82) Google Scholar, 36Griffel L.H. Amenta P.S. Das K.M. Use of a novel monoclonal antibody in diagnosis of Barrett’s esophagus.Dig Dis Sci. 2000; 45: 40-48Crossref PubMed Scopus (38) Google Scholar These data support that Barrett’s epithelium is a colonic or incomplete type of intestinal metaplasia.35Das K.M. Prasad I. Garla S. et al.Detection of a shared colon epithelial epitope on Barrett epithelium by a novel monoclonal antibody.Ann Intern Med. 1994; 120: 753-756Crossref PubMed Scopus (82) Google Scholar Although normal small-intestinal epithelium does not react with mAb Das-1, small-intestinal adenoma and adenocarcinoma strongly react with the antibody, suggesting a phenotypic change in the precancerous state and in carcinoma.37Onuma E.K. Amenta P.S. Jukkola A.F. et al.A phenotypic change of small intestinal epithelium to that of colonocytes in small intestinal adenomas and adenocarcinomas.Am J Gastroenterol. 2001; 96: 2480-2485Crossref PubMed Google Scholar We also reported that GIM of colonic phenotype, such as type II or III (incomplete type) detected by the mucin histochemistry38Filipe M.I. Jass J.R. Intestinal metaplasia subtypes and cancer risk.in: Filipe M.I. Jass J.R. Gastric carcinoma. Churchill Livingstone, Edinburgh1986: 212-236Google Scholar and detected by mAb Das-1, is associated strongly with gastric cancer.39Mirza Z.K. Das K.K. Slate J. et al.Gastric intestinal metaplasia as detected by a novel biomarker is highly associated with gastric adenocarcinoma.Gut. 2003; 52: 807-812Crossref PubMed Scopus (37) Google Scholar Ninety-three percent of GIM as well as gastric cancer from the same patients at a field away from the cancer area reacted with mAb Das-1, whereas GIM from patients without gastric cancer reacted less frequently (35%) with the antibody (P < .0001).39Mirza Z.K. Das K.K. Slate J. et al.Gastric intestinal metaplasia as detected by a novel biomarker is highly associated with gastric adenocarcinoma.Gut. 2003; 52: 807-812Crossref PubMed Scopus (37) Google ScholarMore recently, during screening a complementary DNA library prepared from a human colon cancer cell line, T84, we isolated and cloned a novel human tropomyosin (hTM) isoform, termed TC22.40Lin J.L. Geng X. Bhattacharya S.D. et al.Isolation and sequencing of a novel tropomyosin isoform preferentially associated with colon cancer.Gastroenterology. 2002; 123: 152-162Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar The amino acid sequence analysis of TC22 showed that it is identical to normal colon epithelial tropomyosin isoform 5 (hTM5), except the C-terminal peptide amino acids 222–247. By using this C terminal peptide, we developed an mAb, termed TC22-4.40Lin J.L. Geng X. Bhattacharya S.D. et al.Isolation and sequencing of a novel tropomyosin isoform preferentially associated with colon cancer.Gastroenterology. 2002; 123: 152-162Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar The expression of TC22, identified by the TC22-4 mAb, progressively increased in benign adenomatous polyps of colon (35%), in polyps with mild (57%) and severe dysplasia (100%), and in colon cancer (100%).40Lin J.L. Geng X. Bhattacharya S.D. et al.Isolation and sequencing of a novel tropomyosin isoform preferentially associated with colon cancer.Gastroenterology. 2002; 123: 152-162Abstract Full Text Full Text PDF PubMed Scopus (36) Google Scholar hTMs are microfilament-associated proteins present in all eukaryotic cells with organ-specific isoforms and distinct functions,41Lees-Miller J.P. Helfman D.M. The molecular basis for tropomyosin isoform diversity.Bioessays. 1991; 13: 429-437Crossref PubMed Scopus (296) Google Scholar, 42Pittenger M.F. Helfman D.M. In vitro and in vivo characterization of four fibroblast tropomyosins produced in bacteria: TM-2, TM-3, TM-5a, and TM-5b are co-localized in interphase fibroblasts.J Cell Biol. 1992; 118: 841-858Crossref PubMed Scopus (64) Google Scholar, 43Lin J.J. Warren K.S. Wamboldt D.D. et al.Tropomyosin isoforms in nonmuscle cells.Int Rev Cytol. 1997; 170: 1-38Crossref PubMed Google Scholar and at least 8 isoforms of hTM are detected in human beings.43Lin J.J. Warren K.S. Wamboldt D.D. et al.Tropomyosin isoforms in nonmuscle cells.Int Rev Cytol. 1997; 170: 1-38Crossref PubMed Google Scholar, 44Novy R.E. Lin J.L. Lin C.S. et al.Human fibroblast tropomyosin isoforms: characterization of cDNA clones and analysis of tropomyosin isoform expression in human tissues and in normal and transformed cells.Cell Motil Cytoskeleton. 1993; 25: 267-281Crossref PubMed Scopus (52) Google Scholar hTM5 is the predominant isoform in normal colon epithelium and it acts as an autoantigen in ulcerative colitis.45Das K.M. Dasgupta A. Mandal A. et al.Autoimmunity to cytoskeletal protein tropomyosin: a clue to the pathogenetic mechanism for ulcerative colitis.J Immunol. 1993; 150: 2487-2493PubMed Google Scholar, 46Geng X. Biancone L. Dai H.H. et al.Tropomyosin isoforms in intestinal mucosa: production of autoantibodies to tropomyosin isoforms in ulcerative colitis.Gastroenterology. 1998; 114: 912-922Abstract Full Text Full Text PDF PubMed Scopus (114) Google Scholar, 47Onuma E.K. Amenta P.S. Ramaswamy K. et al.Autoimmunity in ulcerative colitis (UC): a predominant colonic mucosal B cell response against human tropomyosin isoform 5.Clin Exp Immunol. 2000; 121: 466-471Crossref PubMed Scopus (43) Google Scholar, 48Biancone L. Mandal A. Yang H. et al.Production of immunoglobulin G and G1 antibodies to cytoskeletal protein by lamina propria cells in ulcerative colitis.Gastroenterology. 1995; 109: 3-12Abstract Full Text PDF PubMed Scopus (58) Google Scholar, 49Sakamaki S. Takayanagi N. Yoshizaki N. et al.Autoantibodies against the specific epitope of human tropomyosin(s) detected by a peptide based enzyme immunoassay in sera of patients with ulcerative colitis show antibody dependent cell mediated cytotoxicity against HLA-DPw9 transfected L cells.Gut. 2000; 47: 236-241Crossref PubMed Scopus (35) Google Scholar, 50Taniguchi M. Geng X. Glazier K.D. et al.Cellular immune response against tropomyosin isoform 5 in ulcerative colitis.Clin Immunol. 2001; 101: 289-295Crossref PubMed Scopus (20) Google ScholarEpidemiologic studies have indicated that Asian countries have a high prevalence of H pylori infection, with a correspondingly high incidence of gastric cancer. The annual incidence of gastric cancer is very high in Japan.51Parkin D.M. Whelan S.L. Ferlay J. Cancer incidence in five countries. Vol. VII. International Agency for Research on Cancer, World Health Organization and International Association of Cancer Registries, Lyon1997Google Scholar In this study, we examined if the eradication of H pylori in the Japanese population affects the following: (1) subsequent histologic grade of GIM, (2) mAb Das-1 reactivity that identifies the colonic phenotype of GIM associated with gastric carcinogenesis, and (3) the expression of the novel TM isoform TC22 in GIM. p53 expression also was examined.Patients and MethodsIn this prospective study, gastric biopsy samples (from 288 endoscopic procedures) from 96 H pylori–positive Japanese patients at Asahikawa Medical College Hospital between October 1995 and October 2003 were obtained before introduction of therapy, and, subsequently, over a follow-up period of up to 4 years. To assess H pylori infection, biopsy specimens, 2 from each site, were taken from the greater curvature of the antrum and body of the stomach. Additional samples were taken from grossly abnormal areas. H pylori status was analyzed in each patient by 2 methods: Wartin–Starry staining and H pylori culture. A patient was regarded as positive for H pylori if at least 1 method was positive, and the patient received anti–H pylori therapy with lansoprazole (30 mg), amoxicillin (750 mg), and clarithromycin (400 mg), all taken twice daily for 1 or 2 weeks. All patients underwent upper endoscopy again after 2 to 3 months posttherapy to ensure successful eradication of H pylori, and then were followed up with yearly endoscopy, for up to 4 years (mean, 2.6 y; range, 1–4 y). At each endoscopy, successful eradication again was documented. Written informed consent was obtained and approved by the Ethics Committee of Asahikawa Medical College.Histology and Patient ClassificationGIM was defined as replacement of the gastric epithelium by intestinal-type epithelium, and was composed of 2 types: (1) absorptive enterocytes with brush border along with goblet cells, or (2) columnar cells with foamy cytoplasm but lacking brush border.11Filipe M.I. Munoz N. Matko I. et al.Intestinal metaplasia types and the risk of gastric cancer: a cohort study in Slovenia.Int J Cancer. 1994; 57: 324-329Crossref PubMed Scopus (389) Google ScholarIn this study, patients with chronic gastritis with gastric ulcers or gastroduodenal ulcers were included. Almost half of the patients (53.9%) had gastric ulcers and the remainder had both gastric as well as duodenal ulcers.8Take S. Mizuno M. Ishiki K. et al.The effect of eradicating Helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease.Am J Gastroenterol. 2005; 100: 1037-1042Crossref PubMed Scopus (187) Google Scholar The patients with duodenal ulcers only were excluded because most duodenal ulcers are categorized as antral-predominant gastritis7Uemura N. Okamoto S. Yamamoto S. et al.Helicobacter pylori infection and the development of gastric cancer.N Engl J Med. 2001; 345: 784-789Crossref PubMed Scopus (3612) Google Scholar or nonatrophic gastritis,20Mera R. Fontham E.T. Bravo L.E. et al.Long term follow up of patients treated for Helicobacter pylori infection.Gut. 2005; 54: 1536-1540Crossref" @default.
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