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1. Mader AM, Patrício FR, Rigueiro MP, Lourenço LG: [Analysis of clinicopathological, tumor cell proliferation and apoptosis parameters in adenocarcinoma of the gastric cardia]. Arq Gastroenterol; 2006 Jul-Sep;43(3):184-90
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  • [Title] [Analysis of clinicopathological, tumor cell proliferation and apoptosis parameters in adenocarcinoma of the gastric cardia].
  • [Transliterated title] Estudo clínico-patológico, da proliferação celular e da apoptose no adenocarcinoma gástrico da cárdia.
  • MATERIAL AND METHODS: Forty cases of adenocarcinoma of the cardia were studied between 1988 and 2001, with a minimum clinical follow-up of 3 years.
  • Patients were excluded if they had previous chemotherapy or radiotherapy treatment, presented early neoplasia, or died during the operations or for other reasons unrelated to cancer.
  • Gender; age, Laurén and Ming histological type, staging, and the presence or absence of intestinal metaplasia, epithelial dysplasia and Helicobacter pylori in the adjacent mucosa were analyzed.
  • For the survival analysis, cases with distant metastasis upon diagnosis were excluded.
  • There was predominance of the male gender (72.5%), diffuse histological type (55%) and infiltrative histological type (72.5%), and the more advanced stages (III and IV: 67.5%).
  • There was no association with intestinal metaplasia and/or H. pylori.
  • There was a positive correlation for intestinal histological type with PCNA and apoptotic indices, in 10 high power fields.
  • CONCLUSIONS: Adenocarcinoma of the cardia predominated in male adults of mean age 61 years, and the predominant type was diffuse in more advanced stages.
  • Survival in cases of adenocarcinoma of the cardia is still low.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Cardia / pathology. Cell Proliferation. Stomach Neoplasms / pathology

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  • (PMID = 17160232.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen
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2. Vats HS, Banerjee TK, Resnick J, Khan Q: Esophageal adenocarcinoma arising from Barrett's dysplasia: a case report of double occurrence and prolonged survival after chemotherapy. Clin Med Res; 2006 Sep;4(3):184-8
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  • [Title] Esophageal adenocarcinoma arising from Barrett's dysplasia: a case report of double occurrence and prolonged survival after chemotherapy.
  • A relatively young patient with chronic gastroesophageal reflux disease (GERD), obesity, smoking, and alcohol intake presented with widespread metastatic disease in lymph nodes, liver and lungs from a lower esophageal adenocarcinoma extending into the gastroesophageal junction associated with Barrett's mucosa and dysplasia.A complete response was achieved with six cycles of chemotherapy that sustained for more than 4 years without further recurrence.
  • Unfortunately, there was presence of esophageal metaplasia after complete response which eventually converted to low to high grade dysplasia and ultimately to a second primary localized lower esophageal adenocarcinoma that was treated with thoracoabdominal esophagectomy and lymphadenectomy.
  • The pathogenesis of a recent increase in the incidence of GERD, Barrett's esophagus and lower esophageal adenocarcinoma are discussed.
  • Surgery, radiotherapy and combination chemotherapy are effective in the early stages leading to tumor shrinkage and prolongation of life and even cure in some cases.
  • Lower esophageal adenocarcinoma is frequently associated with Barrett's high-grade dysplasia.
  • Since there has been a dramatic increase in the incidence of Barrett's dysplasia, appropriate surveillance with upper gastrointestinal endoscopy and preventive strategies, such as the use of aspirin, cyclo-oxygenase II inhibitors and other nonsteroidal antiinflammatory drugs known to be chemopreventive agents against colon, esophagus, gastric and bladder cancers, need to be studied.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Gastroesophageal Reflux / complications. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / pathology. Time Factors

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  • [Cites] Ann Surg Oncol. 2004 Jul;11(7):641-3 [15197008.001]
  • [Cites] J Gastroenterol Hepatol. 2004 Jan;19(1):4-12 [14675236.001]
  • [Cites] J Natl Cancer Inst. 1995 Jan 18;87(2):104-9 [7707381.001]
  • [Cites] N Engl J Med. 1996 Aug 15;335(7):462-7 [8672151.001]
  • [Cites] Am J Gastroenterol. 1998 Apr;93(4):536-41 [9576444.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1826-34 [9586897.001]
  • [Cites] Cancer. 1998 Nov 15;83(10):2049-53 [9827707.001]
  • [Cites] N Engl J Med. 1998 Dec 31;339(27):1979-84 [9869669.001]
  • [Cites] Gut. 1998 Sep;43(3):327-33 [9863476.001]
  • [Cites] JAMA. 1999 May 5;281(17):1623-7 [10235156.001]
  • [Cites] Eur J Cancer. 2005 Mar;41(5):664-72 [15763640.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1554-66 [15887151.001]
  • [Cites] Clin Gastroenterol Hepatol. 2005 Jun;3(6):529-37 [15952094.001]
  • [Cites] CA Cancer J Clin. 2005 Nov-Dec;55(6):334-51 [16282279.001]
  • [Cites] Oncologist. 2004;9(2):147-59 [15047919.001]
  • [Cites] Am J Gastroenterol. 2001 May;96(5):1355-62 [11374668.001]
  • [Cites] Am J Med. 2001 Jul;111(1):33-7 [11448658.001]
  • [Cites] Aliment Pharmacol Ther. 2001 Aug;15(8):1087-100 [11472311.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1167-74 [11870157.001]
  • [Cites] Ann Surg. 2002 Sep;236(3):376-84; discussion 384-5 [12192324.001]
  • [Cites] Surgery. 2003 Jan;133(1):24-31 [12563234.001]
  • [Cites] Cancer Treat Rev. 2003 Dec;29(6):525-32 [14585262.001]
  • [Cites] N Engl J Med. 1992 Jun 11;326(24):1593-8 [1584260.001]
  • (PMID = 16988098.001).
  • [ISSN] 1539-4182
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC1570486
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3. Leung WK, Ng EK, Chan FK, Chan WY, Chan KF, Auyeung AC, Lam CC, Lau JY, Sung JJ: Effects of long-term rofecoxib on gastric intestinal metaplasia: results of a randomized controlled trial. Clin Cancer Res; 2006 Aug 1;12(15):4766-72
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  • [Title] Effects of long-term rofecoxib on gastric intestinal metaplasia: results of a randomized controlled trial.
  • PURPOSE: Gastric cancer and its premalignant gastric lesion, intestinal metaplasia (IM), frequently express cyclooxygenase-2 (COX-2) at high levels.
  • We tested whether long-term use of specific COX-2 inhibitors regress gastric IM.
  • Patients on rofecoxib (19.1%) and on placebo (16.1%) had no IM detected in the stomach (P = 0.59).
  • There was also no significant difference in the severity of IM between the two treatment groups (P >or= 0.3).
  • CONCLUSIONS: There was no trend to suggest that treatment with rofecoxib for 2 years resulted in the regression of gastric IM.
  • Although our findings cast doubt on the reversibility of gastric IM by COX-2 inhibitor, further studies are needed to establish the role of COX-2 inhibitors in different stages of gastric carcinogenesis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Gastrointestinal Neoplasms / drug therapy. Lactones / administration & dosage. Metaplasia / drug therapy. Sulfones / administration & dosage
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Double-Blind Method. Drug Administration Schedule. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Placebos. Prospective Studies. Treatment Outcome

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  • (PMID = 16899628.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lactones; 0 / Placebos; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib
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4. Stepanov EA, Razumovskiĭ AIu, Bataev S-, Alkhasov AB, Nurik VI, Mart'ianov AV, Bogaeva II: [Treatment policy for children with gastroesophageal reflux complicated by Barrett esophagus]. Khirurgiia (Mosk); 2002;(11):8-13
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  • [Title] [Treatment policy for children with gastroesophageal reflux complicated by Barrett esophagus].
  • Twenty-four-hour pH-metry and manometry of the esophagus, scintigraphy and contrast roentgenoscopy of the esophagus were used for diagnosis of GER.
  • All the children underwent biopsy of mucosa membrane of distal esophagus.
  • Metaplasia of esophageal epithelium by intestinal type (IT) in combination with one by gastric type (GT) were revealed in 8 children, metaplasia by gastric type alone (epithelium of gastric and fundal parts of the stomach)--in 8 children.
  • Six children with IT metaplasia of the esophagus with long strictures underwent extirpation of the esophagus with one-stage esophagoplasty.
  • It esophageal stenosis is not long or is absent, fundoplication by Nissen (4 children) and drug therapy (6 children) are performed.
  • It is concluded that in IT metaplasia of the esophagus with long peptic esophageal strictures resistant to bouginage extirpation of the esophagus with one-stage coloesophagoplasty is desirable.
  • Other methods of treatment do not exclude probability of esophageal adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / etiology. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / therapy
  • [MeSH-minor] Adolescent. Biopsy. Child. Child, Preschool. Combined Modality Therapy / standards. Diet, Reducing. Drug Therapy, Combination. Esophagoplasty / methods. Esophagus / drug effects. Esophagus / pathology. Esophagus / physiopathology. Esophagus / surgery. Female. Humans. Infant. Male. Metaplasia. Supine Position / physiology


5. Keto Y, Ebata M, Okabe S: [Pharmacological study on the pathological changes of the gastric mucosa in Helicobacter pylori-infected Mongolian gerbils]. Nihon Yakurigaku Zasshi; 2001 Oct;118(4):259-68
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  • [Title] [Pharmacological study on the pathological changes of the gastric mucosa in Helicobacter pylori-infected Mongolian gerbils].
  • Helicobacter pylori (H. pylori) infection has been recognized to be a causal factor of gastritis, ulcers and gastric cancer in man.
  • Using Mongolian gerbils (M. gerbils), which are suitable for an H. pylori infection animal model, we examined 1) how H. pylori infection, indomethacin and their combination affects the healing of gastric ulcers and whether or not such factors provoke a relapse of healed acetic acid ulcers; and 2) whether or not eradication of the bacteria with drugs at specified times after infection prevents the development of mucosal changes, including gastric adenocarcinoma.
  • Indomethacin treatment showed a tendency to delay ulcer healing.
  • 2) Four or 8 months after H. pylori inoculation, eradication was performed by concurrent treatment with omeprazole + clarithromycin.
  • Immediately after treatment ended in both the 5 and 9 month groups, it was verified that H. pylori were completely eradicated.
  • Autopsy performed 18 months after H. pylori inoculation revealed gastric hyperplastic polyps with erosive lesions and ulcers that were grossly visible; and atrophic gastritis, intestinal metaplasia, carcinoids, and adenocarcinomas were histologically observed in the non-treated control group.
  • In contrast, intestinal metaplasia and mucosal atrophy was observed in animals eradicated after 8 months and autopsied after 18 months.
  • It was concluded that 1) H. pylori infection delayed the healing of preexisting gastric ulcers and resulted in the relapse of healed ulcers, yet indomethacin had little or no effect on ulcer healing or relapse; and 2) early eradication of H. pylori infection with drug therapy can prevent severe gastric mucosal changes, to include adenocarcinomas, in M gerbils.
  • [MeSH-major] Gastric Mucosa / pathology. Helicobacter Infections. Helicobacter pylori. Stomach Ulcer / microbiology
  • [MeSH-minor] Adenocarcinoma / microbiology. Adenocarcinoma / prevention & control. Animals. Anti-Bacterial Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Ulcer Agents / therapeutic use. Clarithromycin / therapeutic use. Disease Models, Animal. Gerbillinae. Indomethacin / adverse effects. Omeprazole / therapeutic use. Recurrence. Stomach Neoplasms / microbiology. Stomach Neoplasms / prevention & control

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  • (PMID = 11680169.001).
  • [ISSN] 0015-5691
  • [Journal-full-title] Nihon yakurigaku zasshi. Folia pharmacologica Japonica
  • [ISO-abbreviation] Nippon Yakurigaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anti-Ulcer Agents; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole; XXE1CET956 / Indomethacin
  • [Number-of-references] 60
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6. Keto Y, Ebata M, Okabe S: Gastric mucosal changes induced by long term infection with Helicobacter pylori in Mongolian gerbils: effects of bacteria eradication. J Physiol Paris; 2001 Jan-Dec;95(1-6):429-36
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  • [Title] Gastric mucosal changes induced by long term infection with Helicobacter pylori in Mongolian gerbils: effects of bacteria eradication.
  • Helicobacter pylori infection has been reported to induce various mucosal changes, including gastric adenocarcinoma, in Mongolian gerbils 62 weeks after inoculation.
  • Using Mongolian gerbils, this study examined whether or not eradication of the bacteria with drugs at specified times after infection prevents the development of mucosal changes.
  • Four or 8 months after H. pylori inoculation, eradication was performed by concurrent treatment with omeprazole+clarithromycin.
  • Immediately after treatment ended, in both the 5 and 9 month groups, it was verified that H. pylori was completely eradicated.
  • Autopsy performed 18 months after H. pylori inoculation revealed gastric hyperplastic polyps with erosive lesions and ulcers that were grossly visible in the non-treated control group.
  • In addition, atrophic gastritis, intestinal metaplasia, carcinoids, and adenocarcinomas were histologically observed in the animals.
  • In contrast, intestinal metaplasia and mucosal atrophy was observed in animals eradicated after 8 months and autopsied after 18 months.
  • It was concluded that early eradication of H. pylori infection with drug therapy can prevent severe gastric mucosal changes, to include adenocarcinomas, in Mongolian gerbils.
  • [MeSH-major] Gastric Mucosa / pathology. Helicobacter Infections / pathology. Helicobacter pylori
  • [MeSH-minor] Animals. Anti-Bacterial Agents / therapeutic use. Anti-Ulcer Agents / therapeutic use. Body Weight. Chronic Disease. Clarithromycin / therapeutic use. Gerbillinae. Male. Omeprazole / therapeutic use. Proton Pump Inhibitors. Time Factors

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  • (PMID = 11595471.001).
  • [ISSN] 0928-4257
  • [Journal-full-title] Journal of physiology, Paris
  • [ISO-abbreviation] J. Physiol. Paris
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
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7. Shiotani A, Uedo N, Iishi H, Tatsuta M, Ishiguro S, Nakae Y, Kamada T, Haruma K, Merchant JL: Re-expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia. Int J Cancer; 2007 Sep 15;121(6):1182-9
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  • [Title] Re-expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia.
  • Loss of Sonic Hedgehog (Shh) and aberrant CDX2 expression are early changes correlating with the presence of intestinal metaplasia that occur in the gastric mucosa prior to neoplastic transformation.
  • The aim of this study was to compare the improvement in corpus gastritis with Shh and CDX2 expression after H. pylori eradication between subjects at high risk for gastric cancer and controls.
  • Seventy patients with endoscopic resection for early gastric cancer and 30 controls were studied.
  • 1.6-13.5) and in the mucosa with incomplete intestinal metaplasia rather than in those without incomplete intestinal metaplasia (OR 7.6 95% C.I. 2.4-24.3).
  • Atrophy, expression of Shh and CDX2 at the corpus lesser curve significantly improved in mucosa without incomplete intestinal metaplasia (p < 0.01), but not in mucosa with incomplete intestinal metaplasia.
  • In conclusion, H. pylori eradication prior to development of incomplete intestinal metaplasia improves corpus gastritis and may prevent gastric cancer.
  • Pepsinogen I may be a useful marker in patients with a residual higher risk of gastric cancer after H. pylori eradication.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17520681.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK062041; United States / NIDDK NIH HHS / DK / R01 DK61410; United States / NIDDK NIH HHS / DK / R01 DK061410-04; United States / NIDDK NIH HHS / DK / DK061410-04; United States / NIDDK NIH HHS / DK / R01 DK061410
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents; 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / SHH protein, human; 804826J2HU / Amoxicillin; 9001-10-9 / Pepsinogen A; H1250JIK0A / Clarithromycin
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8. Tepes B: Can gastric cancer be prevented? J Physiol Pharmacol; 2009 Dec;60 Suppl 7:71-7
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  • [Title] Can gastric cancer be prevented?
  • Gastric adenocarcinoma is the fourth most common malignancy worldwide and is globally the second leading cause of cancer-related deaths each year.
  • Among the risk factors are genetic factors (genetic diffuse gastric cancer - E-cadherin mutation (CDH1), pro- and anti-inflammatory cytokine genes and innate immune response gene polymorphisms), environmental factors (infection with the bacterium Helicobacter pylori (H. pylori), Epstein-Barr virus, nutrition: nitroso compounds, salt and antioxidants intake) and other factors (pernicious anemia, gastric polyps, gastric surgery, reproductive hormones, smoking).
  • The bacterium H. pylori has been found to be the major carcinogen in gastric cancer development.
  • Approximately 65%-80% of non-cardia gastric adenocarcinoma is attributable to H. pylori infection.
  • One percent of patients infected with H. pylori will develop gastric cancer.
  • American and European guidelines on the management of H. pylori infection recommend H. pylori eradication in all patients with atrophy and/or intestinal metaplasia and in all first-degree relatives of gastric cancer patients.
  • In the Asian Pacific Gastric Cancer Consensus, it was suggested for the first time that it is time for population-based screening and treatment of H. pylori infection in regions with gastric cancer incidence above 20/100000 per year.
  • Population screen and treat of H. pylori infection should be recommended in regions with gastric cancer incidence above 20/100000 per year.
  • This can be a good approach in H. pylori infected patients before they develop premalignant gastric lesions.
  • In patients with intestinal metaplasia, atrophy or dysplasia, regular endoscopic and histological surveillance should be done.
  • [MeSH-major] Adenocarcinoma / prevention & control. Stomach Neoplasms / prevention & control
  • [MeSH-minor] Animals. Early Detection of Cancer. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter Infections / physiopathology. Helicobacter pylori. Humans. Mass Screening. Patient Education as Topic. Risk Factors. Stomach Diseases / physiopathology. Stomach Diseases / prevention & control. Stomach Diseases / therapy

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  • (PMID = 20388948.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 74
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9. Niki T, Matsumoto I, Nishisaki H, Inoue H, Hamano K, Maeda T, Okutani T, Hirohata S, Nakashima T, Yasutake K, Kawaguchi K, Sashikata T: [A case of advanced gastric adenocarcinoma with mild elevation of serum SCC that responded remarkably to adjuvant chemotherapy of ADM, CDDP, ETP and 5-FU (ACVF)]. Gan To Kagaku Ryoho; 2003 Jan;30(1):117-20
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  • [Title] [A case of advanced gastric adenocarcinoma with mild elevation of serum SCC that responded remarkably to adjuvant chemotherapy of ADM, CDDP, ETP and 5-FU (ACVF)].
  • Endoscopic examination and computed tomography (CT) revealed an advanced gastric cancer with multiple abdominal lymph node swellings.
  • Distal partial gastrectomy was performed but lymph node resection was not done, since it was not thought to be curative.
  • Adjuvant chemotherapy was performed for 4 courses with a regimen of ADM 20 mg/m2 day 1, CDDP 50 mg/m2 day 1, ETP 100 mg/day days 3-7, 5-FU 600 mg/m2 every other day on days 3-29.
  • After 3 courses of ACVF therapy, the patient's serum CEA and SCC level normalized and the lymph node metastases became undetectable by CT scan.
  • No severe side effects were observed at any time during the administration of these medications.
  • In this case, serum SCC level was elevated even though histologic examination did not reveal squamous cell carcinoma but poorly differentiated adenocarcinoma.
  • On immunohistochemical analysis, these tissues were stained diffusely with CEA, locally with AE1 + 3, and partially with PAS or Alcian blue.
  • We speculate that this tumor could have developed the potency of SCC secretions without structural change into squamous metaplasia.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antigens, Neoplasm / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Serpins. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Drug Combinations. Etoposide / administration & dosage. Fluorouracil / administration & dosage. Gastrectomy. Humans. Lymphatic Metastasis. Male. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Remission Induction. Tegafur / administration & dosage

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  • (PMID = 12557715.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Drug Combinations; 0 / Pyridines; 0 / Serpins; 0 / squamous cell carcinoma-related antigen; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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10. Lamarque D, Levy M, Chaumette MT, Roudot-Thoraval F, Cavicchi M, Auroux J, Courillon-Mallet A, Haioun C, Delchier JC: Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma. Am J Gastroenterol; 2006 Aug;101(8):1886-93
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  • [Title] Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma.
  • OBJECTIVES: Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported.
  • The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment.
  • METHODS: Forty-five patients (mean age 45 +/- 2.1 yr) with gastric MALT lymphoma, treated by Helicobacter pylori eradication, chemotherapy with per os single alkylating agents, or both treatments have been followed by gastroscopy with biopsies in antrum and corpus at least once a year.
  • Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment.
  • In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis.
  • RESULTS: At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia.
  • Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients.
  • Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up.
  • CONCLUSIONS: Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition.
  • [MeSH-major] Gastric Mucosa / pathology. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] Atrophy. Chi-Square Distribution. Disease Progression. Female. Gastroscopy. Helicobacter Infections / drug therapy. Helicobacter Infections / pathology. Helicobacter pylori. Humans. Male. Metaplasia. Middle Aged. Risk Factors

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  • (PMID = 16780555.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Xiao F, Crissey MA, Lynch JP, Kaestner KH, Silberg DG, Suh E: Intestinal metaplasia with a high salt diet induces epithelial proliferation and alters cell composition in the gastric mucosa of mice. Cancer Biol Ther; 2005 Jun;4(6):669-75
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  • [Title] Intestinal metaplasia with a high salt diet induces epithelial proliferation and alters cell composition in the gastric mucosa of mice.
  • Intestinal metaplasia of the gastric mucosa is an important component in the pathway to adenocarcinoma.
  • The mechanisms that induce the progression from intestinal metaplasia to cancer have not been elucidated.
  • High dietary salt has been known as one of the risk factors for gastric cancer development in humans.
  • Therefore, we investigated the role of high salt diet on gastric epithelial cell proliferation and differentiation, using our mouse model that ectopically expressed Cdx2 homeodomain transcription factor and induced an intestinal metaplastic phenotype in the gastric epithelia.
  • Sixty Cdx2 transgenic and sixty age-matched wild-type littermates were studied.
  • Fifty-percent Cdx2 transgenic and wild type mice were administered a high-salt diet and the other fifty-percent was fed a standard diet starting at 12 weeks after birth.
  • Cell types and cell kinetics were assessed by immunohistochemistry.
  • At 52 weeks, significant alterations in pathology were observed in the Cdx2 transgenic mice fed a high-salt diet, including elongation of gastric pits, reduction of the glandular zone in the gastric corpus, and deepening of glands in the antrum.
  • In the Cdx2 transgenic mice fed a high salt diet, the parietal and chief cells were significantly decreased in the gastric corpus.
  • A significant increase in cell proliferation and apoptosis in the corpus and antrum were observed in Cdx2 transgenic mice fed a high-salt diet as compared to wild-type littermates.
  • Taken together, these data implicate that intestinal metaplasia in concert with a high-salt diet induces epithelial proliferation, apoptosis, and alters cellular types in the gastric mucosa of mice.
  • Alteration in the composition of the gastric epithelium may play a role in influencing the microenvironment to engender susceptibility to carcinogens.
  • [MeSH-major] Gastric Mucosa / pathology. Intestine, Small / pathology. Sodium Chloride, Dietary / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Differentiation / drug effects. Cell Lineage. Cell Proliferation / drug effects. Homeodomain Proteins / physiology. Immunohistochemistry. Metaplasia. Mice. Mice, Transgenic. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / physiology

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  • (PMID = 15970710.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30-DK-50306; United States / NIDDK NIH HHS / DK / R01-DK46704; United States / NIDDK NIH HHS / DK / R01-DK59539
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Sodium Chloride, Dietary; 0 / Transcription Factors
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12. Tseng HH, Hsu PI, Chen HC, Lai KH, Lo GH, Lo CC, Chou NH, Mok KT, Chen IS, Chou NH, Yang HB, Liu L, Hsu PN: Compartment theory in Helicobacter pylori-associated gastric carcinogenesis. Anticancer Res; 2003 Jul-Aug;23(4):3223-9
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  • [Title] Compartment theory in Helicobacter pylori-associated gastric carcinogenesis.
  • BACKGROUND: The compartment theory has not been well investigated in gastric carcinogenesis.
  • This study was aimed at examining the compartment alterations through the Helicobacter pylori (H. pylori)-related chronic gastritis-intestinal metaplasia-carcinoma sequence, and investigating the long-term effect of bacterial eradication on the compartment changes.
  • PATIENTS AND METHODS: Gastric biopsy specimens were obtained from subjects with H. pylori-negative normal mucosa (N = 12), H. pylori-positive non-metaplastic gastritis (N = 42), H. pylori-positive intestinal metaplasia (N = 21) and intestinal-type adenocarcinoma (N = 20).
  • Additionally, 50 patients with H. pylori-positive gastritis were enrolled to investigate the long-term effect of bacterial eradication on the compartment changes of gastric epithelium.
  • RESULTS: The mean PCNA labeling indices (L.I.) of non-metaplastic gastritis, intestinal metaplasia and adenocarcinoma were significantly higher than that of normal mucosa (31.1, 49.2 and 40.7 vs. 21.4; p < 0.01, 0.001 and 0.001, respectively).
  • In patients with intestinal metaplasia, there was a full expansion (phase 1 change) of proliferating zone to the middle compartment of gastric pits (ratio of L.I. between middle and lower compartment = 1.00).
  • The proliferating cells were evenly distributed in adenocarcinoma (complete loss of compartmentalization).
  • Eradiation of H. pylori led to a reversion of compartment changes of gastric epithelium in patients with chronic gastritis.
  • CONCLUSION: H. pylori-related gastric carcinogenesis is a multistep process involving progressive alterations of proliferating activity as well as loss of compartmentalization.
  • Eradication of H. pylori reverses the changes in growth kinetics of gastric epithelium.
  • [MeSH-major] Adenocarcinoma / microbiology. Gastritis / microbiology. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter pylori. Stomach Neoplasms / microbiology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Aged. Cell Cycle / physiology. Cell Division / physiology. Chronic Disease. Disease Progression. Drug Therapy, Combination. Female. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Humans. Lansoprazole. Male. Metaplasia / microbiology. Metaplasia / pathology. Metronidazole / therapeutic use. Middle Aged. Omeprazole / analogs & derivatives. Omeprazole / therapeutic use. Tetracycline / therapeutic use

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  • (PMID = 12926056.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0K5C5T2QPG / Lansoprazole; 140QMO216E / Metronidazole; F8VB5M810T / Tetracycline; KG60484QX9 / Omeprazole
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13. Zivny J, Wang TC, Yantiss R, Kim KH, Houghton J: Role of therapy or monitoring in preventing progression to gastric cancer. J Clin Gastroenterol; 2003 May-Jun;36(5 Suppl):S50-60; discussion S61-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of therapy or monitoring in preventing progression to gastric cancer.
  • It is generally accepted that intestinal-type gastric adenocarcinoma arises through a multistep process originating with chronic gastritis, progressing through stages of atrophy, intestinal metaplasia, and dysplasia and finally invasive carcinoma.
  • Clinical studies have shown that the eradication of H. pylori can lead to resolution of chronic gastritis, and a few studies have suggested some improvement in gastric atrophy.
  • Intestinal metaplasia, however, does not appear to be as reversible.
  • Nevertheless, results of several intriguing studies of high-risk populations support the notion that eradication of H. pylori may decrease or delay progression to gastric carcinoma despite the inability to reverse all mucosal damage.
  • Currently, in the United States, there is no widely accepted screening program for H. pylori infection in asymptomatic individuals, and consensus regarding surveillance for gastric intestinal metaplasia or dysplasia is lacking.
  • The purpose of this report is to evaluate the available data regarding the epidemiology of H. pylori and associated carcinoma, discuss relevant human and animal data that address eradication strategies in the prevention of gastric carcinoma, and finally discuss current recommendations regarding screening programs aimed at high-risk populations.
  • [MeSH-major] Adenocarcinoma / prevention & control. Stomach Neoplasms / prevention & control
  • [MeSH-minor] Animals. Disease Progression. Gastritis, Atrophic / complications. Gastritis, Atrophic / pathology. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter Infections / pathology. Helicobacter pylori. Humans. Metaplasia / pathology. Monitoring, Physiologic. Risk Factors

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  • (PMID = 12702966.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 92
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14. Guarner J, Mohar A: [The association between Helicobacter pylori and gastric neoplasia. Epidemiologic evidence]. Rev Gastroenterol Mex; 2000 Oct-Dec;65(4 Suppl 2):20-4
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  • [Title] [The association between Helicobacter pylori and gastric neoplasia. Epidemiologic evidence].
  • Helicobacter pylori (HP) causes chronic gastritis and, together with non-steroidal anti-inflammatory drugs, is considered the most frequent etiologic agent of peptic ulcer.
  • Since there are numerous epidemiologic and pathogenesis studies that demonstrate an association between infection by HP and gastric neoplasias, the World Health Organization declared, in 1994, HP infection a Group 1 carcinogen (a definitive cause of human neoplasias, similar to tobacco).
  • This article reviews the epidemiological evidence supporting the association between HP infection and two gastric neoplasias: adenocarcinoma and B cell lymphoma associated to mucosas (MALT).
  • This article also presents preliminary results of a project performed in the mountainous region of Chiapas, Mexico, in which the decrease of precancerous gastric lesions were studied one year after treatment for HP infection.
  • [MeSH-major] Adenocarcinoma / epidemiology. Helicobacter Infections / epidemiology. Helicobacter pylori / pathogenicity. Lymphoma, B-Cell, Marginal Zone / epidemiology. Stomach Neoplasms / epidemiology
  • [MeSH-minor] Amoxicillin / therapeutic use. Clarithromycin / therapeutic use. Comorbidity. Double-Blind Method. Drug Therapy, Combination / therapeutic use. Enzyme Inhibitors / therapeutic use. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Gastritis, Atrophic / microbiology. Gastritis, Atrophic / pathology. Humans. Metaplasia. Mexico / epidemiology. Omeprazole / therapeutic use. Precancerous Conditions / epidemiology. Precancerous Conditions / etiology. Prospective Studies. Randomized Controlled Trials as Topic. Retrospective Studies. Stomach Ulcer / epidemiology. Stomach Ulcer / etiology. Stomach Ulcer / microbiology. Stomach Ulcer / prevention & control

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  • (PMID = 11464618.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
  • [Number-of-references] 43
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15. Brien TP, Farraye FA, Odze RD: Gastric dysplasia-like epithelial atypia associated with chemoradiotherapy for esophageal cancer: a clinicopathologic and immunohistochemical study of 15 cases. Mod Pathol; 2001 May;14(5):389-96
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  • [Title] Gastric dysplasia-like epithelial atypia associated with chemoradiotherapy for esophageal cancer: a clinicopathologic and immunohistochemical study of 15 cases.
  • Preoperative chemotherapy combined with radiotherapy (chemrad) is a common type of neoadjuvant treatment for esophageal adenocarcinoma or squamous cell carcinoma.
  • The purpose of this study was to describe the clinical, histologic, proliferative (MIB-1), and oncogenetic (p53) features of 15 patients with gastric dysplasia-like epithelial atypical changes associated with preoperative chemrad for esophageal cancer.
  • The findings were compared with 12 age- and sex-matched patients with known gastric dysplasia.
  • Cases with gastric dysplasia-like epithelial atypia were significantly associated with a flat gross appearance, a patchy distribution, foveolar and gland involvement, surface maturation, an open nuclear chromatin pattern with prominent nucleoli, retention of nuclear polarity, mitoses confined to the pits, lack of atypical mitoses, cytoplasmic hypereosinophila and/or vacuolization, a lack of association with intestinal metaplasia, and finally, irregular glandular microcystic change, in comparison to the dysplasia controls.
  • In summary, a number of histologic and immunohistochemical features may distinguish gastric dysplasia-like epithelial atypia associated with chemrad for esophageal cancer from true dysplasia.
  • Pathologists should be aware of this entity and its histologic and immunohistochemical features to avoid misinterpretation and prevent unnecessary treatment.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Antineoplastic Agents / adverse effects. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy. Neoadjuvant Therapy / adverse effects. Radiation Injuries
  • [MeSH-minor] Adult. Aged. Antigens, Nuclear. Epithelium / chemistry. Epithelium / drug effects. Epithelium / pathology. Epithelium / radiation effects. Female. Gastric Mucosa / chemistry. Gastric Mucosa / drug effects. Gastric Mucosa / pathology. Gastric Mucosa / radiation effects. Humans. Immunohistochemistry. Ki-67 Antigen. Male. Middle Aged. Nuclear Proteins / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 11353047.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Antineoplastic Agents; 0 / Ki-67 Antigen; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p53
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16. Piazuelo E, Cebrián C, Escartín A, Jiménez P, Soteras F, Ortego J, Lanas A: Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus. World J Gastroenterol; 2005 Dec 21;11(47):7436-43
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  • [Title] Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus.
  • AIM: To test whether antioxidant treatment could prevent the progression of Barrett's esophagus to adenocarcinoma.
  • METHODS: In a rat model of gastroduodenoesophageal reflux by esophagojejunal anastomosis with gastric preservation, groups of 6-10 rats were randomized to receive treatment with superoxide dismutase (SOD) or vehicle and followed up for 4 mo.
  • RESULTS: All rats undergoing esophagojejunostomy developed extensive esophageal mucosal ulceration and inflammation by mo 4.
  • The process was associated with a progressive presence of intestinal metaplasia beyond the anastomotic area (9% 1st mo and 50% 4th mo) (94% at the anastomotic level) and adenocarcinoma (11% 1st mo and 60% 4th mo).
  • Exogenous administration of SOD decreased mucosal superoxide levels, increased mucosal SOD levels and reduced the risk of developing intestinal metaplasia beyond the anastomotic area (odds ratio = 0.326; 95%CI: 0.108-0.981; P = 0.046), and esophageal adenocarcinoma (odds ratio = 0.243; 95%CI: 0.073-0.804; P = 0.021).
  • CONCLUSION: Superoxide dismutase prevents the progression of esophagitis to Barrett's esophagus and adenocarcinoma in this rat model of gastrointestinal reflux, supporting a role of antioxidants in the chemoprevention of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Free Radical Scavengers / pharmacology. Superoxide Dismutase / pharmacology

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  • (PMID = 16437713.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Free Radical Scavengers; EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ PMC4725177
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17. Raderer M, Püspök A, Stummvoll G, Längle F, Chott A: Early cancer of the stomach arising after successful treatment of gastric MALT lymphoma in patients with autoimmune disease. Scand J Gastroenterol; 2003 Mar;38(3):294-7
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  • [Title] Early cancer of the stomach arising after successful treatment of gastric MALT lymphoma in patients with autoimmune disease.
  • BACKGROUND: Extranodal marginal zone B-cell lymphoma of the mucosa associated lymphoid tissue (MALT lymphoma) arises in lymphoid tissue acquired through chronic antigenic stimulation as exemplified by Helicobacter pylori.
  • Secondary development of gastric cancer, however, is thought to be a rare event.
  • The detection of a signet ring cell carcinoma during follow-up endoscopy after successful therapy of MALT lymphoma in a patient with Sjögren's syndrome prompted us to analyse the frequency of subsequent gastric cancer in patients with underlying autoimmune disease (AD).
  • METHODS: Patients with early stage MALT lymphoma and an underlying AD were evaluated for the occurrence of a secondary gastric cancer during the course of follow-up.
  • Data analysed included the type of AD, stage of MALT lymphoma, H. pylori status, treatment for MALT lymphoma and response, follow-up, the presence of a secondary cancer, and time to development of cancer.
  • In all patients, histologic samples were reassessed for the extent of gastritis, presence of intestinal metaplasia or focal atrophy at the time of lymphoma diagnosis.
  • RESULTS: A total of eight patients with overt AD at the time of diagnosis of MALT lymphoma were identified.
  • All patients had early stage MALT lymphoma restricted to the mucosa and submucosa at the time of diagnosis, and the presence of H. pylori was found in all cases.
  • Two of these patients achieved complete remission (CR) of the lymphoma following H. pylori eradication, while six were judged unresponsive and underwent chemotherapy, resulting in CR in all cases.
  • One patient died from stroke while being in CR for 2 months following chemotherapy.
  • Two patients (25%) developed early cancer limited to the gastric mucosa while being in CR from lymphoma for 9 and 27 months, respectively, and underwent partial gastrectomy.
  • Final staging of gastric cancer revealed pT1pN0M0 in both cases.
  • In the remaining 4 patients, no evidence of lymphoma recurrence or a second malignancy has been found so far by regular follow-up every 3 months for a time-span between 52 and 63 months after initial diagnosis.
  • CONCLUSION: Patients with concurrent MALT lymphoma and an underlying autoimmune condition show not only an impaired response to H. pylori eradication but might also be at increased risk for the development of gastric cancer.
  • [MeSH-major] Autoimmune Diseases / therapy. Gastric Mucosa / pathology. Lymphoma, B-Cell, Marginal Zone / therapy. Stomach Neoplasms / therapy
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Aged. Antineoplastic Combined Chemotherapy Protocols. Austria. Biopsy. Carcinoma, Signet Ring Cell / diagnosis. Carcinoma, Signet Ring Cell / therapy. Endosonography. Female. Follow-Up Studies. Humans. Metaplasia. Middle Aged. Neoplasm Staging. Polymyalgia Rheumatica / diagnosis. Polymyalgia Rheumatica / therapy. Pyloric Antrum / pathology. Remission Induction. Severity of Illness Index. Sjogren's Syndrome / diagnosis. Sjogren's Syndrome / therapy. Time Factors. Treatment Outcome

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  • (PMID = 12737445.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Norway
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18. Rokkas T, Pistiolas D, Sechopoulos P, Robotis I, Margantinis G: The long-term impact of Helicobacter pylori eradication on gastric histology: a systematic review and meta-analysis. Helicobacter; 2007 Nov;12 Suppl 2:32-8
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  • [Title] The long-term impact of Helicobacter pylori eradication on gastric histology: a systematic review and meta-analysis.
  • BACKGROUND: Helicobacter pylori infection is a crucial factor in the multistep carcinogenic process of gastric cancer.
  • In this process the gastric mucosa evolves through the stages of acute gastritis, chronic gastritis, gastric atrophy (GA), and intestinal metaplasia (IM) before developing gastric adenocarcinoma.
  • AIMS: The main aim of this study was to systematically review the long-term effects of H. pylori eradication on gastric histology (i.e. effects on GA and IM for both antrum and corpus) by meta-analyzing all relevant studies.
  • [MeSH-major] Gastric Mucosa / pathology. Helicobacter Infections / drug therapy. Helicobacter Infections / pathology
  • [MeSH-minor] Atrophy. Humans. Metaplasia

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  • (PMID = 17991174.001).
  • [ISSN] 1083-4389
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Number-of-references] 32
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19. de Korwin JD: [Eradication of Helicobacter pylori. Is it necessary to eradicate Helicobacter pylori in gastric reflux?]. Presse Med; 2001 Sep 22;30(26):1313-20
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  • [Title] [Eradication of Helicobacter pylori. Is it necessary to eradicate Helicobacter pylori in gastric reflux?].
  • PYLORI: Epidemiological studies have not demonstrated an association between H. pylori infection and symptoms of gastroesophageal reflux, reflux esophagitis, or Barrett's esophagus with or without dysplasia or esophageal adenocarcinoma.
  • An inverse association is also observed between the severity of reflux complications and infection by strains of H. pylori expressing certain virulence markers (cogA) associated with the more severe gastric lesions.
  • The prevalence of gastroesophageal reflux-related disease has increased steadily for more than fifty years while the incidence of H. pylori infection has decreased in developed countries.
  • Pangastritis with significant lesions of the gastric body leading to a reversible decrease in the secretion of acid after H. pylori eradication might lower the risk of gastroesophageal reflux.
  • Antisecretion treatments reduce the quantity of gastric acid favoring H. pylori colonization of the fundic mucosa and possibly aggravating fundic gastritis.
  • The risk of progression from H. pylori gastritis to atrophy or intestinal metaplasia of the fundus under prolonged proton pump inhibitor treatment remains to be determined.
  • Eradication of H. pylori reduces the efficacy of antisecretory drugs according to poorly understood mechanisms.
  • [MeSH-major] Anti-Bacterial Agents. Anti-Ulcer Agents / therapeutic use. Drug Therapy, Combination / therapeutic use. Esophagitis, Peptic / drug therapy. Helicobacter Infections / drug therapy. Helicobacter pylori
  • [MeSH-minor] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control. Humans. Risk Factors. Treatment Outcome

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  • (PMID = 11603095.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents
  • [Number-of-references] 59
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20. Toller IM, Altmeyer M, Kohler E, Hottiger MO, Müller A: Inhibition of ADP ribosylation prevents and cures helicobacter-induced gastric preneoplasia. Cancer Res; 2010 Jul 15;70(14):5912-22
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  • [Title] Inhibition of ADP ribosylation prevents and cures helicobacter-induced gastric preneoplasia.
  • Gastric adenocarcinoma develops as a consequence of chronic inflammation of the stomach lining that is caused by persistent infection with the bacterium Helicobacter pylori.
  • Gastric carcinogenesis progresses through a sequence of preneoplastic lesions that manifest histologically as atrophic gastritis, intestinal metaplasia, and dysplasia.
  • We show here in several preclinical models of Helicobacter-induced atrophic gastritis, epithelial hyperplasia, and metaplasia that the inhibition of ADP ribosylation by the small-molecule inhibitor PJ34 not only prevents the formation of gastric cancer precursor lesions, but also efficiently reverses preexisting lesions.
  • PJ34 exerts its chemopreventive and therapeutic effects by impairing Helicobacter-specific T-cell priming and T(H)1 polarization in the gut-draining mesenteric lymph nodes.
  • The subsequent infiltration of pathogenic T cells into the gastric mucosa and the ensuing gastric T cell-driven immunopathology are prevented efficiently by PJ34.
  • The immunosuppressive and chemoprotective effects of PJ34 therefore result from impaired T-cell activation and T(H)1 polarization, and lead to the protection from preneoplastic gastric immunopathology.
  • In conclusion, ADP-ribosylating enzymes constitute novel targets for the treatment of Helicobacter-associated gastric lesions predisposing infected individuals to gastric cancer and may also hold promise for the treatment of other T cell-driven chronic inflammatory conditions and autoimmune pathologies.
  • [MeSH-major] Gastritis, Atrophic / drug therapy. Helicobacter Infections / drug therapy. Helicobacter pylori / growth & development. Phenanthrenes / pharmacology. Precancerous Conditions / drug therapy. Stomach Neoplasms / drug therapy

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  • [Copyright] (c)2010 AACR.
  • (PMID = 20634404.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / N-(oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide hydrochloride; 0 / Phenanthrenes; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 61D2G4IYVH / Adenosine Diphosphate; 82115-62-6 / Interferon-gamma
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21. Hao Z, Li X, Qiao T, Li S, Lv Y, Fan D: Downregulated expression of CIAPIN1 may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression. Cancer Biol Ther; 2009 Jun;8(11):1064-70
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  • [Title] Downregulated expression of CIAPIN1 may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression.
  • Our previous studies revealed that cytokine induced apoptosis inhibitor 1 (CIAPIN1), which was reported to be essential in mouse definitive hematopoiesis, was related to multidrug resistance in gastric cancer cells and that the distribution of CIAPIN1 in normal human tissues was similar to the distribution of Ras.
  • This study aimed to explore whether CIAPIN1 plays a role in gastric carcinogenesis.
  • Expression of CIAPIN1 in normal, inflammatory gastric mucosa, gastric precancerous lesions and gastric adenocarcinoma was detected by immunohistochemistry and western blotting and, influence of CIAPIN1 on the proliferation of gastric cancer cells was investigated by ectopic expression of CIAPIN1 and RNA interference (RNAi).
  • Our immunohistochemical results demonstrated that the expression of CIAPIN1 in gastric antral mucosa was progressively reduced along the sequence of normal/inflammatory gastric mucosa-atrophy-intestinal metaplasia-dysplasia-adenocarcinoma.
  • The downregulation of CIAPIN1 in cancerous tissues was further confirmed by western blotting.
  • No relationship between the expression level of CIAPIN1 and the clinicopathological parameters such as age, gender, differentiation, TNM stage and the existence of metastasis was found in gastric cancer patients.
  • In in vitro cellular experiments, ectopic expression of CIAPIN1 by cDNA transfection resulted in suppression of cell proliferation and inhibition of cell cycle progression while knockdown of CIAPIN1 with siRNA accelerated cell proliferation and promoted cell cycle progression in SGC7901 and MKN28 gastric cancer cells.
  • These results suggest that downregulated CIAPIN1 expression may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Intracellular Signaling Peptides and Proteins / genetics. RNA, Small Interfering / genetics. Stomach Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Blotting, Western. Cell Cycle / physiology. Cell Growth Processes / physiology. Cell Line, Tumor. Down-Regulation. Drug Resistance, Multiple. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Transfection

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  • (PMID = 19471113.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CIAPIN1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering
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22. Cai X, Carlson J, Stoicov C, Li H, Wang TC, Houghton J: Helicobacter felis eradication restores normal architecture and inhibits gastric cancer progression in C57BL/6 mice. Gastroenterology; 2005 Jun;128(7):1937-52
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  • [Title] Helicobacter felis eradication restores normal architecture and inhibits gastric cancer progression in C57BL/6 mice.
  • BACKGROUND & AIMS: The impact of Helicobacter eradication therapy on the progression or regression of gastric lesions is poorly defined.
  • This study examined the effects of eradication therapy on inflammation, atrophy, metaplasia, dysplasia, and cancer progression.
  • METHODS: C57BL/6 mice were infected with Helicobacter felis and received bacterial eradication therapy after 2, 6, or 12 months of infection.
  • The gastric mucosa was examined at early, mid, and late intervals after eradication and graded for histology, expression pattern of alpha-catenin and beta-catenin, and IQGAP1.
  • Progression to adenocarcinoma was prevented.
  • Infected mice developed antral adenocarcinoma and gastric outlet obstruction by 24 months.
  • Only 30% of the mice receiving bacterial eradication therapy at 12 months developed antral carcinoma.
  • Bacterial eradication at any time during the first year of infection prevented death due to gastric outlet obstruction.
  • The expression pattern of alpha-catenin, beta-catenin, and IQGAP1 varied with cell type and paralleled histologic changes.
  • CONCLUSIONS: Inflammation, metaplasia, and dysplasia are reversible with early eradication therapy; progression of dysplasia was arrested with eradication therapy given as late as 1 year and prevented gastric cancer-related deaths.
  • [MeSH-major] Adenocarcinoma / microbiology. Helicobacter Infections / drug therapy. Helicobacter felis / pathogenicity. Precancerous Conditions / microbiology. Stomach Neoplasms / microbiology
  • [MeSH-minor] Animals. Anti-Bacterial Agents / therapeutic use. Atrophy. Disease Models, Animal. Gastric Mucosa / immunology. Gastric Mucosa / pathology. Male. Mice. Mice, Inbred C57BL. Tetracycline / therapeutic use

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  • (PMID = 15940628.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K22 CA96485
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; F8VB5M810T / Tetracycline
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23. Hunt RH: Will eradication of Helicobacter pylori infection influence the risk of gastric cancer? Am J Med; 2004 Sep 6;117 Suppl 5A:86S-91S
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Will eradication of Helicobacter pylori infection influence the risk of gastric cancer?
  • Gastric adenocarcinoma is a disease of high mortality and poor prognosis that is second only to lung cancer as a leading cause of cancer-related deaths worldwide.
  • Although gastric cancer has a multifactorial etiology, infection with Helicobacter pylori is highly associated with its development.
  • New information on bacterial and host genetics and results of epidemiologic studies suggest that better identification of individuals at high risk for gastric malignancy may be possible.
  • Studies suggest that cure of H pylori infection may be associated with retardation of glandular atrophy and intestinal metaplasia but not reversal of dysplasia.
  • Theoretically, it is attractive to believe that eradication of H pylori infection might prevent gastric cancer; however, studies supporting this hypothesis are not yet available.
  • Public policy strategies for the identification of patients at risk for H pylori-related gastric malignancy are likely to be complex, but testing and treating for the infection earlier rather than later in life is anticipated to be the more beneficial approach.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anti-Bacterial Agents. Drug Therapy, Combination / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori / isolation & purification. Stomach Neoplasms / prevention & control
  • [MeSH-minor] Adult. Age Distribution. Aged. Comorbidity. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Randomized Controlled Trials as Topic. Risk Assessment. Sex Distribution. Treatment Outcome

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  • (PMID = 15478858.001).
  • [ISSN] 0002-9343
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents
  • [Number-of-references] 46
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24. Basseri B, Conklin JL, Mertens RB, Lo SK, Bellack GS, Shaye OA: Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature. Dis Esophagus; 2009;22(4):E1-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature.
  • The inlet patch is an area of heterotopic gastric mucosa most commonly located in the postcricoid portion of the esophagus at, or just below, the level of the upper esophageal sphincter.
  • Esophageal and supraesophageal symptoms are commonly associated with inlet patch, while esophageal adenocarcinoma rarely complicates it.
  • Laryngeal adenocarcinoma associated with inlet patch is not described in the literature.
  • A 33-year-old female with long-standing asthma and presumed gastroesophageal reflux developed laryngeal cancer at age 22 years that was treated with concomitant radiation and induction chemotherapy.
  • Biopsies showed columnar mucosa (predominantly gastric cardiac/fundic type) consistent with inlet patch, with focal intestinal metaplasia.

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  • (PMID = 19473208.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
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25. de Vries AC, Kuipers EJ, Rauws EA: Helicobacter pylori eradication and gastric cancer: when is the horse out of the barn? Am J Gastroenterol; 2009 Jun;104(6):1342-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Helicobacter pylori eradication and gastric cancer: when is the horse out of the barn?
  • Helicobacter pylori infection is a major risk factor for gastric cancer development.
  • Therefore, H. pylori eradication may be an important approach in the prevention of gastric cancer.
  • This report describes two patients who developed gastric cancer at, respectively, 4 and 14 years after H. pylori eradication therapy.
  • These patients were included in a study cohort of H. pylori-infected subjects who received anti-H. pylori therapy during the early years of development of H. pylori eradication therapy and underwent strict endoscopic follow-up for several years.
  • In both patients, gastric ulcer disease and premalignant gastric lesions, i.e., intestinal metaplasia at baseline and dysplasia during follow-up, were diagnosed before gastric cancer development.
  • These case reports demonstrate that H. pylori eradication does not prevent gastric cancer development in all infected patients after long-term follow-up.
  • In patients with premalignant gastric lesions, in particular in patients with a history of gastric ulcer disease, adequate endoscopic follow-up is essential for early detection of gastric neoplasia.
  • [MeSH-major] Adenocarcinoma / etiology. Anti-Bacterial Agents / therapeutic use. Gastric Mucosa / microbiology. Helicobacter Infections / drug therapy. Helicobacter pylori / isolation & purification. Stomach Neoplasms / etiology
  • [MeSH-minor] Adult. Biopsy. Endoscopy, Gastrointestinal. Fatal Outcome. Female. Follow-Up Studies. Gastrectomy. Humans. Male. Middle Aged. Time Factors

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  • [CommentIn] Am J Gastroenterol. 2009 Dec;104(12):3100; author reply 3101-2 [19956126.001]
  • [CommentIn] Am J Gastroenterol. 2009 Dec;104(12):3099; author reply 3101-2 [19956125.001]
  • [CommentIn] Am J Gastroenterol. 2009 Dec;104(12):3100-1; author reply 3101-2 [19956127.001]
  • (PMID = 19491846.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents
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26. Laine L, Ahnen D, McClain C, Solcia E, Walsh JH: Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitors. Aliment Pharmacol Ther; 2000 Jun;14(6):651-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors.
  • Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins.
  • Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions.
  • Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen.
  • However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g.
  • Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events.
  • [MeSH-major] Adenocarcinoma / chemically induced. Anti-Ulcer Agents / adverse effects. Carcinoid Tumor / chemically induced. Gastric Acid / metabolism. Proton Pump Inhibitors. Stomach Neoplasms / chemically induced
  • [MeSH-minor] Helicobacter Infections / complications. Humans. Malabsorption Syndromes / chemically induced. Risk Factors. Stomach Diseases / chemically induced. Stomach Ulcer / drug therapy

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  • [CommentIn] Aliment Pharmacol Ther. 2001 Jul;15(7):1085-6 [11421886.001]
  • [CommentIn] Aliment Pharmacol Ther. 2000 Nov;14(11):1537-8 [11069327.001]
  • [CommentIn] Aliment Pharmacol Ther. 2001 May;15(5):729-30 [11328270.001]
  • (PMID = 10848649.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors
  • [Number-of-references] 141
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27. Stein HJ, Feith M, Siewert JR: Cancer of the esophagogastric junction. Surg Oncol; 2000 Jul;9(1):35-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the Western world, there has been an alarming rise in the incidence and prevalence of adenocarcinoma arising at the esophagogastric junction during recent decades.
  • Epidemiological, clinical and pathological data support a sub-classification of adenocarcinomas arising in the vicinity of the esophagogastric junction (AEG) into adenocarcinoma of the distal esophagus (Type I), true carcinoma of the cardia (Type II) and subcardial carcinoma (Type III).
  • While most, if not all, adenocarcinomas of the distal esophagus arise from areas with specialized intestinal metaplasia, which develop as a consequence of chronic gastroesophageal reflux, the etiology and pathogenesis of true carcinoma of the gastric cardia and subcardial gastric cancer is not clear at present.
  • Although a subgroup of true carcinomas of the gastric cardia may also develop within short segments of intestinal metaplasia at the esophagogastric junction, a causal relation between these tumors and gastroesophageal reflux has been difficult to establish.
  • Irrespective of the etiology, a complete removal of the primary tumor and its lymphatic drainage has to be the primary goal of any surgical approach to adenocarcinoma of the esophagogastric junction.
  • Our experience in the management of more than 1000 such patients during the past 18 years suggests that an individualized therapeutic strategy oriented by tumor type and stage results in survival rates superior to those reported with a more indiscriminate approach.
  • This individualized strategy prescribes a transmediastinal esophagectomy with lymphadenectomy in the lower posterior mediastinum and along the celiac axis for Type I tumors, extended total gastrectomy with transhiatal resection of the distal esophagus and D2 lymphadenectomy for Type II and Type III tumors, a limited resection of the esophagogastric junction and distal esophagus with interposition of a pedicled jejunal segment for uT1N0 tumors, and neoadjuvant chemotherapy followed by resection for uT3/T4 tumors.
  • Extensive preoperative staging is essential to allow correct selection of the appropriate therapeutic strategy using this tailored approach.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / therapy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / therapy. Esophagogastric Junction. Stomach Neoplasms / diagnosis. Stomach Neoplasms / therapy
  • [MeSH-minor] Algorithms. Combined Modality Therapy. Decision Trees. Esophagectomy. Gastrectomy. Gastroesophageal Reflux / complications. Humans. Incidence. Lymph Node Excision. Neoplasm Staging. Preoperative Care. Prevalence. Splenectomy. Survival Analysis. Treatment Outcome

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  • (PMID = 11525305.001).
  • [ISSN] 0960-7404
  • [Journal-full-title] Surgical oncology
  • [ISO-abbreviation] Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 36
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28. Fitzgerald RC, Lascar R, Triadafilopoulos G: Review article: Barrett's oesophagus, dysplasia and pharmacologic acid suppression. Aliment Pharmacol Ther; 2001 Mar;15(3):269-76
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  • [Title] Review article: Barrett's oesophagus, dysplasia and pharmacologic acid suppression.
  • Barrett's oesophagus, a significant complication of gastro-oesophageal reflux disease (GERD), is the single most important risk factor for oesophageal adenocarcinoma.
  • The progression of Barrett's oesophagus from specialized intestinal metaplasia to dysplasia and finally invasive carcinoma is incompletely understood, but increased and disordered proliferation is a key cellular event.
  • In ex vivo organ culture experiments, cell proliferation is increased after exposure to short pulses of acid, whilst proliferation is reduced in Barrett's oesophagus specimens taken from patients with oesophageal acid exposure normalized by antisecretory therapy.
  • In clinical practice, proton pump inhibitors relieve symptoms and induce partial regression to squamous epithelium, but abnormal oesophageal acid exposure and the risk for dysplasia or adenocarcinoma persist in many patients.
  • [MeSH-major] Barrett Esophagus / drug therapy. Barrett Esophagus / pathology. Gastric Acid / physiology. Gastroesophageal Reflux / complications. Proton Pump Inhibitors
  • [MeSH-minor] Adenocarcinoma. Cell Division. Cell Transformation, Neoplastic. Disease Progression. Epithelium / drug effects. Epithelium / pathology. Esophageal Neoplasms / etiology. Humans. Risk Factors

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  • (PMID = 11207503.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors
  • [Number-of-references] 34
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29. Hahm KB, Kim DH, Lee KM, Lee JS, Surh YJ, Kim YB, Yoo BM, Kim JH, Joo HJ, Cho YK, Nam KT, Cho SW: Effect of long-term administration of rebamipide on Helicobacter pylori infection in mice. Aliment Pharmacol Ther; 2003 Jul;18 Suppl 1:24-38
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  • BACKGROUND: It has been suggested that chronic, persistent, uncontrolled inflammations in the stomach could provide the basic step for the beginning of carcinogenesis.
  • One of the potential clinical applications of rebamipide is the inhibition of the immunoinflammatory response in gastric mucosa imposed by Helicobacter pylori.
  • AIM: To determine the implications of long-term rebamipide treatment in H. pylori infection, we studied the underlying moleculo-pathological changes in gastric lesions in mice infected with H. pylori (SS1 strain), following this treatment.
  • Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels of IL-1beta, TNF-alpha, IFN-gamma and IL-10, mRNA transcripts of various mouse cytokines and chemokines, and NF-kappaB binding activities, and finally the presence of gastric adenocarcinoma were compared between an H. pylori infected group (HP), and an H. pylori infected group administered with long-term rebamipide-containing pellet diets (HPR).
  • RESULTS: Serum levels of IL-1beta, IFN-gamma and TNF-alpha, the gastric mucosal expression of ICAM-1, HCAM and MMP, and transcriptional regulation of NF-kappaB-DNA binding were all significantly decreased in the HPR group compared with the HP group.
  • In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not different in either group.
  • CONCLUSION: The long-term administration of rebamipide should be considered in the treatment of H. pylori since it demonstrated molecular and biological advantages like a lessening of gastric inflammation and a possible chemopreventive effect.
  • [MeSH-major] Alanine / analogs & derivatives. Alanine / therapeutic use. Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Quinolones / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cytokines / metabolism. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Gastritis / microbiology. Gastritis / pathology. Immunohistochemistry. Matrix Metalloproteinases / metabolism. Mice. Mice, Inbred C57BL. NF-kappa B / metabolism. Protein Binding. Proteins / metabolism. RNA, Messenger / metabolism

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  • (PMID = 12925138.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Cytokines; 0 / NF-kappa B; 0 / Proteins; 0 / Quinolones; 0 / RNA, Messenger; 111911-87-6 / rebamipide; EC 3.4.24.- / Matrix Metalloproteinases; OF5P57N2ZX / Alanine
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30. Jankowski J, Sharma P: Review article: approaches to Barrett's oesophagus treatment-the role of proton pump inhibitors and other interventions. Aliment Pharmacol Ther; 2004 Feb;19 Suppl 1:54-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review article: approaches to Barrett's oesophagus treatment-the role of proton pump inhibitors and other interventions.
  • In those who are identified, the management options include acid reduction therapies with proton pump inhibitors or anti-reflux surgery.
  • Endoscopic ablative therapies have also been attempted.
  • In addition to having inherent procedure-related risks with ablative therapies, these alternatives may be limited by high rates of failure, need for continued acid suppressive therapy, metaplasia persistence under otherwise normal appearing tissue, need for procedural expertise, and continued risk for adenocarcinoma development.
  • Therefore, a widely applicable chemoprevention strategy that cost-effectively reduces the rate of progression from oesophagitis to adenocarcinoma in high-risk patients and perhaps those at lower rates of risk is highly desirable.
  • The AspECT trial currently underway is seeking to determine the effects of high- and low-dose proton pump inhibitor therapy with and without low-dose aspirin as Barrett's oesophagus chemoprevention.
  • [MeSH-major] Barrett Esophagus / drug therapy. Proton Pump Inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / drug therapy. Esophagitis / complications. Gastric Mucosa. Gastroesophageal Reflux / surgery. Humans. Photochemotherapy / methods

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  • (PMID = 14725580.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors
  • [Number-of-references] 31
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31. Mörk H: [Acid reflux on the esophagus. What helps in acute reflux esophagitis, how to prevent a recurrence?]. MMW Fortschr Med; 2000 Apr 27;142(17):26-9

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  • Gastro-esophageal reflux disease--one of the most common diagnoses in gastroenterology--is characterized by its symptoms or mucosal lesions caused by the non-physiological exposure of the esophagus to gastric juice.
  • For its acute treatment, proton pump inhibitors are distinctly superior to histamine 2 receptor antagonists, and are the treatment of choice.
  • Since relapse is common, long-term treatment is often necessary.
  • While, in such cases, laparoscopic antireflux surgery offers an alternative, neither long-term data nor controlled studies comparing this approach with long-term medical treatment have been carried out.
  • A major complication of reflux disease is Barrett's metaplasia with its associated risk for adenocarcinoma development.
  • However, as endoscopic therapy bears risks and data on long-term efficacy are still lacking, the significance of thermal ablation has further to be evaluated in specialized centers.
  • [MeSH-major] Anti-Ulcer Agents / therapeutic use. Esophagitis, Peptic / drug therapy

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  • (PMID = 10879017.001).
  • [ISSN] 1438-3276
  • [Journal-full-title] MMW Fortschritte der Medizin
  • [ISO-abbreviation] MMW Fortschr Med
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors
  • [Number-of-references] 0
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32. Kandulski A, Selgrad M, Malfertheiner P: Helicobacter pylori infection: a clinical overview. Dig Liver Dis; 2008 Aug;40(8):619-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Helicobcater pylori colonizes the stomach of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases.
  • Colonization of the gastric mucosa with Helicobcater pylori results in the development of chronic gastritis in all infected individuals and in a subset of patients chronic gastritis progresses to complications (i.e. ulcer disease, gastric neoplasias, some distinct extragastric disorders).
  • Helicobcater pylori eradication for gastric cancer prevention has been suggested by preclinical research and clinical trials, showing even reversibility of precancerous lesions (atrophic gastritis and intestinal metaplasia) after Helicobcater pylori eradication.
  • [MeSH-major] Helicobacter Infections / diagnosis. Helicobacter Infections / microbiology. Helicobacter pylori
  • [MeSH-minor] Adenocarcinoma / microbiology. Adenocarcinoma / prevention & control. Anemia, Iron-Deficiency / microbiology. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Asthma / microbiology. Dyspepsia / microbiology. Gastroesophageal Reflux / microbiology. Humans. Hypersensitivity, Immediate / microbiology. Lymphoma, B-Cell, Marginal Zone / microbiology. Peptic Ulcer / chemically induced. Peptic Ulcer / diagnosis. Peptic Ulcer / drug therapy. Peptic Ulcer / microbiology. Purpura, Thrombocytopenic, Idiopathic / microbiology. Stomach Neoplasms / microbiology. Stomach Neoplasms / prevention & control

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  • (PMID = 18396114.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Number-of-references] 80
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33. Gisbert JP, Piqué JM: [Indications and consequences of Helicobacter pylori eradication on gastroesophageal reflux disease]. Med Clin (Barc); 2005 May 14;124(18):697-709
MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • On the other hand, most studies demonstrate that the presence of the infection in patients with GERD does not negatively affect the therapeutic efficacy of proton pump inhibitors (PPIs), and, in case of negatively influencing it, the effects are not clinically relevant and are easily controllable with standard antisecretory treatment.
  • Therefore, the decision to administer H. pylori eradication treatment to a patient should not be influenced by the concomitant presence of GERD.
  • Nevertheless, when the gastritis pattern is unknown before the antibiotic administration, the effect of H. pylori eradication on gastric acid secretion and the incidence of GERD is unpredictable.
  • In the exceptional cases in which H. pylori eradication could have negative effects on GERD, its clinical relevance will be limited, and reflux symptoms or endoscopic esophagitis will favourably respond to the standard PPI antisecretory treatment.
  • Therefore, again, when H. pylori eradication is indicated in a particular patient, the concomitant diagnosis of GERD should not change our attitude.
  • Finally, is has recently been recommended to eradicate H. pylori infection in those patients with GERD needing long-term treatment with PPI, as some studies have reported that these drugs induce, in presence of the organism, an atrophic gastritis, with the consequent risk of gastric cancer.
  • In any case, the appearance in the gastric mucosa of clinically relevant lesions, such as intestinal metaplasia, dysplasia or adenocarcinoma, in patients treated with PPI for several years, has not yet been demonstrated, although this could simply be a problem of time.
  • In the meantime, as it occurs with any controversial indication, the decision of the doctor facing a patient infected by H. pylori and needing maintenance therapy with PPIs should be assessed on a case by case basis.
  • [MeSH-major] Gastritis / drug therapy. Gastritis / microbiology. Gastroesophageal Reflux / drug therapy. Gastroesophageal Reflux / microbiology. Helicobacter Infections / drug therapy. Helicobacter pylori
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Drug Therapy, Combination. Gastritis, Atrophic. Gastrointestinal Agents / therapeutic use. Humans. Proton Pump Inhibitors

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  • (PMID = 15899166.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Gastrointestinal Agents; 0 / Proton Pump Inhibitors
  • [Number-of-references] 185
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34. Bretagne JF: [Could Helicobacter pylori treatment reduce stomach cancer risk?]. Gastroenterol Clin Biol; 2003 Mar;27(3 Pt 2):440-52
MedlinePlus Health Information. consumer health - Stomach Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Could Helicobacter pylori treatment reduce stomach cancer risk?].
  • Despite its dramatic decline in incidence in developed countries, gastric cancer is a major public health issue in the world.
  • Accumulating evidence for considering H. pylori as a causal factor for gastric cancer comes from recent epidemiologic studies, the advent of an animal model of gastric cancer and from new insights into the biological mechanisms for gastric carcinogenesis.
  • The stomach cancer risk for people infected with H. pylori is rather low, inferior to 1%.
  • The occurrence of gastric adenocarcinomas in patients after complete remission of gastric MALT lymphoma induced by H. pylori eradication suggests also the limits of the preventive strategy against gastric cancer.
  • Furthermore, the effectiveness of eradication to reverse precancerous gastric lesions such as severe atrophy and intestinal metaplasia is questionable.
  • By waiting for effective anti-H. pylori vaccine, public health measures such as dietary modification should be promoted to further decrease the gastric cancer incidence.
  • On the individual basis the specialist has a role in the diagnosis of gastric precancerous lesions by endoscopy and also in the prevention of gastric cancer by selecting indications for H. pylori therapy.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Helicobacter Infections / complications. Helicobacter Infections / drug therapy. Helicobacter pylori / pathogenicity. Lymphoma, B-Cell, Marginal Zone / etiology. Lymphoma, B-Cell, Marginal Zone / prevention & control. Stomach Neoplasms / etiology. Stomach Neoplasms / prevention & control
  • [MeSH-minor] Cell Transformation, Neoplastic. Diet. Endoscopy, Gastrointestinal. Epidemiologic Studies. Humans. Incidence. Precancerous Conditions / diagnosis. Public Health. Risk Factors

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  • (PMID = 12700501.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 143
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