Cases reported "Stomach Neoplasms"

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1/27. Endoscopic and histological reversibility of gastric adenoma after eradication of helicobacter pylori.

    Although epidemiological studies strongly suggest an association between helicobacter pylori infection and gastric carcinogenesis via a multistage process, a causal link between them has not been demonstrated. We evaluated the endoscopic and histological changes of gastric adenoma, which is considered a premalignant condition, after eradication of H. pylori. Thirty-five H. pylori-infected patients with gastric adenoma were treated with triple therapy (lansoprazole 30mg/day, clarithromycin 400mg/day, and amoxicillin 1500 mg/day) for 1 week. Of these 35 patients, 30 (86%) exhibited no H. pylori by culture or histology after the therapy. Of the 30 gastric adenomas, 7 decreased in size endoscopically; three gastric adenomas especially showed apparent remission, although histological cure in these three patients was not apparent. Our results suggest that removal of H. pylori infection may only mask a gastric adenoma endoscopically owing to the change around the gastric mucosa.
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ranking = 1
keywords = carcinogenesis
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2/27. Deletion 7p in gastric MALT lymphoma.

    Deletion of the long arm of chromosome 7 has been related to loss of tumor suppressor genes which may constitute a primary step of carcinogenesis in many kinds of malignancies, including low-grade B-cell lymphoma. However, deletion of the short arm of chromosome 7, del(7p), in low-grade B-cell lymphoma has not been reported. Here, we report a case of gastric MALT lymphoma with the chromosome aberration del(7p) which progressed in spite of eradication of Helicobactor pylori. Deletion 7p may represent a new karyotypic change that is possibly related to autonomous growth of MALT lymphoma.
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ranking = 1
keywords = carcinogenesis
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3/27. Multiple gastric carcinomas 21 years after gastrojejunostomy without gastrectomy. Report of a case.

    We report a case of gastric carcinoma after gastrojejunostomy (GJ-stomy) without gastrectomy. Multiple gastric carcinomas were discovered 21 years after GJ-stomy without gastrectomy which had been performed for treatment of pyloric stenosis due to severe gastric ulcer. Multiple gastric carcinomas were found in the stomach, or the esophagocardiac junction, and in the corpus and anastomotic lesion of the GJ-stomy. Under the light microscope, intestinal metaplasia was detected in the antral mucosa and the area around the anastomosis. In immunohistochemical analysis, p53-specific antibodies gave a positive reaction in every gastric carcinoma and in the noncancerous gastric glands around the carcinoma at the anastomosis and in the corpus. cells positive for immunostaining with Ki-67-specific antibodies were more numerous in all gastric carcinomas and in the area around the anastomotic lesion than in the normal gastric mucosa. Hsp70-specific antibodies reacted with cells in the noncancerous glands around the carcinoma in the anastomotic area. Mucosal injury and the potential for carcinogenesis due to exposure to gastroduodenal reflux are discussed. The results of this study suggest that similar cases with gastroduodenal reflux should be followed carefully.
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ranking = 1
keywords = carcinogenesis
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4/27. Chromosomal imbalances in gastric cancer. Correlation with histologic subtypes and tumor progression.

    DNA copy number changes were analyzed by comparative genomic hybridization (CGH) in 38 gastric carcinomas and correlated with tumor histologic type and progression. Gains of copy numbers were observed in all tumors, affecting all chromosomes except chromosome 16. The average number of copy number gains was 7 (range, 1-13), most frequently located on chromosomes 11, 12, 15, 17, and 20 in 45% to 97% of tumors. High-level amplifications were found on chromosomes 12, 15, 17, and 20; the latter was affected most frequently (66%). Loss of DNA copy numbers was detected in 14 tumors affecting 7 chromosomes. No statistically significant differences in the frequency and pattern of chromosomal imbalances were observed in tumor histologic type (Lauren classification) and grade of differentiation, as well as the prognostic parameters depth of invasion (pT) and lymph node involvement (pN). Our results indicate that in gastric cancer there is no specific recurrent pattern of DNA aberrations to be correlated with tumor histologic type or stage. However, CGH analysis could reveal new, recurrent genetic changes in gastric cancer affecting chromosomes sites that harbor genes known to participate in tumorigenesis and progression of several human malignant neoplasms.
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ranking = 0.58858692519554
keywords = tumorigenesis
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5/27. Altered expression of the fragile histidine triad gene in primary gastric adenocarcinomas.

    Genomic alterations and abnormal expression of the fragile histidine triad (FHIT) gene in gastric carcinomas were examined to determine whether the FHIT gene is actually a frequent target for alteration during gastric carcinogenesis. To correlate DNA and RNA lesions of the FHIT gene with the effect on FHIT protein expression, we have investigated the FHIT gene for loss of heterozygosity (LOH), aberrant transcripts, point mutations, and protein expression in 35 gastric adenocarcinomas. Allelic loss at D3S1300 was detected in 7 of 33 (21%) informative cases. Aberrant transcripts, with deletions and/or insertions, were observed in 20 of 35 (57.1%) cases and resulted from alternative splicing through exon skipping and/or insertion of the FHIT intron 5 sequence or activation of the cryptic splice site. Point mutations were not found in the FHIT coding region but detected in noncoding exon 2, 3, 4, or 5 of eight aberrant transcripts. Significant reduction of FHIT protein expression was observed in 22 of 35 (62.9%) cases. Aberrant FHIT transcription was shown to be associated with loss of FHIT protein expression. However, aberrant FHIT transcripts themselves were not associated with any clinicopathological parameters, such as age, sex, tumor site, or clinical stage. Moreover, there was no association between the presence of LOH at D3S1300 and the expression of aberrant FHIT transcripts. Nevertheless, high frequency of aberrant FHIT transcripts, significant rate of LOH at D3S1300, and altered expression of the FHIT protein indicate that alterations of the FHIT gene can play an important role in gastric carcinogenesis.
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ranking = 2
keywords = carcinogenesis
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6/27. Hemorrhagic gastric carcinoma in an acromegalic patient.

    A rare case of hemorrhagic gastric carcinoma in an acromegalic patient is reported. A 79-year-old Japanese man was referred to our hospital with diagnoses of upper gastrointestinal hemorrhage and angina pectoris. This patient showed typical clinical features of acromegaly, with increased serum growth hormone (GH) and insulin-like growth factor i (IGF-I) level. A high titer of serum anti-helicobacter pylori (H. pylori) IgG was also observed. After percutaneous transluminal coronary angioplasty treatment for stenosis of the right coronary artery, the patient underwent distal gastrectomy. Gastric cancer was Type 2 macroscopically and was diagnosed histologically as a papillary and well to moderately differentiated tubular adenocarcinoma. reverse transcription-polymerase chain reaction analysis estimated that the amount of IGF-I receptor mRNA expression in the gastric cancer tissue was 1.6 times higher than that in the adjacent atrophic mucosa, whereas the amount of IGF-I mRNA expression in the cancer tissue was only half that in the atrophic mucosa. Both the stimulatory effects of GH and/or IGF-I on cell proliferation and H. pylori infection in gastric tumorigenesis may have been responsible for the development and growth of gastric carcinoma in this patient.
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ranking = 0.58858692519554
keywords = tumorigenesis
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7/27. A novel germline mutation of hMLH1 in a patient with hereditary non-polyposis colorectal cancer.

    dna mismatch repair genes, hMLH1 and hMSH2, assigned on chromosome 3p21-23 and 2p21-22 are involved in hereditary non-polyposis colorectal cancer (HNPCC). The heterozygous carrier of the mutated allele results in a mutator phenotype and accelerating tumorigenesis, which especially causes carcinomas in the gastrointestinal and genitourinary tracts. We screened germline mutations of mismatch repair genes hMLH1 and hMSH2 in a patient with multiple primary neoplasms (multiple stomach cancers, colon cancer and brain tumor) in a cancer clustered HNPCC family. Screening by long RT-PCR from the RNA extracted from puromycin-treated heparinized blood showed skipping of the exon 2 in hMLH1. The analysis of the genomic DNA showed a GT deletion in the splice-donor site of the exon 2, which is compatible with the splicing variant detected by long RT-PCR analysis. This is a novel germline mutation that has not been reported previously.
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ranking = 0.58858692519554
keywords = tumorigenesis
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8/27. Different types of epithelial cadherin alterations play different roles in human carcinogenesis.

    Epithelial cadherin (E-cadherin) gene and protein alterations are implicated in the existence of two clearly distinct types of tumors in the stomach (isolated cell and glandular carcinomas), breast (lobular and ductal carcinomas), and thyroid (papillary and follicular carcinomas), as well as in the occurrence of poorly differentiated foci in colorectal and prostate adenocarcinomas. A thorough correlation between clinicopathologic features and molecular data, and the study of early lesions from familial cases provide clues for the understanding of the role played by E-cadherin in these settings.
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ranking = 4
keywords = carcinogenesis
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9/27. Familial gastric cancer.

    BACKGROUND: Familial aggregation of gastric cancer has pointed out to a possible hereditary and genetic factor involved in the carcinogenesis of this disease. The diffuse type gastric cancer patients are frequently younger and the tumor has locally infiltrative growth pattern early in its development. observation of families with frequent early onset gastric cancer has led to the identification of a novel gene implicated in gastric cancer susceptibility: CDH1/E-cadherin. Diffuse familiar gastric cancer is defined as any family presenting: two first-degree relatives with diffuse gastric cancer, one of them with age under 50 years or at least 3 first-degree relatives irrespective age of onset. CASE REPORT: The family reported by us does not fit in any of the classification proposed. The precise identification of these families by clinical and molecular tools is of great importance. The case reported is an example of a family that probably is a form of hereditary gastric cancer not yet fully understood. CONCLUSION: Soon there will be new criteria, possibly including genetic and molecular characteristics.
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ranking = 1
keywords = carcinogenesis
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10/27. Simultaneous EBV-positive lymphoepithelioma-like carcinoma and EBV-negative intestinal-type adenocarcinoma in a patient with helicobacter pylori-associated chronic gastritis.

    We report the case of a 72-year-old man with 2 simultaneous gastric carcinomas. The larger, ulcerated mass in the antrum was a conventional infiltrating intestinal-type adenocarcinoma. The associated antral-type mucosa showed moderate chronic gastritis, foci with complete and incomplete intestinal metaplasia, and mild to moderate helicobacter pylori infection. The second, smaller tumor was found within fundic-type mucosa and was a lymphoepithelioma-like carcinoma associated with Epstein-Barr virus (EBV) infection shown by the EBV-encoded small RNA (EBER) test. The EBER test result was negative in the intestinal type adenocarcinoma. To our knowledge, this is the first report of simultaneous gastric carcinomas with 2 different morphologic phenotypes, in which only one tumor was associated with EBV infection, while the second tumor was related to H pylori-associated chronic gastritis. Our report demonstrates 2 different but simultaneous etiologic pathways of gastric carcinogenesis in the same patient.
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ranking = 1
keywords = carcinogenesis
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