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Molecular aspects of the endocrine tumors of the pancreas and the gastrointestinal tract
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Loss of heterozygosity at 18q21 region in gastric cancer involves a number of cancer-related genes and correlates with stage and histology, but lacks independent prognostic value
No full textSeveral studies support a role of 18q21 LOH, involving the DCC locus, in colorectal cancer progression; however, its contribution to the natural history of gastric cancer is less clear. Recently, a number of cancer-related genes have been mapped in the 18q21 region, either centromeric or telomeric to DCC. This study searched for 18q21 LOH in 161 gastric cancers representative of all tumour stages and main histological types. To this purpose, seven highly polymorphic markers were used flanking the 18q21 band and spanning the entire region. Thirty-four out of 147 (23.1%) informative cases showed LOH. In 27 of 34 cases (79%), LOH involved all the informative loci. The remaining seven cases showed LOH at more telomeric sites and retained heterozygosity at more centromeric markers, mostly those proximal to the DCC gene. A strong correlation between 18q21 LOH and level of gastric wall invasion, lymph node metastases, or stage was found in cohesive (glandular+solid) and mixed tumours, but not in diffuse cancers. Cox univariate and multivariate analysis showed that invasion level, lymph node metastases, distant metastases, TNM stage, and histology were effective predictors of survival, whereas 18q21 LOH did not show predictive power. The simultaneous deletion of a variety of cancer-related genes with different and even opposite roles might explain why, apparently, 18q21 LOH does not per se contribute significantly to the natural history of gastric cancer, despite strong correlation with stage
Intracellular, Intercellular, and Stromal Invasion of Gastric Mucosa, Preneoplastic Lesions, and Cancer by Helicobacter pylori
No full textBACKGROUND AND AIMS: It is not clear how Helicobacter pylori, an apparently extracellular pathogen colonizing the luminal side of the gastric epithelium, invariably causes an immune-inflammatory response on the stromal side of the mucosa. Penetration of H pylori into epithelial cell lines and its interaction with immune-inflammatory cells have been documented in vitro. Several investigations also showed in vivo bacterial penetration into the epithelium up to the lamina propria; however, the identification as H pylori of the bacteria-like bodies observed in unchanged, metaplastic, or neoplastic mucosa remained sometimes questionable.
METHODS: To search for bacteria-like organisms, we used transmission electron microscopy on endoscopic biopsy specimens from 20 dyspeptic subjects and surgical specimens of neoplastic and nonneoplastic mucosa from 20 cancerous stomachs. To ascertain the H pylori nature of the organisms found, we used 6 different antibodies directed against bacterial lysates, purified vacuolating cytotoxin A, or purified cytotoxin-associated antigen A in immunogold tests. The results were compared with those of H pylori strains cultivated in vitro.
RESULTS: In nonmetaplastic gastric epithelium, cytochemically proven H pylori were detected, in the majority of cases, inside cytoplasm of epithelial cells, in intraepithelial intercellular spaces, and in underlying lamina propria, often in direct contact with immune-inflammatory cells and sometimes inside small blood vessels. Cytochemically proven H pylori were also observed inside 6 of 8 intestinal metaplasias and 9 of 20 cancers.
CONCLUSIONS: H pylori penetrates normal, metaplastic, and neoplastic gastric epithelium in vivo, intracellularly, or interstitially to cause a strong immune-inflammatory response and promote gastric carcinogenesis
Loss of heterozygosity for chromosome 17p, p53 gene, and chromosome 18q, DCC gene, in aggressive endocrine tumors of the stomach
No full textTargeted ablation of secretin cells reveals a close developmental relationship with CCK and L cells
No full textLoss of heterozygosity at 18q21 region in gastric cancer involves a number of cancer-related genes and correlates with stage and histology, but lacks independent prognostic value
No full textSeveral studies support a role of 18q21 LOH, involving the DCC locus, in colorectal cancer progression; however, its contribution to the natural history of gastric cancer is less clear. Recently, a number of cancer-related genes have been mapped in the 18q21 region, either centromeric or telomeric to DCC. This study searched for 18q21 LOH in 161 gastric cancers representative of all tumour stages and main histological types. To this purpose, seven highly polymorphic markers were used flanking the 18q21 band and spanning the entire region. Thirty-four out of 147 (23.1%) informative cases showed LOH. In 27 of 34 cases (79%), LOH involved all the informative loci. The remaining seven cases showed LOH at more telomeric sites and retained heterozygosity at more centromeric markers, mostly those proximal to the DCC gene. A strong correlation between 18q21 LOH and level of gastric wall invasion, lymph node metastases, or stage was found in cohesive (glandular+solid) and mixed tumours, but not in diffuse cancers. Cox univariate and multivariate analysis showed that invasion level, lymph node metastases, distant metastases, TNM stage, and histology were effective predictors of survival, whereas 18q21 LOH did not show predictive power. The simultaneous deletion of a variety of cancer-related genes with different and even opposite roles might explain why, apparently, 18q21 LOH does not per se contribute significantly to the natural history of gastric cancer, despite strong correlation with stage
PYY-Tag transgenic mice displaying abnormal (H(+)-K(+)ATPase activity and gastric mucosal barrier impairment
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