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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrophic gastritis with intestinal metaplasia cannot be regarded as a form of precancerous change, but it is of profound significance in the development of gastric carcinoma. It would be reasonable to infer that those subjects who have atrophic gastritis with intestinal metaplasia to any great extent represent a high-risk population for gastric cancer. Environmental factors, especially dietary habits, are implicated in the etiology of gastric carcinoma. Intake of high concentrations of sodium chloride is assumed to promote the development of carcinoma of the stomach. Cigarette smoking is also one of the risk factors in the pathogenesis of gastric cancer, supposedly acting as an initiator in gastric tumorigenesis. Although a controversy exists as to whether gastric resection for benign ulcers enhances the subsequent development of gastric carcinoma, it appears likely that an increased amount of long-term duodenogastric reflux after partial gastrectomy results in a higher incidence of carcinoma in the stomach remnant.
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PMID:[High-risk population of gastric cancer patients]. 363 68

Although many genetic alterations have been reported in gastric cancer, it is not known whether all gastric tumors are capable of indefinite proliferative potential, e.g., immortality. The expression of telomerase and stabilization of telomeres are concomitant with the attainment of immortality in tumor cells; thus, the measurement of telomerase activity in clinically obtained tumor samples may provide important information useful both as a diagnostic marker to detect immortal cancer cells in clinical materials and as a prognostic indicator of patient outcome. Telomerase activity was analyzed in 66 primary gastric cancers with the use of a PCR-based assay. The majority of tumors (85%) displayed telomerase activity, but telomerase was undetectable in 10 tumors (15%), 8 of which were early stage tumors. Most of the tumors with telomerase activity were large and of advanced stages, including metastases. Survival rate of patients of tumors with detectable telomerase activity was significantly shorter than that of those without telomerase activity. Alterations of telomere length (reduced/elongated terminal restriction fragments) were detected in 14 of 66 (21%) gastric cancers, and all 14 had telomerase activity. Cellular DNA contents revealed that all 22 aneuploid tumors had detectable telomerase activity. The present results indicate that telomerase activation may be required as a critical step in the multigenetic process of tumorigenesis, and that telomerase is frequently but not always activated as a late event in gastric cancer progression.
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PMID:Telomerase activity in gastric cancer. 761 59

A transforming gene was cloned from a focus of rat fibroblast cell line Rat 1 transfected with DNA of a gastrocarcinoma cell line. The transforming gene is the activated form of oncogene c-Ha-ras, and the lesion was identified as a single nucleotide substitution at codon 12 by sequencing. We further used polymerase chain reaction (PCR)-restriction analysis to detect the mutations at codon 12 of c-Ha-ras. By using this method, 11 cases out of 24 solid tumors and 3 cell lines of gastric cancer were shown to contain mutations, and there was a strong correlation between mutations and metastasis and survival of the patients. The role of the activated c-Ha-ras in tumorigenesis of stomach cancer was further proved through the assay in which the malignant phenotypes of the c-Ha-ras-transformed cells were partially inhibited by blocking the c-Ha-ras expression with antisense oligonucleotides or exogenous plasmid expressing antisense RNA.
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PMID:Activation of oncogene c-Ha-ras in gastric cancer of Chinese patients. 805 87

c-erbB-2 oncogene encodes a growth factor receptor whose amino acid sequence has extensive homology with human epidermal growth factor receptor. It is frequently overexpressed in human breast, ovary, lung, and stomach cancers, where its overexpression is related significantly to the prognosis. Tl investigate the possible role of c-erbB-2 oncogene in the oncogenesis of stomach cancer, we examined the genetic alterations of c-erbB-2 oncogene in 4 stomach cancer cell lines, SNU-1, SNU-5, SNU-16 and KATO III. There were no differences in c-erbB-2 mRNA level as well as c-erbB-2 gene copy number among them. But gp185-erbB-2, c-erbB-2 gene product, was increased from 2- to 4-fold in SNU-1 and SNU-5 cells, compared with that in SNU-16 or KATO III cells. Our results suggest that post-transcriptional regulation of gp185erbB-2 expression may underlie gp185erbB-2 overexpression in cancer cells.
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PMID:The mechanism of c-erbB-2 gene product increase in stomach cancer cell lines. 810 20

On the basis of our recent findings that licochalcone A isolated from Xin-jiang licorice showed anti-inflammatory and anti-tumorigenic activities, we synthesized more than 40 chalcone derivatives to examine their anti-tumorigenic activities. In vitro inhibitory activity against phosphorylation of phospholipids promoted by tetradecanoylphorbol-13-acetate (TPA) in HeLa cells was adopted as a screening test for anti-tumor-promoting effect. In vivo experimental mouse skin tumors initiated by dimethylbenz[a]-anthracene (DMBA) and promoted by TPA were used to test the anti-tumor-promoting effect of chalcones. In the results, 3'- and 4'-methyl-3-hydroxychalcone showed the highest potency in inhibiting tumorigenesis. They also showed a remarkable inhibitory effect on the proliferation of HGC-27 cells derived from human gastric cancer. We discuss the structure-activity relationship, including stereo-chemical phototransformation, of some chalcone derivatives with reference to their ultraviolet (UV) and nuclear magnetic resonance (NMR) spectroscopic data.
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PMID:Anti-tumorigenic chalcones. 814 19

Simultaneous multiple gastric cancers are rarely observed in clinical practice, and its association with p53 gene mutation has not been mentioned in any previous reports. We report a case of advanced gastric cancer with two primary lesions in the stomach who received total gastrectomy. Tumor and surrounding normal tissues from the surgical specimen were studied by using polymerase chain reaction-single strand conformation polymorphism analysis, restriction enzyme digestion method and direct sequencing. Point mutations of p53 gene at codon 248 (CGG-->TGG) were found in both primary tumor foci. The patient developed cancerous peritonitis eight months after the operation and expired six months later. This report suggests that p53 gene mutation can occur at an earlier stage in the tumorigenesis of gastric cancer than previously reported and it might be associated with an unusual clinical and pathological presentation.
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PMID:A case of simultaneous multiple gastric cancers with p53 gene mutation. 817 66

In order to identify relevant genetic lesions in gastric carcinoma, we searched for tumor suppressor gene inactivation and K-ras gene mutations by analyzing tumor and control DNAs from 34 patients. These were from an epidemiologically defined area of Italy characterized by one of the world's highest incidences of stomach cancer. Allele losses were investigated by the Southern blotting procedure at 16 polymorphic loci on 11 different chromosomes. Our data demonstrate that chromosomal regions 5q, 11p, 17p and 18q are frequently deleted, and that 7q and 13q chromosome arms are also involved, although at a lower frequency. Loss of heterozygosity (LOH) at region 11p was not found during other surveys carried out on patients of different geographic origins. No specific combination of allelic losses could be recognized in the samples analyzed, the only exception being that tumors with 17p allelic loss also showed LOH on the 18q region. When matching frequent LOH events and the stage of progression of the tumors, we observed a trend of association between advanced stages and allelic losses on 17p and 18q chromosome arms. The analysis of K-ras, carried out by the polymerase chain reaction and denaturing gradient gel electrophoresis, demonstrated transforming mutations in only 3 out of 32 cases. Colorectal tumorigenesis proceeds by the accumulation of genetic alterations, including K-ras mutations and inactivation of tumor suppressor genes on the 5q, 17p and 18q regions. Our data indicate that, although gastric and colorectal neoplasias share common genetic alterations, they probably progress through different pathways.
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PMID:Loss of heterozygosity and K-ras gene mutations in gastric cancer. 840 32

The aim of this study was to survey the expression of an embryonic cytokine gene, MK, in the normal organs and neoplastic tissues of adults. Northern analysis showed that MK mRNA was exclusively expressed in the kidney among murine organs including thymus, lung, heart, spleen, liver, and kidney. In situ hybridization analysis revealed that MK expression was localized in the proximal tubules and metaplastic Bowman's epithelium, but not in other nephron segments such as glomeruli, loop of Henle, distal tubules, and collecting ducts. To investigate whether MK expression is a marker of tubular cell lineage, several cell lines originating from renal tubules were tested. No expression of MK was detected in PtK1 and LLC-PK1 cells derived from marsupial and porcine proximal tubules or in MDBK and MDCK cells from bovine and canine distal/collecting tubules. Unexpectedly, the MK gene was expressed in a human renal cell carcinoma line, VMRC-RCW, and the expression was up-regulated in the presence of retinoic acid. To elucidate the involvement of MK in the development of tumors, we further examined its expression in a variety of human neoplastic cell lines: YMB-1-C (breast cancer), EBC-1 (lung squamous cell carcinoma), RERF-LC-OK (lung adenocarcinoma), SBC-3 (lung small cell carcinoma), HSC-2 (mouth squamous cell carcinoma), NUGC-2 (gastric cancer), COLO201 (colon cancer), HepG2 (hepatoma), MIA PaCa-2 (pancreatic cancer), MCAS (ovarian cancer), HeLa (cervical cancer), BeWo (chorionic carcinoma), ITO-II (testicular tumor), T24 (urinary bladder tumor), and G-401 (Wilms' tumor). Strong signals were detected in COLO201, HepG2, ITO-II, T24, G-401, and weaker but distinct signals were detected in YMB-1-C, HSC-2, and MCAS cells. The MK gene was, therefore, widely expressed in neoplastic cells originating from genital organs, intestinal tract, liver, mammary gland, and urinary tract, and the expression was not restricted to adenocarcinomas, but was also observed in other types of tumor cells. These findings suggest that a retinoic acid responsive gene, MK, may play a role in the pathophysiology of renal proximal tubules and tumorigenesis in many types of neoplasms.
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PMID:A retinoid responsive cytokine gene, MK, is preferentially expressed in the proximal tubules of the kidney and human tumor cell lines. 843 39

Generalized gastrointestinal juvenile polyposis is a rare form of diffuse polyposis in which cancer infrequently develops. A clinical case is described in which gastric polyps showed a variety of histological features, including both in situ and invasive adenocarcinoma. Many mixed lesions were observed, confirming a morphological sequence already documented in colorectal tumorigenesis but still undefined in gastric tumors. The patient seems strongly predisposed to gastric cancer, presumably on a genetic basis, because he developed a malignancy in a hyperplastic juvenile polyp, usually not considered a precancerous lesion. There is no doubt that cases like this may be important for accurate genetic evaluation and biological characterization.
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PMID:Generalized juvenile polyposis with mixed pattern and gastric cancer. 844 Apr 42

This study examined p53 gene alterations in human gastric mucosa, intestinal metaplasia and well-differentiated (cohesive type) adenocarcinomas to clarify to the role of the p53 gene in gastric tumorigenesis by means of fluorescence in situ hybridization (FISH), polymerase-chain-reaction-single-strand-conformation polymorphism (PCR-SSCP) and immunohistochemistry. Gene alterations were compared with numerical changes of chromosome 17. Samples were obtained from 31 surgically resected stomachs affected with gastric cancer. There was no nuclear p53 protein in cells from normal gastric mucosa. Among 23 specimens of intestinal metaplasia, cells with p53 protein were variably detected in 5 incomplete metaplasias (colonic type). A histological study revealed a mildly dysplastic appearance. PCR-SSCP identified p53-gene mutation in exons 5 and 8 in 2 of the 5 samples. Numerical aberrations of chromosome 17 and the p53 gene were undetectable both in normal mucosa and in intestinal metaplasia. Variable numbers of tumor cells contained p53 protein in 13 (54%) of 24 carcinomas, and PCR-SSCP revealed abnormal bands in 5 of them. Mutations were detected in exons 5, 7, 7, 7 and 8. FISH analysis demonstrated that 6 carcinomas emitted 3 or 4 signals for chromosome 17, and 7 gave one signal for the p53 gene in over 20% of the cells. Ten (77%) of 13 carcinomas examined by FISH appeared to show a p53-gene deletion.
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PMID:Numerical aberration and point mutation of p53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: analysis by fluorescence in situ hybridization (FISH) and PCR-SSCP. 864 18


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