Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated p53 overexpression and the proliferative activity of the primary lesion as well as the clinicopathological features of 75 patients with gastric cancer invading the submucosa (sm cancer), of whom 14 (18.7%) had lymph node metastasis. Among the clinicopathologic features studied, only lymphatic invasion by the primary tumor was related to lymph node metastasis. There was no relationship between immunohistochemical staining for p53 protein or Ki-67 and lymph node metastasis. The p53-positive rate was 35.7 and 57.1% in patients with and without metastasis, respectively, while the mean Ki-67 labeling index was 38.9 and 38.1%, respectively. Our results suggest that p53 mutation or the proliferative activity of sm cancer do not influence lymph node metastasis, even though p53 mutation may enhance the proliferative activity and metastatic potential of advanced gastric cancer.
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PMID:p53 overexpression and proliferative activity do not correlate with lymph node metastasis in early gastric cancer. 901 4

We report 8 newly established gastric-carcinoma cell lines (SNU-216, 484, 520, 601, 620, 638, 668, 719) from Korean patients. Morphologic study was carried out using light and electron microscopes. CEA, alpha FP, and CA 19-9 and TPA in supernatant and in cell lysate were measured by radioimmunoassay. p53 and c-Ki-ras gene mutations were screened and confirmed by sequencing. The cell lines, derived from tumors with moderate differentiation, grew as a diffuse monolayer, and those from tumors with poor differentiation and minimal desmoplasia grew exclusively as non-adherent. Out of the 8 gastric-cancer cell lines, 5 had detectable levels of CEA both in supernatant and in cell lysate; there was no expression or secretion of alpha FP in these cells; 4 cell lines showed high levels of CA 19-9 in cell pellets. All cell lines except SNU-484 had high concentrations of TPA both in cell lysate and in supernatants. p53 mutation was found in 6 cell lines (75%): 2 (SNU-216 and SNU-668) had mutations in exon 6, and other 3 in exon 8. The c-Ki-ras mutation was found in 2 cell lines (25%), SNU-601 and SNU-668. The former showed GGT-to-GAT transition mutation at codon 12, while the latter showed CAA-to-AAA transversion mutation at codon 61. DNA profiles using restriction endonuclease HinfI and polymorphic DNA probes ChdTC-15 and ChdTC-114 showed different unique patterns; which suggests that these cell lines are unique and not cross-contaminated. We believe that the newly characterized gastric-cancer cell lines presented in this paper will provide a useful in vitro model for studies related to human gastric cancer.
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PMID:Establishment and characterization of human gastric carcinoma cell lines. 903 53

The relationship between p53 overexpression and clinicopathologic variables in gastric cancer was evaluated using 304 paraffin-embedded gastric tumor tissues. DO7, a murine monoclonal antiserum to p53 protein, was used for the immunohistochemical analysis. Positive staining was found in 129 tumors (42.2% of all tumors). Overexpression of p53 was not associated with sex, location of the tumor in the stomach or the type of Borrman's tumor. The overexpression rate of p53 protein was 30.4% (28/92) in stage II and 47.6% (101/212) in stage III (p = 0.007). While there was no significant association between p53 protein accumulation and T stage, there was a significant association with N stage, i.e. p53 overexpression was 27.4% (17/62) in the node-negative group and 46.3% (112/242) in the node-positive group (p = 0.011). In 79 patients, in whom corresponding primary gastric tumor and regional lymph node metastases were available, overexpression was found in 34 (43%) primary tumors and in 38 (48.1%) node samples, with a concordance rate of 67.1% in terms of p53 expression. Mean numbers of regional lymph node involvement by the tumor were 6.1 in the group with p53 overexpression and 5.2 in the group showing no immunoreactivity (p = 0.051). These findings suggest that p53 overexpression is related to gastric cancer progression and that immunoreactivity in the metastatic lymph nodes show the dependency on p53 expression in the primary tumor.
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PMID:Relationship between p53 overexpression and gastric cancer progression. 907 90

Gastric carcinogenesis has been studied in various aspects. Helicobacter pylori (Hp) infection and mutation of the p53 tumor suppressor gene have recently been argued to be important factors of gastric carcinogenesis. There have been many studies to determine the precise mechanism of how Hp is related to gastric cancer, but it is so far still unknown. We studied the relationship of Hp infection and p53 overexpression and tried to discover some significance in clinicopathologic factors such as age, sex, stage, site, differentiation and gross morphology. Ninety-six patients who were diagnosed with gastric cancer at Severance Hospital, Yonsei University Medical College from November 1995 to March 1996, and 96 control patients of non-ulcer dyspepsia (NUD) were studied by endoscopic biopsy of normal gastric tissue and cancer tissue. They also underwent the CLO (Delta West, Melbourne, Western Australia) test for Hp positivity and p53 immunohistochemical stain for p53 positivity. These data were analyzed for comparison with the clinicopathologic characteristics of gastric cancers. In conclusion, the differentiated group cancer had a significantly high Hp positivity and p53 positivity. There is a possibility that Hp infection and p53 tumor suppressor gene mutation might be significantly related in the gastric carcinogenic process of well- and moderately-differentiated adenocarcinomas, but further study is necessary to determine more direct clues on the carcinogenic roles of these factors.
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PMID:P53 overexpression in gastric adenocarcinoma with Helicobacter pylori infection. 917 90

To examine in vivo the validity of the results of experiments in vitro, we analyzed the relationship between p53 gene status and apoptotic cell death of human gastric intestinal-type adenocarcinomas. Surgical specimens were classified into two categories: 18 gastric cancers with nuclear p53 protein (A), and 17 gastric cancers without nuclear p53 protein (B). Polymerase chain reaction-single strand conformation polymorphism disclosed a shifted band that corresponded to a mutation in the p53 gene in 13 cases (72%) in category A and 3 cases (18%) in category B, the frequency being significantly higher in the former (P < 0.05). Apoptotic cells were identified from routinely stained sections and by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The TUNEL index [TI; (the number of TUNEL-positive apoptotic cells/the total number of tumor cells) x 100] was 3.8 +/- 1.4% in category A and 4.9 +/- 1.2% in category B, the value being significantly lower in the former (P < 0.05). The proliferating cell nuclear antigen index, defined similarly to the TI, was 56.4 +/- 16.3% in category A, and it was significantly higher than that in category B (P < 0.05). The immunohistochemically detected expression of p21CIP1/WAP1 did not differ between the two categories, while Bax-positive tumor cells were more frequently detected in category A. These results indicate that (1) expression of a mutated p53 gene attenuates apoptotic cell death of gastric cancer, in accordance with the previous in vitro finding that p53 gene mutation provides a possible selective advantage for tumor cell proliferation, and (2) apoptosis is related not only to expression of p53 and the stage of the cell cycle, but also to p53-independent and cell cycle-independent events.
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PMID:Evidence that expression of a mutated p53 gene attenuates apoptotic cell death in human gastric intestinal-type carcinomas in vivo. 924 3

We examined the expression of p53, p21, cyclin D1, E, and PCNA in 75 cases of gastric cancer by immunohistochemical study and the expression of p21 RNA in cases by in situ hybridization. The rate of stage III, IV cases of p53(+) p21(-) group was significantly higher than that of any other groups. The apportinately 3-year survival rate of p53(+) p21(-) group was significantly lower than either that of p21(+) p53(-) or p53(-) p21(-) group. The 3-year survival rates of positive cases were significantly lower than those of negative cases on both cyclin D1 and E. The positive rate of cyclin E of the p53(-) p21(+) group was significantly lower than that of the p53(+) p21(-) group. The average PCNA Labeling. Index (LI) of the p53(+) p21(-) group was significantly higher than that of the p53(-) p21(+) group. The 3-year survival rate of cases with expression of p21 RNA was higher than that of cases without p21 RNA. Average PCNA L1 of cases with expression of mutant-type p53 was high and the number of poor prognostic cases in cases with expression of mutant-type p53 was large. In contrast, the average PCNA LI of cases with expression of p21 was low and the number of good prognostic cases with expression of p21 was large. These results suggest that p21 suppresses synthesis of DNA via cyclin E and PCNA.
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PMID:[The significance of p21 expression in gastric cancer]. 926 17

The results of surgical treatment for gastric cancer are apparently better in Japan than in Western countries. It has been proposed that this is because of a biological difference between the tumours in Japan and in the West. We have previously reported very similar frequencies of positive immunohistochemical staining for the c-erbB2 oncogene and mutant p53 proteins in British and Japanese gastric cancers, findings which do not seem to support the 'biological difference' hypothesis. We realized that these studies did not rule out differences in the mechanism of cancer progression which might show themselves by a different association between p53 and c-erbB2 expression and stage in the two populations. We therefore re-analysed our data to look for differences in the frequency of p53 and c-erbB2 expression in the British and Japanese populations. Comparison of fixed tissue from 88 British and 89 Japanese tumours showed no significant association of c-erbB2 or p53 with stage progression in either population. Logistic regression showed no difference between the two populations in the relationship between stage and oncogene expression. These results do not support the idea of biologically different cancers in Japan and Britain. Other possible explanations for the difference in results such as the stage migration effect, better efficacy of Japanese-style surgery, or a difference in the host resistance to cancer in the two countries should be considered.
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PMID:c-erbB2 and p53 expression are not associated with stage progression of gastric cancer in Britain or Japan. 931 57

Five lines (MKN-28, MKN-45, MKN-74, KATO-III, and HSC-39) of human gastric carcinoma cells were treated with 1 microgram/ml cisplatin for 12, 24, 36, 48, and 72 h. Apoptotic indices (percentages of apoptotic cells) were analyzed at each time point. After incubation with cisplatin, apoptotic cells were detected more frequently among MKN-45 and MKN-74 cells with a wild-type gene for p53 and without expression of the bcl-2 protein than among HSC-39, MKN-28, and KATO-III cells with a mutation or complete deletion of the gene for p53 and with overexpression of the bcl-2 protein. The levels of p53 protein increased after treatment with cisplatin in MKN-74 cells. However, levels of bcl-2 protein were reduced in KATO-III after treatment with cisplatin. Thus, p53 status and the expression of bcl-2 by tumor cells might be good indicators of sensitivity to chemotherapy for patients with gastric cancer.
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PMID:Changes in levels of expression of p53 and the product of the bcl-2 in lines of gastric cancer cells during cisplatin-induced apoptosis. 932 93

The nm23-H1 gene has been suggested to be a metastasis suppressor gene. Studies about the events of loss of heterozygosity (LOH) at the nm23 locus and its correlation to metastasis are controversially discussed. To optimize detection of LOH at the nm23 locus, we screened two P1 clones for additional microsatellites. Tumor and normal DNA from 37 colorectal, 16 gastric, and 8 germ cancer patients were examined for LOH. We found two new CA repeats, one 5' to nm23-H1 and another 3' to nm23-H2. Using these nm23 locus-specific CA repeats and five other chromosome 17 loci (D17S1522, D17S1566, D17S855, D17S515, and TP53), allele loss was observed in 4/32 (12.5%) patients with colon cancer, 2/14 (14.3%) with gastric cancer, and 1/7 (14%) with germ cancer. No isolated LOH of the nm23 region was observed.
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PMID:Isolation and characterization of new microsatellites at the nm23-H1 and nm23-H2 gene loci and application for loss of heterozygosity (LOH) analysis. 934 64

The association between genetic instability in repetitive DNA domains and cancer has been reported in different types of malignancies. In this work we perform a comparative study of 29 gastric tumors with paired normal tissue using seven tetra-(FES/FPS, VWA31/A, HTPO, TH01, MBPB) and pentanucleotide (CD4, TP53) STR polymorphic markers regarding loss of heterozygosity and replication error status. Furthermore, we compare the gene frequencies obtained in normal tissue from patients with those of a normal control population from the same area, looking for allele associations between any of these polymorphic loci and gastric cancer risk. The results have shown that FES/FPS and TP53 present the higher rates of somatic instability. The observed results for TP53 are in accordance with those previously reported in gastric carcinogenesis, while instability of FES/FPS is for the first time reported in this tumor type. Our data suggest that different loci show different rates of instability and/or loss of heterozygosity and do not seem to consist of a result of an RER+ phenotype affecting several genomic repetitive domains. Furthermore, the instability in markers TH01, MBPB, TP53, and FES was generally detected in genotypes involving alleles with a high number of repeats. Comparing gene frequencies in patients and normal controls, no significant differences were found, although longer alleles are consistently more frequent in patients for the markers MBPB, TH01, and CD4.
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PMID:Tetra- and pentanucleotide short tandem repeat instability in gastric cancer. 937 35


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