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)

The effects of treatment in a hydrated autoclave (121 degrees C, 2 atm for 20 min), microwave oven (in water), and simple heating (60 degrees C overnight in distilled water or 90 degrees C for 10 min in ZnSO4) on the stainability of 56 antigens by commercially available antibodies in formalin-fixed paraffin-embedded tissue sections were evaluated. The detectability of nuclear antigens, glycoprotein, lymphocytic surface markers, and chromogranin A was significantly and reproducibly improved by these treatments, whereas the detectability of viral antigens and peptide hormones was attenuated or unchanged. This enhancement includes not only the distinctiveness of the positive staining, but also the number of positive cells, as revealed by comparing serial sections. Among these four heating procedures, microwave heating and autoclaving were more effective than the others on p53, c-erbB-2, and CA125, whereas simple heating was best for smooth-muscle actin (HHF35 and CGA7). Generally the effects of the heating procedures for these antigens were consistent among the cases, but the effects on GFAP varied with the case. The alterations we observed could significantly influence the interpretation of immunohistochemical staining of currently popular tumor markers such as p53 in terms of their prevalence (28% vs 64% in gastric cancer; 36% vs 82% in metastatic liver cancer) and other diagnostically important markers.
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PMID:Alteration of immunoreactivity by hydrated autoclaving, microwave treatment, and simple heating of paraffin-embedded tissue sections. 751 73

Tumour-associated cell-surface glycoprotein is associated with tumour progression in gastric cancer. We investigated the biological significance of tumour-associated cell-surface glycoprotein, determined by the binding of Helix pomatia agglutinin (HPA), with regard to survival time and to the malignant potential of cancer cells in serosally invasive gastric cancer in 119 patients. HPA was positively stained in 75 of 119 patients (63.0%) with gastric cancer with serosal invasion. In patients with HPA-positive tissue, the tumour was larger than in HPA-negative cases and was frequently located in the middle third of the stomach. The incidence of lymph node metastasis was higher than in patients with HPA-negative tissue. There were no differences between the cases staining negatively and positively with HPA with respect to the other factors examined. Gastric cancer tissues with HPA-positive staining revealed a higher positive rate of abnormal p53 staining and a higher concentration of proliferating cell nuclear antigen (PCNA) labelling. The survival time of the patients with HPA positive staining was shorter than for those whose tissues were HPA negative. Thus, tumour-associated cell-surface glycoprotein is apparently closely related to the malignant potential of serosally invasive gastric cancer.
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PMID:A tumour-associated cell-surface glycoprotein accompanying p53 overexpression and higher growth potential for gastric cancer. 753 20

In order to detect regions of DNA containing tumor suppressor genes involved in the development of gastric cancer, we performed an allelotype study on 78 gastric adenocarcinomas from a population composed largely of Texan Hispanics and Anglos, two ethnic groups that have a ratio of incidence rates of gastric cancer of approximately 2:1. In total, 42 microsatellite markers were employed, which detected at least one site per arm of each autosome in the human genome. These included several markers linked to known tumor suppressor genes (TP53, APC, DCC, RB1, and BRCA1). Sites showing quantitative allelic imbalance (AI) greater than 30% were located on 3p (36%), 11q (31%), 12q (38%), 13q (33%), 17p near TP53 (74%), and 17q near BRCAI (32%). Among the 22% of cases showing microsatellite instability (MI), a subset (4 of 17) showed instability at 59% or more of sites tested. No ethnic bias was detected in cases showing MI or in cases with AI at sites with rates of AI above 30%. Tumors of the intestinal subtype were significantly more likely than diffuse tumors to show AI at DI3S170 (P = 0.01). A deletion map of chromosome arm 3p was prepared for tumors with AI at D3S1478. These data indicate that a tumor suppressor gene on chromosome arm 3p is involved in the development of a subset of gastric cancers.
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PMID:Allelic imbalance in gastric cancer: an affected site on chromosome arm 3p. 754 34

The expression of p53 was studied immunohistochemically in combination with the DNA ploidy pattern by gland isolation in 97 alcohol-fixed gastric lesions. A polyclonal antibody, CM-1, was applied to the paraffin-embedded sections in this study. Overexpression of the p53 protein was found in 73.2% of 41 well or moderately differentiated gastric carcinomas and 52.2% of 23 cases with poor differentiation (P < 0.05). Immunoreactivity of p53 was also detected in isolated cancerous glands. No p53 immunoreactivity was detected in benign gastric lesions including adenomas, hyperplastic polyps and regions of intestinal metaplasia. In addition, flow cytometric DNA analysis was performed on isolated glandular epithelium adjacent to the portions used for immunostaining. DNA aneuploidy (DA) was detected in 85.7% of the well or moderately differentiated carcinomas and 42.9% of those with poor differentiation (P < 0.05). There was a positive correlation between DA, p53 positivity and the presence of regional lymph node metastasis, but not with other clinicopathological variables. In spite of the limited applicability of this method to poorly differentiated gastric cancer, we found that immunostaining and flow cytometry in combination with the gland isolation method facilitates analysis of gastric carcinogenesis.
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PMID:Expression of p53 and flow cytometric DNA analysis of isolated neoplastic glands of the stomach: an application of the gland isolation method. 765 35

We studied p53 gene at the DNA and protein level in human gastric cancer tissues and corresponding normal gastric mucosae from 20 cases of patients undergone radical surgery. By Southern blotting, the p53 gene was found to be partially deleted in 30% (6/20) of gastric cancer tissues. ABC immunohistochemical study of p53 expression was carried out on cryostat sections using monoclonal antibodies (PAb 1801) to p53. High level expression of mutated p53 protein was detected in 55% (11/20) gastric cancer tissues. The staining pattern was intranuclear and/or intracytoplamic. There was no detectable staining of any of the normal gastric tissues with 1801 antibody. The positive rate of p53 overexpression was higher in poorly-differenciated glandular carcinomas than well-differenciated cancer (P = 0.0116). Highly significant association exists between high level p53 expression and allele deletion (r = 0.59). The date indicate that inactivation of p53 gene is important in human gastric carcinogenesis and tumor progression. The assay of p53 gene structure and products may provide new biologically relevant tumor marks for predicting the behavior of gastric carcinomas, identifying more aggressive tumors, determining prognosis of the patients and guiding treatment.
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PMID:[p53 gene deletion and abnormal expression in gastric carcinoma]. 765 19

Gastric cancer involves changes in multiple oncogenes and multiple suppressor genes, and it causes genetic instability. Aberrant expression and amplification of the c-met gene, inactivation of the p53 gene, and CD44 abnormal transcripts are common events of both well differentiated and poorly differentiated gastric cancers. Amplification of the cyclin E gene is also observed in gastric cancer regardless of histologic type. Decreased expression of the pic1 (p21) gene occurs independent of the p53 mutations. In addition, K-ras mutations, c-erbB-2 gene amplification, loss of heterozygosity (LOH) and mutations of the APC gene, LOH of the bcl-2 gene, and LOH at the DCC locus are preferentially associated with well differentiated gastric cancer. Moreover, LOH on chromosome 1q is involved in the progression of well differentiated cancer. Precancerous lesions, including hyperplastic polyp, intestinal metaplasia, and adenoma, share genetic changes found in well differentiated cancers. Conversely, genetic instability may be involved in the first step of stomach carcinogenesis of the poorly differentiated type. Reduction or loss of cadherin and catenins, K-sam gene amplification, and c-met gene amplification are necessary for the development and progression of poorly differentiated or scirrhous carcinoma. Interaction between cell-adhesion molecules in the c-met expressed tumor cells and hepatocyte growth factor from stromal cells is implicated in the morphogenesis of two types of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular biology of gastric cancer. 767 88

Preoperative staging of gastric cancer plays a crucial role every multimodal treatment protocol. At present, staging intends to be far more than evaluation of the depth of tumor infiltration into the organ wall, that is, T stage, nodular status (N category), and the presence of distant metastases (M stage) according to UICC criteria. In modern surgical oncology it includes more often the evaluation of prognostic factors such as the RAS-protein, p53 tumor suppressor gene, growth factor receptors, cell adhesion molecules, proteolytic factors, and proliferation-associated antigens. Furthermore, evaluation of nodular status is possible by sophisticated computer programs. The conventional staging of gastric cancer using endoscopy and sonography, conventional ultrasonography, computed tomography, and magnetic resonance imaging is discussed. Possible improvements of staging in oncologic centers should include surgical laparoscopy, laparoscopic ultrasonography, and meticulous evaluation of an abdominal lavage including immunohistochemical detection of free tumor cells. The most promising tumor biology-related prognostic factors in gastric cancer are briefly discussed.
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PMID:Preoperative staging of gastric cancer as precondition for multimodal treatment. 767 91

To determine the role and timing of p53 alteration in gastric adenomas, sequentially biopsied gastric adenomas were immunohistochemically studied for p53 overexpression. From a total of 29 cases, 32 adenomas were endoscopically followed up more than 1 year and used in this study. Immunohistochemically, p53 positivity with diffuse or focal staining was observed in 12 of 32 adenomas. During the follow-up period, only four adenomas transformed to adenocarcinoma, of which three showed p53 positivity by immunohistochemistry. The mutation of the p53 gene in exon 5 through 8 was examined in 18 gastric adenomas including four adenomas with malignant transformation. The PCR-SSCP analysis and DNA sequencing revealed four missense mutations and one silent mutation in five adenomas. The missense mutation was present in three adenomas with diffuse p53 staining and in one adenoma with focal p53 staining. The predominant type of mutation was the G:C to A:T transition. In addition to the p53 gene analysis, Ki-ras gene was also investigated, but no mutation in codon 12 and 13 was found in the adenomas investigated. This study indicated that gastric adenomas might be one of the precursor lesions of gastric cancer but somewhat different from colon adenomas in regard to growth potential, p53 staining pattern and the rate of Ki-ras gene mutation.
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PMID:Clinicopathological and molecular biological studies of gastric adenomas with special reference to p53 abnormality. 770 44

In order to investigate the relationship between altered patterns of p53 expression and risk factors for stomach cancer, we have analyzed a group of 35 patients with early stage intestinal-type adenocarcinoma of the stomach. We assessed p53 nuclear overexpression by immunohistochemistry, using monoclonal antibody PAb 1801, and identified 15 out of 35 patients (43%) displaying nuclear overexpression of p53 protein. Significantly elevated odds ratios (O.R.) were observed for greater body mass index (highest quartile versus lowest quartile: O.R. = 7.9; 95% confidence interval (CI): 1.1 to 56.1) and younger age (< 60 vs. > or = 70 years: O.R. = 10; 95% CI, 1.43 to 50). The odds ratio for p53 overexpression in cigarette smokers was 2.8 (95% CI: 0.7 to 11.6) but not statistically significant. These data indicate that p53 mutations may be involved in the early stages of gastric carcinogenesis, especially in the development of intestinal-type adenocarcinoma.
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PMID:Risk factors and p53 nuclear overexpression in early stage intestinal-type adenocarcinoma of the stomach. 775 Jan 3

Abnormalities of the tumour suppressor gene p53 have been shown in approximately 60% of advanced gastric adenocarcinomas and it has been suggested that the immunohistochemical finding of increased p53 expression is a prognostic marker in gastric cancer. No studies of early (T1) tumours have been reported. Over expression of p53 protein in 95 early gastric carcinomas and in adjacent mucosa was investigated using immunohistochemistry with antibody CM1. Thirty five per cent of the tumours were positive. The frequency of p53 positivity in tumours of tubular histological type (46%) was significantly higher than that in signet ring tumours (10%) (p = 0.006), and neoplasms that invaded deeply into the submucosa were more frequently positive (45%) than others (30%). Five of eight (62%) T1 tumours with lymph node metastases showed immunoreactive p53. In signet ring tumours, immunopositivity correlated with the frequency of DNA aneuploidy. p53 Over expression was also found in 15% of 26 examples of high grade dysplasia in mucosa adjacent to invasive tumours. No positivity was found in intestinal metaplasia or in normal mucosa. The findings show that immunocytochemically demonstrable over expression of p53 correlates with other morphological markers of aggressiveness in T1 gastric adenocarcinoma. The increasing frequency of p53 immunoreactivity in the sequence of high grade dysplasia-->early gastric cancer-->advanced gastric cancer supports the view that abnormalities of p53 are related to tumour progression in gastric carcinogenesis.
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PMID:Expression of p53 in early (T1) gastric carcinoma and precancerous adjacent mucosa. 782 4


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