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)

P53 gene mutation has been described with variable frequency in gastric cancer and its biological significance remains unclear. We studied 101 gastric carcinomas to evaluate the association between this genetic alteration and the evolution of gastric cancer. Of these, 67 patients were men and 34 were women. The median age at diagnosis was 68 years. The tumors were obtained from gastrectomies. The p53 gene mutation was determined with the monoclonal antibody DO7 (Novocastra). The neoplasms were classified as tumors with high or low level p53 expression according to the intensity and distribution of the nuclear staining. Forty eight tumors showed high level of p53 immunoreactivity. The association of p53 expression with age, sex, tumor size, histologic type, histologic grade, depth of invasion, localization, lymph node metastases, type of surgery and 5 year survival rate was investigated. The results did not demonstrate any significant association between p53 expression and the factors mentioned above.
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PMID:[Expression of p53 in gastric carcinoma. Prognostic value]. 785 87

Loss or inactivation of p53 gene--a suppressor oncogene has been considered to be one of the important mechanisms in the development of human tumors. One of the evidences for mutation of allelic gene of p53 is the identification of p53 protein concentrated in the nuclei of related cells. By using ABC immunohistochemical method, we studied the expression of p53 in cryostatic sections of the tumor tissue and adjacent mucosa resected from 38 patients with gastric cancer. p53 was found to be positive in the nuclei with intensive staining in 24 out of 38 cases with carcinoma (63.2%). p53 positive cells were distributed diffusively in the cancer tissue. All the adjacent mucosa specimens except 10 were negatively stained with p53 monoclonal antibody. These 10 specimens including 3 with dysplasia and 4 with metaplasia were only weakly stained. p53 was also found to be positive in 18 out of 23 cancer patients with metastasis in perigastric lymph nodes (78.3%). We also studied in the same section the nucleolar organizer region-associated proteins (AgNORs) with using silver staining technique to find if there is any relationship between p53 gene mutation and the activity of rRNA transcription of tumor cells. The number of AgNORs dots per nucleus detected in gastric cancer sections with positive staining of p53 (9.9 + 2.14) was greater than those with p53 negative staining (7.2 + 1.68). There was a significant statistical difference between the two groups (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The expression of mutant p53 gene in gastric carcinoma]. 786 23

Gastrointestinal cancers involve genetic alterations in multiple oncogenes, multiple tumor suppressor genes, and multiple DNA repair genes. However, common and different genetic changes are observed in esophageal, gastric, and colorectal carcinomas, respectively. Inactivation of the p53 gene and expression of CD44 abnormal transcripts are common events that serve as a powerful tool for cancer diagnosis. Gene amplification of cyclin D is found preferentially in esophageal cancer, whereas gene amplification of cyclin E and c-met is frequently associated with gastric cancer. Mutations of the cyclin-dependent kinase inhibitor genes also occur in esophageal and gastric cancers. However, the scenario of multiple gene changes differs depending on the two histologic types of gastric cancer, because they may have different genetic pathways. Interestingly, the frequency of genetic instability is also quite different between the two types of gastric cancer. A new strategy of molecular diagnosis for gastrointestinal cancers, which started as routine work at Hiroshima City Medical Association Clinical Laboratory last August, may provide a new approach to cancer diagnosis for the next decade.
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PMID:Genetic alterations in human gastrointestinal cancers. The application to molecular diagnosis. 788 67

Our previous study revealed that mutations of the p53 gene were detected by cDNA sequencing in one of four (25%) primary gastric tumors and in five of six (83%) gastric cancer cell lines. It was of interest that all five cell lines established from metastatic lesions had p53 gene mutations, while the single cell line established from a primary tumor lacked an abnormality. Thus, the current study was initiated to determine the frequency of p53 mutations in 10 pairs of samples from primary gastric carcinomas and their lymph node metastases, in addition to morphologically normal gastric mucosa. In addition, we correlated the findings with other relevant molecular markers including the metastasis associated nm23-H1 gene and loss of heterozygosity (LOH) using multiple polymorphic markers for chromosome 17p and sequencing the entire open reading frame (ORF) of the p53 gene. Five of ten (50%) patients were constitutionally heterozygous for one or more 17p and/or p53 probes (pYNZ 22, BamHI RFLP; pMct35.1, Mspl RFLP; php53cl, Bg/II RFLP), while none had LOH at the 17p and/or p53. A Bg/II RFLP for analysis of possible nm23-H1 somatic allelic deletion revealed no LOH out of four informative cases. One paired sample demonstrated the substitution of valine for isoleucine at codon 41 (GTT to ATT) in both primary gastric tumor and metastasis. Another metastatic sample demonstrated the substitution of proline for threonine at codon 278 (CCT to C/ACT) in addition to a non-mutated codon, while only the wild-type p53 sequence was present in the paired primary gastric tumor tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of p53 gene mutations in paired primary and metastatic gastric tumor tissues. 790 5

Intragenic restriction site polymorphisms in amino acid residue 72 in exon 4 and a Mspl polymorphism in intron 6 of the p53 tumour suppressor gene can both serve as polymorphic markers. Probe YNZ22 (D17S5) is a highly polymorphic, variable number of tandem repeat (VNTR) marker which maps to chromosome 17p13.1 where the p53 gene is located. Locus specific amplification by polymerase chain reaction (PCR) technique and subsequent non-isotopic single-strand conformation polymorphism analysis of the PCR fragments was used for the detection of loss heterozygosity (LOH) of 17p including the p53 gene locus. In combination with a PCR-based method for the analysis of the VNTR locus D17S5 using unique sequences flanking the polymorphic region of YNZ22 we investigated tumour DNA and corresponding constitutional DNA from 69 patients, including 39 patients with gastric cancer, 21 patients with osteosarcomas and 9 patients with Ewing's sarcomas. Using all three methods, 49/69 (71%) patients were informative for LOH, which revealed allelic loss in 5/39 (12.8%) gastric cancers, 1/9 (11.1%) Ewing's sarcoma, and 4/20 (20%) osteosarcomas.
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PMID:Rapid detection of loss of heterozygosity of chromosome 17p by polymerase chain reaction-based variable number of tandem repeat analysis and detection of single-strand conformation polymorphism of intragenic p53 polymorphisms. 791 80

Immunohistochemical detection of p53 was performed in archival material of 129 early gastric cancers. Positive staining was detected in 22.5% (29/129) of the cases. No significant association could be established with any clinicopathological criteria but a trend of a higher rate of p53 detection was observed among large tumors (> 6 cm) and in cases with lymph node involvement. Prognosis was significantly worse for patients with p53-positive staining tumors. The 5-year survival rate was 92.1% for patients with p53-negative tumors and 71.2% for those with positive malignancies (p = 0.001). p53 detection and lymph node involvement emerged as independent prognostic factors in a Cox model including other clinicopathological criteria. Immunochemical detection of p53 may become an important aid in the preoperative evaluation of patients with early gastric cancer.
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PMID:p53 detection as a prognostic factor in early gastric cancer. 797 Apr 91

A case with primary triple cancers including thyroid cancer is reported. A 57-year old woman complaining of laryngeal discomfort was found to have an firm elastic lump on the right anterior neck. On 123I scan, the nodule in the right thyroid lobe accumulated considerable amounts of radioiodine as a warm nodule, while the remainder of the gland showed decreased uptake. Thyroid hormone levels remained within normal ranges. Cytological findings obtained by fine-needle aspiration biopsy showed papillary carcinoma. Right lobectomy was performed. The histological examinations revealed papillary carcinoma embedded within adenomatous thyroid tissue. It is probable that the surrounding adenomatous tissue accumulated radioiodine, since the warm nodule on 123I scan was larger than the size of the carcinoma. Examinations of the gastrointestinal tract revealed the presence of poorly differentiated adenocarcinoma in the stomach and well differentiated adenocarcinoma (carcinoma in adenoma) in the rectum. Expressions of ras p21 and p53 were examined immunohistochemically in these carcinoma tissues. The ras p21 product was clearly detected in not only the thyroid carcinoma but in a part of the surrounding adenomatous regions as well. Both ras p21 and p53 proteins were observed in the rectal cancer tissue. In contrast, these oncoproteins were not found in the gastric cancer tissue. In this case ras oncogene activation may be an early event in the tumorigenic process of the thyroid and rectum. However, different genetic alterations seem to occur during the development of these three carcinomas.
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PMID:[A case report of primary triple cancers in the thyroid, stomach and rectum with evidence of variable oncoprotein expressions]. 800 92

To plan a strategy for DNA-based diagnosis of gastric cancer, which is still one of the major causes of death in Akita Prefecture, I reviewed recent studies on genomic instability and genetic changes in gastric cancers. Complex chromosome changes, pathohistology-dependent activation of some proto-oncogenes and -independent inactivation of tumor suppressor genes have been found, which suggests that gastric carcinogenesis is caused by the accumulation of multiple genetic changes in stomach cells. Although the primary change in the carcinogenesis is still unknown, the loss of the 13 locus on the short arm of chromosome 17 or the mutation of the p53 gene, or both, may be essential, since the change occurs frequently in gastric cancer as well as in other various cancers. The approach to DNA-based diagnosis of gastric cancer should be made at three size levels of human genome, chromosome banding (2 x 10(6) bp-), linkage analysis (10(4)-2 x 10(6) bp) and DNA (-10(4) bp) levels.
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PMID:[A proposal for chromosome and genetic analysis in gastric cancer]. 806 34

This study was conducted to investigate the p53 gene alterations in 25 surgically-resected gastric adenocarcinomas in the Korea Cancer Center Hospital by polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) for exons 4-8 and immunohistochemical staining (IHCS) with anti-p53 antibody, DO-7. p53 mutations were detected in nine (36%) out of 25 cancer tissues by PCR-SSCP in exon 4-8: 0,1,1,6 and 1 mutations in exons 4,5,6,7 and 8, respectively. All tissues were also tested by IHCS, and positive staining was observed in 11 cases (44%). A discrepancy of the results between the two methods was observed in four cases. In one which showed positivity by PCR-SSCP a negative reaction by IHCS, the two base deletion was observed in exon 7. On the other hand, in three cases the mutation was detected only in IHCS but not in PCR-SSCP. The exact mechanism by which this discrepancy develops is not clear at present, although it may be due to the mutation of other exons not tested in this study or the relatively low sensitivity of the PCR-SSCP method. The incidence of p53 gene mutations was analysed according to pathologic stage and histological differentiation, but no significant difference was observed between the p53 alterations and these factors. By combined use of PCR-SSCP and IHCS, 48% of the 25 primary gastric cancer were considered to have mutations of the p53 gene. These results suggest that p53 mutation is not an infrequent event in primary gastric cancer and the p53 gene plays an important role in the carcinogenesis process of gastric cancer.
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PMID:Alterations of p53 gene in primary gastric cancer tissues. 806 92

To study the involvement of the p16 tumor suppressor gene in esophageal cancer development, we examined homozygous deletion of the p16 gene in 13 human esophageal cancer cell lines and 9 gastric cancer cell lines, in which some of genetic alterations have already been characterized. By Southern blot analysis, homozygous deletion was observed in 12 out of the 13 esophageal cancer cell lines (92%), in 2 out of a total of 9 gastric cancer cell lines (22%). It was also found that the p16 gene loss, cyclin D1 amplification and p53 gene mutations occurred independently in these cell lines. These findings suggest that loss or mutations of the p16 gene are involved in most esophageal cancers and that mutation of this gene plays a critical role in the development of esophageal cancer.
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PMID:Highly frequent homozygous deletion of the p16 gene in esophageal cancer cell lines. 809 26


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