p53 Gene Mutations in Esophageal Cancer Detected by Polymerase Chain Reaction Single‐strand Conformation Polymorphism Analysis

Tamura, Gen; Maesawa, Chihaya; Suzuki, Yasushi; Satodate, Ryoichi; Ishida, Kazunari; Saito, Kazuyoshi

doi:10.1111/j.1349-7006.1992.tb00125.x

Cited by 101 publications

(95 citation statements)

References 13 publications

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“…Chromosome 4 aneuploidy has also been implicated in another upper GI malignancy, oesophageal, by our group (Croft et al, 2002;Doak et al, 2003). P53 is the most frequently mutated gene in human cancer (Levine et al, 1991;Tamura et al, 1991;Vogelstein and Kinzer, 1992;Sipponen et al, 1998) and is commonly found to be abnormal in 30 -58% of intestinal and diffuse gastric tumours (Grady, 2001). Hence, here we assessed whether copy number changes of these four chromosomes occurred in gastritis or intestinal metaplasia, as well as dysplasia and adenocarcinoma.…”

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Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

et al. 2005

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In this series of experiments, a novel protocol was developed whereby gastric cells were collected using endoscopic cytology brush techniques, and prepared, such that interphase fluorescence in situ hybridization (FISH) could be performed. In total, 80 distinct histological samples from 37 patients were studied using four chromosome probes (over 32 000 cells analysed). Studies have previously identified abnormalities of these four chromosomes in upper GI tumours. Using premalignant tissues, we aimed to determine how early in Correa's pathway to gastric cancer these chromosome abnormalities occurred. Aneuploidy of chromosomes 4, 8, 20 and 17(p53) was detected in histologically normal gastric mucosa, as well as in gastritis, intestinal metaplasia, dysplasia and cancer samples. The levels of aneuploidy increased as disease severity increased. Amplification of chromosome 4 and chromosome 20, and deletion of chromosome 17(p53) were the more common findings. Hence, a role for these abnormalities may exist in the initiation of, and the progression to, gastric cancer. Helicobactor pylori infection was determined in premalignant tissue using histological analysis and PCR technology. Detection rates were comparable. PCR was used to subtype H. pylori for CagA status. The amplification of chromosome 4 in gastric tissue was significantly more prevalent in H. pylori-positive patients (n ¼ 7) compared to H. pylori-negative patients (n ¼ 11), possibly reflecting a role for chromosome 4 amplification in H. pylori-induced gastric cancer. The more virulent CagA strain of H. pylori was associated with increased disease pathology and chromosomal abnormalities, although numbers were small (CagA þ n ¼ 3, CagAÀ n ¼ 4). Finally, in vitro work demonstrated that the aneuploidy induced in a human cell line after exposure to the reactive oxygen species (ROS) hydrogen peroxide was similar to that already shown in the gastric cancer pathway, and may further strengthen the hypothesis that H. pylori causes gastric cancer progression via an ROS-mediated mechanism.

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Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

et al. 2005

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“…1 As underlying genetic and epigenetic alterations, mutations of p53 have been reported in 35-56% of human gastric cancers, [2][3][4] and silencing of p16 by its promoter hypermethylation has been reported in 42.0 -42.2%. 5,6 Mutations of K-RAS and APC genes, however, are observed only at very low frequencies, in the ranges of 0 -3.6% and 0 -1.4%, respectively.…”

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Reduced expression of the insulin‐induced protein 1 and p41 Arp2/3 complex genes in human gastric cancers

Kaneda

Kaminishi

Nakanishi³

et al. 2002

Intl Journal of Cancer

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Aberrantly methylated DNA fragments in a human gastric cancer were searched for by a genome-scanning method, methylation-sensitive-representational difference analysis (MS-RDA). Six DNA fragments flanked by CpG islands (CGIs) and hypermethylated in the cancer were isolated. Four of the 6 fragments possessed genes in their vicinities. Quantitative RT-PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers: Insulin-induced protein 1 (INSIG1/CL-6) and p41 Arp2/3 complex (p41-Arc). As for INSIG1, a DNA fragment was derived from the edge of a CGI in the promoter region. The edge was methylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer. INSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the methylation. By 5-aza-2 -deoxycytidine treatment of 5 cell lines with the methylation of the edge, partial restoration of INSIG1 expression was detected only in 2 of them. These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the CGI in the promoter region, the methylation was likely to be a secondary change. As for p41-Arc, a DNA fragment was derived from a CGI overlapping exon 8, and its methylation did not correlate with its expression. However, methylation of a CGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers. INSIG1 and p41-Arc are known to be involved in cellular differentiation and morphology, respectively, and it was suggested that their reduced expressions might be involved in gastric cancer development or progression. © 2002 Wiley-Liss, Inc. Key words: INSIG1/CL-6; p41-Arc; methylation; carcinogenesis; gastric cancerGastric cancer is one of the major causes of cancer death in many countries. 1 As underlying genetic and epigenetic alterations, mutations of p53 have been reported in 35-56% of human gastric cancers, 2-4 and silencing of p16 by its promoter hypermethylation has been reported in 42.0 -42.2%. 5,6 Mutations of K-RAS and APC genes, however, are observed only at very low frequencies, in the ranges of 0 -3.6% and 0 -1.4%, respectively. 3,7,8 As a factor that influences the accumulation of genetic alterations, microsatellite instability (MSI) is observed at high incidences, ranging from 31-67%. 9,10 MSI is rarely caused by mutations of DNA-mismatch-repair genes such as hMLH1 and hMSH2, 10,11 but hypermethylation of the hMLH1 promoter region is observed in gastric cancers with MSI. 12,13 Promoter hypermethylations are known to cause silencing of genes in various human cancers. 14,15 In addition, methylation alterations of CpG islands (CGIs) outside promoter regions are associated with altered levels of gene expressions. 16 -18 To search for genes whose expressions are altered in association with methylation alterations, we previously established a genome-scanning method for methylation alterations, methylation-sensitive-representational difference analysis (MS-RDA). 19 By this metho...

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“…In recent years, the biological importance of apoptosis has been recognized in tissue homeostasis (2-4), neurological disorders (5), autoimmune diseases (6), and various malignancies (7)(8)(9)(10)(11). Of particular interest has been the important role played by apoptosis in the development of cancers, including hepatocellular carcinoma (7), breast carcinoma (8), gastric cancer (9), colon cancer (10), and brain tumors (11). Among skin cancers, malignant melanoma is still one of the most aggressive malignant neoplasms and carries a poor prognosis (12).…”

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Fas-Mediated Apoptosis of Melanoma Cells and Infiltrating Lymphocytes in Human Malignant Melanomas

2002

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p53 Gene Mutations in Esophageal Cancer Detected by Polymerase Chain Reaction Single‐strand Conformation Polymorphism Analysis

Cited by 101 publications

References 13 publications

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric tissue: the potential involvement of Helicobacter pylori

Reduced expression of the insulin‐induced protein 1 and p41 Arp2/3 complex genes in human gastric cancers

Fas-Mediated Apoptosis of Melanoma Cells and Infiltrating Lymphocytes in Human Malignant Melanomas

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