Role of p53, apoptosis, and cell proliferation in early stage Epstein-Barr virus positive and negative gastric carcinomas

Ishii, Hideaki; Gobé, Glenda C.; Yoneyama, J; Mukaide, Mistuhiro; Ebihara, Yoshiro

doi:10.1136/jcp.2003.015081

Cited by 14 publications

(10 citation statements)

References 39 publications

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“…Therefore, we expected to see an enhanced proliferation rate in these cells due to disruption of the p53 tumor suppressor gene [Milner, 1991;Korkolopoulou et al, 1997;Ishii et al, 2004]. But surprisingly, our results clearly demonstrate that this is not the case in cultured cutaneous cells.…”

Section: Discussioncontrasting

confidence: 34%

A UVB Fingerprint Mutation on the p53 Tumor Suppressor Gene Decreases in vitro

Zhang

Bürger

Hellwig

et al. 2008

Cells Tissues Organs

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The culture of tissue-derived human cells is an important aspect of tissue engineering. Prior to transplantation, the quality of the cultured cells/tissue should be routinely tested so that any enrichment of procarcinogenic cells can be excluded. On this account, a UVB-induced p53 fingerprint mutation would be a valuable quality control marker for skin cells cultured for use in tissue engineering. We developed an allele-specific real-time polymerase chain reaction assay based on SYBR Green which can quantitatively detect CC-TT transitions in the tumor suppressor gene p53. To analyze the transition 281/282, we used DNA from HaCaT cells, a keratinocyte cell line containing the investigated mutation, as a standard to determine the mutation frequency in cultured cutaneous cells. We analyzed a variety of skin cells grown in culture and found a notable decrease in the UVB fingerprint mutation in fibroblasts during proliferation. Furthermore, we quantified the total amount of mutated DNA in different cutaneous cells and detected a significantly higher level in melanocytes. These results are consistent with findings obtained in our laboratory concerning the common deletion, the most frequently reported mutation in the mitochondrial genome, which suggest a positive influence of prolonged in vitro cell proliferation on the quality of genomic DNA.

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Section: Discussioncontrasting

confidence: 34%

A UVB Fingerprint Mutation on the p53 Tumor Suppressor Gene Decreases in vitro

Zhang

Bürger

Hellwig

et al. 2008

Cells Tissues Organs

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“…Seventeen studies determined the presence of a TP53 expression in EBVaGC by performing immunohistochemistry. 14,21,24,26,27,31,32,48,54,[60][61][62][63][64][65][66][67] A TP53 expression was observed in 149 (36.2%) of 412 EBVaGC and in 717 (47.9%) of 1496 EBV-negative carcinomas. While statistical heterogeneity was found among the studies (Q = 36.368, d.f.…”

Section: Tp53 Expression and P53 Mutationmentioning

confidence: 99%

Clinicopathological and molecular characteristics of Epstein–Barr virus‐associated gastric carcinoma: A meta‐analysis

Lee

Kim

Han

et al. 2009

J of Gastro and Hepatol

219

188

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There is conflicting data regarding the clinicopathological significance of the risk factors associated with Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC). To address this controversy, we performed a meta-analysis for the clinicopathological and molecular characteristics of EBVaGC. The relevant published studies were reviewed according to the defined selection criteria. The effect sizes of the outcome parameters were estimated by an odds ratio or a weighted mean difference. This meta-analysis included 48 studies that encompassed a total of 9738 patients. The frequency of EBVaGC was 8.8%, and EBVaGC was significantly associated with ethnicity. It was more predominant in men and in younger individuals. Interestingly, EBVaGC was more prevalent in Caucasian and Hispanic patients than in Asian ones. EBVaGC developed most often in the cardia and body, and it generally showed the diffuse histological type. EBV was highly prevalent in the patients with lymphoepithelial carcinoma. EBVaGC was closely associated with remnant cancer and a CpG island methylator-high status, but not with Helicobacter pylori infection, a TP53 expression, and p53 mutation. In addition, EBVaGC was not significantly associated with the depth of invasion, lymph node metastasis, or the clinical stage. The clinicopathological and molecular characteristics of EBVaGC are quite different from those of conventional gastric adenocarcinoma. However, further study is needed to determine the effect of EBV on the survival of EBVaGC patients.

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“…However, data on hypermethylation of these genes in Caucasian patients are very sparse [19]. The tumor suppressor genes p16, p14 and APC have been reported to be hypermethylated in GC at varying frequencies (range 10%-84%) [3,4,6,17,[20][21][22]. The hypermethylation of the DNA mismatch repair gene hMLH1 often occurs in a setting of microsatellite instability and was found only in EBV-negative GC so far [7].…”

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confidence: 99%

“…Compared to EBV-negative GC, EBV-associated GC (EBVaGC) are characterized by distinct alterations on the molecular, trancriptional and translational level [1,[3][4][5][6][7][8][9][10][11]. In addition, the expression of the BARF1 oncogene of EBV has been identified in EBV-associated GC and has been reported to impact e.g.…”

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confidence: 99%