Interrelationship between Epstein–Barr virus infection in gastric carcinomas and the expression of apoptosis‐associated proteins

Ishii, Hideaki; Gobe, G.; Kawakubo, Yasuaki; Sato, Yuichi; Ebihara, Yoshiro

doi:10.1046/j.1365-2559.2001.01037.x

Cited by 20 publications

(18 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

“…EBV infection is seen in about 10% of gastric adenocarcinoma cases [49,58,67] . Ishii et al [49] found MYC expression in early stages of EBV-positive GC was higher than that of EBV-negative GC, while MYC expression in advanced stages of EBV-positive GC was lower than that of EBV-negative tumors. It was inferred that EBV might cause the host cell to induce MYC expression in early cancer development, but then negatively affect MYC expression in advanced stages of cancers, making them less likely to have a natural regression via apoptosis.…”

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

See 1 more Smart Citation

MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

View full text Add to dashboard Cite

MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer.In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma c a r c i n o g e n e s i s , i n c l u d i n g i t s a s s o c i a t i o n w i t h Helicobacter pylori (H pylori ) MYC AND CANCERMYC gene was found to be the cellular homolog of retroviral v-myc oncogene about 30 years ago [12][13][14] . It is located on chromosomal region 8q24.1, has 3 exons [15,16] and encodes a nuclear phosphoprotein [17] . MYC has to heteromerize with MAX, a protein expressed constitutively, to acquire DNA-binding activity. MYC/MAX dimmers are made viable by a basic region helix-loop-helix leucine-zipper motif (bHLHZip), conserved sequences in the carboxyl terminus of both proteins. MYC/MAX dimmers bind to E-box sequence CACGTG in the promoters of specific target genes and stimulate their transcription [18] . MYC has an effect on up to about 15% of genes in genomes of many organisms, from flies to humans [19] . Groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the Myc target gene network.MYC also consistently represses genes involved in cell growth arrest and cell adhesion [20] . Dominguez-Sola et al [21] recently showed that Myc interacts with the prereplicative complex and localizes to early sites of DNA synthesis. Thus, it also has a direct role in the control of DNA replication.MYC regulates transcription from its targets through several mechanisms, including recruitment of histone acetylases, chromatin modulating proteins, basal transcription factors and DNA methyltransferase [22][23][24][25][26] . Protein products of MYC target genes g o on to mediate the downstream effects of MYC on cell biology. MYC is then rapidly degraded, and the pathway switches to a transcriptionally repressive state when MAX dimerizes with a group of related bHLH-Zip proteins, the MAD family, that act as MYC antagonists [27] ( Figure 1).MYC expression might be regulated transcriptionally (initiation and elongation), post-transcriptionally (mRNA stability and translation) or post-translationally (protein stability) [28] . MYC is generally recognized as an important regulator of proliferation, growth, differentiation and apoptosis [29,30] . Therefore, it is also accepted that the deregulation of MYC expression is a major event in cancer pathogenesis or progression. Deregulated expression of a wild-type MYC protein is suff...

show abstract

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

View full text Add to dashboard Cite

show abstract

“…However, there are some regional differences in the frequency of EBV-positive gastric carcinoma. Countries with higher values include Japan (19.3%), Germany (18%) and United States (12-16%) (18,22,40,47). Two studies conducted in Brazil demonstrated intermediate values, 8% and 11.3% (27,33).…”

Section: Introductionmentioning

confidence: 99%

Epstein-Barr virus-associated gastric carcinoma in Brazil: comparison between in situ hybridization and polymerase chain reaction detection

Lima¹,

Ferreira²,

Barros³

et al. 2012

Braz. J. Microbiol.

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) has been associated with 10% of gastric carcinomas. The aim of this study was to determine the frequency of EBV in gastric carcinomas in Brazil assessed by in situ hybridization (ISH) and PCR, which would contribute to the characterization of the clinical and pathological aspects of EBVassociated gastric carcinomas. One hundred and ninety-two gastric carcinoma cases were collected at hospitals in two Brazilian states. Seventy-three out of 151 cases were PCR(+), while 11/160 cases were ISH(+). Nine out of eleven ISH(+) cases displayed a diffuse staining pattern and 2 out of 11 a focal pattern.Both techniques showed that the EBV(+) cases were characterized by their association with males, older patients, lower gastric region, intestinal type, advanced stage and poorly to moderately differentiated tumors.The concordance between the two techniques was 55.8% (Cohen's kappa index = 0.034).

show abstract

“…Several experimental studies have shown that MYC amplification or overexpression is observed in early GC patients when tumor invasion is confined to the mucosa or submucosa, regardless of the presence of lymph node metastasis (2,18–22). In the study by Onoda et al (20), MYC expression was found to be more frequent and stronger in early lesions compared with advanced lesions, and Ishii et al (21) also documented increased MYC expression in early GCs in comparison with decreased MYC expression in late-stage GCs. Based on these findings and the data from the present study, MYC genetic aberrations may be an early event in the pathogenesis of gastric carcinogenesis, and the detection of MYC locus amplification could be used as an auxiliary tool in GC diagnosis and as a predictor of GC aggressiveness (22).…”

Section: Discussionmentioning

confidence: 93%

Chromosome 8q as the most frequent target for amplification in early gastric carcinoma

Kang¹

2014

Oncology Letters

View full text Add to dashboard Cite

Early gastric carcinoma (GC) is considered to be a curable cancer, as it progresses to the advanced stage following varying durations. Understanding the early stage of GC may provide an insight into its pathogenesis and contribute to reducing the mortality rate of this disease. To investigate the genomic aberrations associated with 22 cases of early GC, high-density microarray comparative genomic hybridization was performed in the present study. The most notable finding was copy number gains (log2 ratio >0.25) on the long arm of chromosome 8, which occurred in 77.3% (17/22) of GC cases, and the delineated minimal common region was 8q22.1-q24.3. More specifically, two amplified (log2 ratio >1) loci in the 8q22.1-q24.3 region were detected in 18.2% (4/22) of GC cases. The first loci covered a region of 102.4–107.9 kb, mapping on 8q22.3-q23.1, and comprised the transcription factor CP2-like 3 gene. The second loci, spanning 128.7–145.7 kb on 8q24.21-q24.3, comprised the representative oncogene of myelocytomatosis. Furthermore, the following possible target genes that were not previously considered to play a pathogenic role in GC were identified: Plasmacytoma variant translocation 1, cysteine/histidine rich 1, kinesin family member C2, forkhead box H1, protein phosphatase 1 regulatory subunit 16A, glutamic-pyruvate transaminase, LOC113655 and RecQ protein-like 4. In the present study, previous findings showing that 8q mutations accumulate early during the multistage pathogenesis of GC were confirmed and expanded upon. The confirmation of previously reported 8q gains and the identification of novel target genes at 8q22.1-q24.3 amplified chromosomal sites should aid in improving our understanding of the molecular mechanisms underlying the tumorigenesis of early GC.

show abstract

Interrelationship between Epstein–Barr virus infection in gastric carcinomas and the expression of apoptosis‐associated proteins

Abstract: The p53 and c-myc expression patterns indicate that EBV-infected gastric carcinomas are less likely to have a natural regression via apoptosis at an early stage and explain, in part, the resistance to treatment of late stage of gastric cancers.

Cited by 20 publications

References 36 publications

MYC and gastric adenocarcinoma carcinogenesis

MYC and gastric adenocarcinoma carcinogenesis

Epstein-Barr virus-associated gastric carcinoma in Brazil: comparison between in situ hybridization and polymerase chain reaction detection

Chromosome 8q as the most frequent target for amplification in early gastric carcinoma

Contact Info

Product

Resources

About