Epstein‐Barr virus‐infected T cells in infectious monoucleosis

Tokunaga, Masayoshi; Uemura, Yoshiko; Tokudome, Takahiro; Satô, Eiichi

doi:10.1111/j.1440-1827.1993.tb01124.x

Cited by 17 publications

(16 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…EBV is also found in a small proportion of more typical gastric adenocarcinomas (Figure 3c) of either diffuse or intestinal type (Shibata and Weiss, 1992;Rowlands et al, 1993;Tokunaga et al, 1993). However, the histological features of these more typical differentiated gastric carcinomas can show heterogeneity, with some cases having lymphoepithelioma-like tumour growth next to adenocarcinoma tumour (Rowlands et al, 1993;Gulley et al, 1996) making the histological distinction between tumours more complicated.…”

Section: Gastric Carcinomamentioning

confidence: 99%

“…EBV-positive gastric cancers are more likely in males compared with females (Shibata and Weiss, 1992;Tokunaga et al, 1993), less likely to be found in the gastric antrum than in the cardia or body of the stomach Yuen et al, 1994;Galetsky et al, 1997), and more likely to be poorly differentiated tumours (Yuen et al, 1994;Gulley et al, 1996;Shin et al, 1996;Galetsky et al, 1997). Less consistent associations have been found for age, with some studies finding more EBV-positive tumours in older people, 60 þ years (Qiu et al, 1997) or 56 þ years (Gulley et al, 1996).…”

Section: Gastric Carcinomamentioning

confidence: 99%

See 1 more Smart Citation

Epstein–Barr virus and oncogenesis: from latent genes to tumours

2003

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with the development of both lymphoid and epithelial tumours. As a common virus infection, EBV appears to have evolved to exploit the process of B cell development to persist as a life-long asymptomatic infection. However, the virus can contribute to oncogenesis as evidenced by its frequent detection in certain tumours, namely Burkitt's lymphoma (BL), post-transplant B cell lymphomas, Hodgkin's disease (HD) and nasopharyngeal carcinoma (NPC), and by its unique ability to efficiently transform resting B cells in vitro into permanently growing lymphoblastoid cell lines (LCLs). These transforming effects are associated with the restricted expression of EBV genes such that only a subset of so-called latent virus proteins are expressed in virus infected tumours and in LCLs. Distinct forms of EBV latency are manifest in the different tumours and these appear to be a vestige of the pattern of latent gene expression used by the virus during the establishment of persistent infection within the B cell pool. This review summarises our current knowledge of EBV latent gene function and how this relates to the role of the virus in the aetiology of different tumours.

show abstract

Section: Gastric Carcinomamentioning

confidence: 99%

Section: Gastric Carcinomamentioning

confidence: 99%

Epstein–Barr virus and oncogenesis: from latent genes to tumours

2003

View full text Add to dashboard Cite

show abstract

“…32 The primary has been reported in some cases of primary gastric antibodies, including MIB-1 (Immunotech, Marseille, lymphoma [22][23][24] and adenocarcinoma. [25][26][27] France), bcl-2 (clone 124; Dako, Glostrup, Denmark), In the current study, the authors analyzed 12 cases p53 (PAb1801; Oncogene Science, Uniondale, NY), and of coexisting primary gastric lymphoma and adenocar-H. pylori (B471; Dako, Glostrup, Denmark), were apcinoma in the same patient observed either synchroplied overnight at 4 ЊC, followed by incubation with nously or metachronously to delineate the clinicosecondary biotinylated antibody for 20 minutes, and pathologic and immunohistochemical features, as well a streptavidin-biotin-peroxidase complex reagent was as to assess the possible association with H. pylori and then applied for 20 minutes at room temperature. The EBV in these double malignancies.…”

mentioning

confidence: 99%

Synchronous and metachronous primary gastric lymphoma and adenocarcinoma

Nakamura

Aoyagi

Iwanaga

et al. 1997

Cancer

View full text Add to dashboard Cite

RESULTS.Two different tumors were found synchronously in 10 patients (5 with Masatoshi Fujishima, M.D. 2 independent tumors and 5 with contiguous/collision tumors) and metachronously in 2. The size of the lymphomas (mean, 7.2 cm) was larger than that of the adeno-1 Second Department of Pathology, Faculty of carcinomas (mean, 3.6 cm) (P õ 0.005). Histologically, 9 of the 12 lymphomas Medicine, Kyushu University, Fukuoka, Japan.(75%) were mucosa-associated lymphoid tissue lymphomas, and all lymphomas 2 Second Department of Internal Medicine, Facinvaded the deep portion of the submucosa or deeper. Conversely, 10 of the 12 ulty of Medicine, Kyushu University, Fukuoka, adenocarcinomas (83%) were early carcinomas. Six adenocarcinomas were intestiJapan.nal type, whereas the other 6 were diffuse type. The MIB-1 index of the adenocarci-3 First Department of Pathology, School of Mednomas (mean, 50.4%) was higher than that of the lymphomas (mean, 29.3%) (P õ icine, Fukuoka University, Fukuoka, Japan. 0.05). Helicobacter pylori (H. pylori) was documented in all 12 patients, whereasEpstein-Barr virus-encoded RNA 1 was detected in only 2. During the followup period after surgery, 6 patients died, 4 due to adenocarcinoma. The survival probability of all 12 patients appeared to be similar to that of previously reported patients with gastric adenocarcinoma alone, and was significantly worse than that of the 217 patients with gastric lymphoma alone (P õ 0.05).CONCLUSIONS. An H. pylori infection is considered to be associated with the development of these double malignancies. In many such synchronously observed cases, lymphomas may precede carcinogenesis, while the prognosis appears to be more closely associated with the adenocarcinoma than the lymphoma. G astric adenocarcinoma is one of the most common malignancies, whereas primary gastric lymphoma is relatively uncommon, oc-The authors thank Dr. Koh-ichi Ohshima and curring in only 1 -7% of all malignant neoplasms of the stomach. Dr. Akinori Iwashita, Fukuoka University, forThe occurrence of both malignant gastric lymphoma and adenocarcitheir kind cooperation, and Brian T. Quinn for noma in the same patient is very rare, and little is known regarding his critical comments.the clinicopathologic characteristics of such cases. 2-13Address for reprints: Shotaro Nakamura, M.D.,Helicobacter pylori (H. pylori) is believed to play a causative role nocarcinomas but also primary gastric lymphomas, especially those of mucosa-associated lymphoid tissue (MALT) type, are associated

show abstract

“…The presence of EBV was determined using in situ hybridization (ISH) with EBER-1, known to be present in large amounts in EBV-infected cells [27]. EBER-1 was detected with a digoxigenin-labeled 30-base oligomer, using previously described procedures [28,29]. Paraffin-embedded 4 mm sections were deparaffinized, rehydrated, predigested with pronase, prehybridized, and then hybridized overnight at 377C.…”

Section: Immunohistochemistry Of Hsp27 and In Situ Hybridization Of Ementioning

confidence: 99%

“…In each EBV-positive case of gastric carcinoma, all of the cells are infected with the virus [6][7][8], which suggests that EBV plays an important role in gastric carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Epstein–Barr virus upregulates phosphorylated heat shock protein 27 kDa in carcinoma cells using the phosphoinositide 3‐kinase/Akt pathway

Fukagawa¹,

Nishikawa²,

Kuramitsu³

et al. 2008

Electrophoresis

View full text Add to dashboard Cite

Gastric cancer is the most common cancer in Japan and infection with Epstein-Barr virus (EBV) is responsible for about 10% of gastric cancers worldwide. Although EBV infection may be involved at an early stage of gastric carcinogenesis, the mechanisms underlying its involvement remain unknown. To investigate the role of EBV in gastric carcinogenesis, we performed proteomic analyses of an EBV-infected gastric carcinoma cell line NU-GC-3 (EBV(+)) and its uninfected control (EBV(-)). 2-DE was combined with MS to identify differentially expressed proteins. We found that EBV infection upregulated one of the phosphorylated heat shock protein 27 kDa (HSP27). The phosphorylated HSP27 isoform which increased in EBV(+) cells can be induced by both heat shock and arsenite. The increase of phosphorylated HSP27 in EBV(+) cells was reduced by treatment with the phosphoinositide 3-kinase (PI3K) inhibitors (LY294002 and wortmannin). In addition, we found increased levels of phosphorylated Akt in EBV(+) cells. These findings suggest that EBV infection upregulates the phosphorylation of HSP27 via the PI3K/Akt pathway. Thus, activation of the PI3K/Akt pathway may contribute to the establishment of a malignant phenotype in EBV-infected gastric carcinomas.

show abstract

Epstein‐Barr virus‐infected T cells in infectious monoucleosis

Cited by 17 publications

References 4 publications

Epstein–Barr virus and oncogenesis: from latent genes to tumours

Epstein–Barr virus and oncogenesis: from latent genes to tumours

Synchronous and metachronous primary gastric lymphoma and adenocarcinoma

Epstein–Barr virus upregulates phosphorylated heat shock protein 27 kDa in carcinoma cells using the phosphoinositide 3‐kinase/Akt pathway

Contact Info

Product

Resources

About