Role of bcl-2 in Epstein-Barr Virus-Induced Malignant Conversion of Burkitt's Lymphoma Cell Line Akata

Komano, Jun; Takada, Kenzo

doi:10.1128/jvi.75.3.1561-1564.2001

Cited by 80 publications

(121 citation statements)

References 26 publications

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“…Their expression is nuclear and although its function is unknown it is strongly believed that they have an oncogenic role. 29 Our PCR-based analysis has shown to be concordant with the EBER results. The semiquantitative results also differentiate between passenger and productive viral presence as absorbance values indicate DNA-relative quantity.…”

Section: Discussionsupporting

confidence: 78%

Epstein–Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas

et al. 2009

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The association of Epstein-Barr virus with pulmonary neoplasms has been restricted to lymphoepithelioma-like carcinomas in Asian patients. We have selected 19 pulmonary adenocarcinomas and squamous-cell carcinomas from 1545 pulmonary neoplasms diagnosed from 1996 to 2007 in an occidental population. All of them showed a low-power appearance confusing between an epithelial and a lymphoid neoplasm, with a dense lymphocytic infiltrate intermingled with neoplastic cells giving an image akin to lymphoepithelial complexes. Five carcinomas presented typical features of Lymphoepithelioma-like lung carcinomas; but six cases could be classified as squamous-cell carcinomas and eight as adenocarcinomas. A semiquantitative polymerase chain reaction method, Early RNA genes 1 and 2 in situ hybridization as well as Latent membrane protein immunostaining for Epstein-Barr virus DNA, RNA and protein detection methods were used in every case. None of Lymphoepithelioma-like carcinomas showed positivity for Epstein-Barr virus in any used method. Otherwise four squamous-cell carcinomas and eight adenocarcinomas (12 cases) demonstrated viral sequences in polymerase chain reaction and/or in situ hybridization analysis in neoplastic cells. Moreover two adenocarcinomas also displayed human herpesvirus 6 DNA sequences coamplification in molecular analysis. Protein immunostaining was focally positive in only three cases. We performed the same analysis in 70 more cases of conventional pulmonary squamous-cell carcinomas and adenocarcinomas that gave negative results. In conclusion, a subset of pulmonary squamous-cell carcinomas and adenocarcinomas show Epstein-Barr DNA and/or RNA sequences in neoplastic cells. This finding expands the spectra of epithelial cell common tumours Epstein-Barr virus associated.

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Section: Discussionsupporting

confidence: 78%

Epstein–Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas

et al. 2009

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“…Various studies have shown that EBV inhibition of apoptosis and up-regulation of the Bcl-2 protein are essential for the malignant phenotype (Marin et al, 1995;Komano et al, 1998). Previous reports also provided direct evidence that EBV up-regulates Bcl-2 expression by repressing the activation of the double-stranded RNA-dependent protein kinase (PKR) (Komano et al, 1999). This allows c-MYC to exert its oncogenic function, and eventually results in the inhibition of apoptosis.…”

Section: Eber-1 and Eber-2 Up-regulate Bcl-2 Protein Expressionmentioning

confidence: 90%

Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells

Mao

2013

J. Zhejiang Univ. Sci. B

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Epstein-Barr virus (EBV), a human gammaherpesvirus carried by more than 90% of the world's population, is associated with malignant tumors such as Burkitt's lymphoma (BL), Hodgkin lymphoma, post-transplant lymphoma, extra-nodal natural killer/T cell lymphoma, and nasopharyngeal and gastric carcinomas in immune-compromised patients. In the process of infection, EBV faces challenges: the host cell environment is harsh, and the survival and apoptosis of host cells are precisely regulated. Only when host cells receive sufficient survival signals may they immortalize. To establish efficiently a lytic or long-term latent infection, EBV must escape the host cell immunologic mechanism and resist host cell apoptosis by interfering with multiple signaling pathways. This review details the apoptotic pathway disrupted by EBV in EBV-infected cells and describes the interactions of EBV gene products with host cellular factors as well as the function of these factors, which decide the fate of the host cell. The relationships between other EBV-encoded genes and proteins of the B-cell leukemia/lymphoma (Bcl) family are unknown. Still, EBV seems to contribute to establishing its own latency and the formation of tumors by modifying events that impact cell survival and proliferation as well as the immune response of the infected host. We discuss potential therapeutic drugs to provide a foundation for further studies of tumor pathogenesis aimed at exploiting novel therapeutic strategies for EBV-associated diseases.

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“…First, EBERs affect membrane signaling by initiating the production of various interleukins (ILs) that are involved in cell growth, such as IL-6, IL-9, or insulin-like growth factor-1 (Ho et al, 1999;Kitagawa et al, 2000;Iwakiri et al, 2003;Iwakiri et al, 2005). They also play a role in regulation of apoptosis by binding the RNA-dependent protein kinase (PKR), subsequently inhibiting PKRmediated apoptosis in the EBV infected cells (Komano et al, 1999;Yamamoto et al, 2000). In addition, EBERs can modulate interferon (IFN)/antiviral response.…”

Section: Treatment Strategies For the Patients With Ebv-associated Chlmentioning

confidence: 99%

“…Nt (Ho et al, 1999;Komano et al, 1999;Kitagawa et al, 2000;Yamamoto et al., 2000;Iwakiri et al, 2003;Iwakiri et al, 2005;Samanta et al, 2006;Samanta et al, 2008;Iwakiri et al, 2009;Iwakiri and Takada, 2010 Immunization with LMP1 gene or polyepitope expression vectors Taylor et al, 2004;Smith et al, 2006;Pan et al, 2009;Lutzky et al, 2010;Chia et al, Immunization with LMP2A gene or polyepitope expression vectors (Taylor et al, 2004;Smith et al, 2006;Pan et al, 2009;Lutzky et al, 2010;Chia et al, 2011) LMP2B Modulation of innate immune response nt TLR: Toll-like receptor, RIG: retinoic acid-inducible gene, PKR: RNA-dependent protein kinase, Nt: not tested, CTL: cytotoxic T lymphocyte, DC: dendritic cells.…”

Section: Inhibition Of Apoptosis (Pkr)mentioning

confidence: 99%

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

Lee¹

2011

Biomolecules and Therapeutics

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Lymphoma is a type of cancer involving cells of the immune system, and has two major categories: Hodgkin lymphoma (HL) and all other lymphomas (non-HL). Although the two types may display the same symptoms, they are readily distinguishable via microscopic examination, and differ in the way they develop, spread and are treated. HL is a unique clinicopathological disorder characterized by the rare presence of malignant cells (usually accounting for 0.1% to 10% of the cells in the total tumor mass) in a background of a nonneoplastic cellular microenvironment comprising T-and Blymphocytes and other cell types (Weiss et al., 1999). In the United States, about 8,500 new cases of HL were expected to be diagnosed in 2010, and the overall incidence is increasing each year (Maggioncalda et al., 2011).Although the pathogenesis of HL is still largely unknown, the association of HL with Epstein-Barr virus (EBV) infection has been demonstrated in many reports. For examples, HL patients show elevated antibody titers to EBV antigens (Levine et al., 1971), and the risk of developing HL is increased up to three-fold in population that have experienced infectious mononucleosis caused by primary EBV infection (Gutensohn Over the past few decades, our understanding of the epidemiology and immunopathogenesis of Hodgkin lymphoma (HL) has made enormous advances. Consequently, the treatment of HL has changed signifi cantly, rendering this disease of the most curable human cancers. To date, about 80% of patients achieve long-term disease-free survival. However, therapeutic challenges still remain, particularly regarding the salvage strategies for relapsed and refractory disease, which need further identifi cation of better prognostic markers and novel therapeutic schemes. Although the precise molecular mechanism by which Epstein-Barr virus (EBV) contributes to the generation of malignant cells present in HL still remains unknown, current increasing data on the role of EBV in the pathobiology of HL have encouraged people to start developing novel and specifi c therapeutic strategies for EBVassociated HL. This review will provide an overview of therapeutic approaches for acute EBV infection and the classical form of HL (cHL), especially focusing on EBV-associated HL cases. and Cole, 1980), and EBV DNA/RNA can be detected in HL tissues (Brink et al., 1997), suggesting that as a primary event in the development of this disease, EBV infection may play a very crucial role in the pathogenesis of HL. AbstractAccording to a population-based cohort study, the frequency of EBV associated HL among total HL cases varies from 30 to 50% (in certain cases even higher; >90% in developing and underdeveloped countries, and >95% in HIV associated cases), and most of them appear in classical Hodgkin lymphoma (cHL), the major type of HL (Herbst et al., 1991;Pallesen et al., 1991;Ambinder et al., 1993;Leoncini et al., 1996). Since EBV is an oncogenic virus that is able to subvert cellular processes supporting growth and survival, the approach to unravel the f...

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Role of bcl-2 in Epstein-Barr Virus-Induced Malignant Conversion of Burkitt's Lymphoma Cell Line Akata

Cited by 80 publications

References 26 publications

Epstein–Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas

Epstein–Barr virus-associated adenocarcinomas and squamous-cell lung carcinomas

Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells

Epstein-Barr Virus-Associated Classical Hodgkin Lymphoma and Its Therapeutic Strategies

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