Lytic Induction Therapy for Epstein-Barr Virus-Positive B-Cell Lymphomas

Feng, Wenzhi; Hong, Gregory K.; Delecluse, Henri Jacques; Kenney, Shannon C.

doi:10.1128/jvi.78.4.1893-1902.2004

Cited by 195 publications

(187 citation statements)

References 49 publications

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“…Nevertheless, killing of gastric carcinoma cells harboring EBV by chemotherapy agent cisplatin is correlated with the induction of the EBV lytic cycle in experimental animals, indicating that the induction of the EBV lytic cycle plays a role in the tumor cell death. 97,99,100 In addition, GCV treatment of lytically infected Burkitt lymphoma cells prevents the lytic form of EBV DNA replication. By coadministering GCV with the cisplatin, tumor cell killing was markedly improved.…”

Section: Zta As a Target Of Anticancer Therapymentioning

confidence: 99%

Regulation of cellular and viral protein expression by the Epstein-Barr virus transcriptional regulator Zta: Implications for therapy of EBV associated tumors

Chen¹,

Li²,

Guo³

2009

Cancer Biology & Therapy

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Section: Zta As a Target Of Anticancer Therapymentioning

confidence: 99%

Regulation of cellular and viral protein expression by the Epstein-Barr virus transcriptional regulator Zta: Implications for therapy of EBV associated tumors

Chen¹,

Li²,

Guo³

2009

Cancer Biology & Therapy

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“…In one study, EBV-positive lymphoma was efficiently treated with ganciclovir (GCV) or azidothymidine (AZT) in vitro and in vivo following radiation-mediated lytic induction (Westphal et al, 2000). The EBV lytic cycle can be induced in EBV-infected cells by treatment with a variety of drugs, such as gemcitabine, doxorubicin, dexamethasone/rituximab, and valporic acid; subsequent treatment with GCV effectively induces apoptosis (Daibata et al, 2005;Feng et al, 2004;Jones et al, 2010). The therapeutic efficacy can be increased by controlling the Akt or MEKK1 signaling pathway in addition to treatment with the aforementioned drugs (He et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Shin

Kim

Lee

2011

Molecules and Cells

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Epstein-Barr virus (EBV) is associated with human cancers such as nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-negative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBVlytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.

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“…6,7] and/or B-cell tumors (gemcitabine, doxorubicin, and methotrexate; refs. 7,8). The ability of chemotherapy to activate the EBV immediate-early BZLF1 promoter requires cis-acting cyclic AMP-responsive element and MEF2D binding motifs in the promoter, as well as activated phosphatidylinositol 3-kinase, mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK) kinase, and p38 kinase pathways (8).…”

Section: Introductionmentioning

confidence: 99%

Valproic Acid Enhances the Efficacy of Chemotherapy in EBV-Positive Tumors by Increasing Lytic Viral Gene Expression

2006

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EBV infection in tumor cells is generally restricted to the latent forms of viral infection. Switching the latent form of viral infection into the lytic form may induce tumor cell death. We have previously reported that certain chemotherapy agents can increase the amount of lytic viral gene expression in EBV-positive tumor cells. In this report, we have explored the potential utility of valproic acid (VPA), an anti-seizure drug that also has strong histone deacetylase inhibitory activity, for activating lytic viral gene expression in EBVpositive tumors. Although VPA treatment alone induced only a modest increase in the level of lytic viral gene expression, it strongly enhanced the ability of chemotherapeutic agents to induce lytic EBV gene expression in EBV-positive epithelial and lymphoid cells in vitro. Furthermore, VPA enhanced cell killing in vitro by chemotherapeutic agents in lymphoblastoid cells and gastric cells (AGS) containing wild-type EBV. In contrast, VPA did not enhance the cytotoxicity of chemotherapy in lymphoblastoid cells containing a lytic-defective (BZLF1-knockout) form of EBV or in EBV-negative AGS cells. Finally, we found that the combination of VPA and chemotherapy was significantly more effective in inhibiting EBVdriven lymphoproliferative disease in severe combined immunodeficient mice than chemotherapy alone. These results suggest that VPA could potentiate the efficacy of chemotherapy for EBV-positive tumors in patients.

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Lytic Induction Therapy for Epstein-Barr Virus-Positive B-Cell Lymphomas

Cited by 195 publications

References 49 publications

Regulation of cellular and viral protein expression by the Epstein-Barr virus transcriptional regulator Zta: Implications for therapy of EBV associated tumors

Regulation of cellular and viral protein expression by the Epstein-Barr virus transcriptional regulator Zta: Implications for therapy of EBV associated tumors

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Valproic Acid Enhances the Efficacy of Chemotherapy in EBV-Positive Tumors by Increasing Lytic Viral Gene Expression

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