Virally targeted therapies for EBV-associated malignancies

Israel, Bruce F.; Kenney, Shannon C.

doi:10.1038/sj.onc.1206548

Cited by 98 publications

(77 citation statements)

References 95 publications

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“…The EBV genome contains more than 100 genes that regulate the expression of EBV-encoded latency proteins such as EBNA-1, which is needed for the replication of EBV episomes (85). Because EBV-associated lymphoproliferative diseases are primarily associated with viral latency, many aspects of the latent antigens have been studied extensively.…”

Section: Epstein-barr Virusmentioning

confidence: 99%

Multiple Infections and Cancer: Implications in Epidemiology

Vedham

Divi

Starks

et al. 2014

Technol Cancer Res Treat

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Approximately 18% of the global cancer burden has been attributed to infectious agents, with estimates ranging from 7% in developed countries to about 22% in developing countries.Chronic infections caused by the hepatitis B and C viruses, human papilloma viruses (HPV), and Helicobacter pylori (H. pylori) are reported to be responsible for approximately 15% of all human cancers. Interestingly, although many of the infectious agents that have been associated with cancer-such as HPV, Epstein-Barr virus (EBV), and H. pylori-are highly prevalent in the world, most infected individuals do not develop cancer but remain lifelong carriers. Malignancies associated with infectious agents may result from prolonged latency as a result of chronic infections. Pathogenic infections are necessary but are not sufficient for cancer initiation or progression. Cancer initiation may require additional cofactors, including secondary infections. Therefore, in patients with chronic infection with one agent, secondary co-infection with another agent may serve as an important co-factor that may cause cancer initiation and progression. Additionally, opportunistic co-infections could significantly inhibit response to cancer treatment and increase cancer mortality. Co-infections are relatively common in areas with a high prevalence of infectious agents, especially in developing countries. These co-infections can cause an imbalance in the host immune system by affecting persistence of and susceptibility to malignant infections. Several articles have been published that focus on infectious agents and cancer. In this article, we discuss the role of infectious agents in malignancies, highlight the role of multiple/co-infections in cancer etiology, and review implications for cancer epidemiology.

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Section: Epstein-barr Virusmentioning

confidence: 99%

Multiple Infections and Cancer: Implications in Epidemiology

Vedham

Divi

Starks

et al. 2014

Technol Cancer Res Treat

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“…A second therapeutic avenue for the strategy of reactivation of latent viruses is oncolytic treatment of virus-associated malignancies. The presence of EBV within nearly all tumor cells in many cancers associated with the virus has made this an ideal test case for this approach (49). The use of HDAC inhibitors, such as VPA or NaB, to induce the viral lytic cycle is one possible tactic (33,95).…”

mentioning

confidence: 99%

Valproic Acid Antagonizes the Capacity of Other Histone Deacetylase Inhibitors To Activate the Epstein-Barr Virus Lytic Cycle

Daigle

Gradoville

Tuck

et al. 2011

J Virol

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“…A number of therapies have been proposed to target EBV-associated tumors based on expression of viral genes, as recently reviewed (46). Some examples are those inhibiting the expression of EBV-encoded oncogenes or induction of EBV episome loss.…”

Section: Discussionmentioning

confidence: 99%

Virus-Associated RNA I–Deleted Adenovirus, a Potential Oncolytic Agent Targeting EBV-Associated Tumors

et al. 2005

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Given the growing number of tumor types recognizably associated with EBV infection, it is critically important that therapeutic strategies are developed to treat such tumors. Replication-selective oncolytic adenoviruses represent a promising new platform for anticancer therapy. Virusassociated I (VAI) RNAs of adenoviruses are required for efficient translation of viral mRNAs. When the VAI gene is deleted, adenovirus replication is impeded in most cells (including HEK 293 cells). EBV-encoded small RNA1 is uniformly expressed in most EBV-associated human tumors and can functionally substitute for the VAI RNAs of adenovirus. It enables replication to proceed through complementation of VAI-deletion mutants. We hypothesized that VAI-deleted adenovirus would selectively replicate in EBV-positive tumor cells due to the presence of EBV-encoded small RNA1 with no (or poor) replication in normal or EBVnegative tumor cells. In this report, we show that high levels of replication occurred in the VAI-deleted mutant in the EBVpositive tumor cells compared with low (or negligible) levels in EBV-negative and normal human primary cells. Correspondingly, high toxicity levels were observed in EBV-positive tumor cells but not in EBV-negative tumor or normal human primary cells. In vivo, VAI-deleted adenovirus showed superior antitumoral efficacy to wild-type adenovirus in EBV-positive tumor xenografts, with lower hepatotoxicity than wild-type adenovirus. Our data suggest that VAI-deleted adenovirus is a promising replication-selective oncolytic virus with targeting specificity for EBV-associated tumors. (Cancer Res 2005; 65(4): 1523-31)

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Virally targeted therapies for EBV-associated malignancies

Cited by 98 publications

References 95 publications

Multiple Infections and Cancer: Implications in Epidemiology

Multiple Infections and Cancer: Implications in Epidemiology

Valproic Acid Antagonizes the Capacity of Other Histone Deacetylase Inhibitors To Activate the Epstein-Barr Virus Lytic Cycle

Virus-Associated RNA I–Deleted Adenovirus, a Potential Oncolytic Agent Targeting EBV-Associated Tumors

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