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CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease.
Blood 1996; 88(8):3129-36Blood

Abstract

The Epstein-Barr virus (EBV) latency C promoter drives expression of a family of viral proteins commonly targeted by CD8 cytotoxic T cells. These proteins are not generally expressed in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. The failure to express these proteins is almost certainly an important factor in the evasion of immunosurveillance by EBV-associated tumors. In a previous study, we have shown that transcriptional activation of the C promoter is inhibited by methylation of a particular CpG site upstream of the promoter that prevents binding of a cellular protein (CBF2), and we have shown that this and adjacent CpG sites are methylated in a Burkitt's lymphoma cell line. In the present study, we show that CpG sites in the CBF2 binding region are predominantly methylated in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. In addition, we present the first direct evidence that the C promoter is transcriptionally silent in Burkitt's lymphoma. In contrast, we show a complete absence of methylation in the CBF2 binding region in a case of reversible EBV-associated B-cell lymphoma arising in an immunocompromised patient whose tumor shows C promoter transcriptional activity. By inhibiting expression of highly antigenic viral proteins, methylation of transcriptional control sequences may veil the presence of virus in tumor tissue from CD8(+) cytotoxic T-cell immune surveillance and thus facilitate viral tumorigenesis.

Authors+Show Affiliations

Department of Oncology, Johns Hopkins University School of Medicine Baltimore, MD, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8874213

Citation

Robertson, K D., et al. "CpG Methylation of the Major Epstein-Barr Virus Latency Promoter in Burkitt's Lymphoma and Hodgkin's Disease." Blood, vol. 88, no. 8, 1996, pp. 3129-36.
Robertson KD, Manns A, Swinnen LJ, et al. CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease. Blood. 1996;88(8):3129-36.
Robertson, K. D., Manns, A., Swinnen, L. J., Zong, J. C., Gulley, M. L., & Ambinder, R. F. (1996). CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease. Blood, 88(8), pp. 3129-36.
Robertson KD, et al. CpG Methylation of the Major Epstein-Barr Virus Latency Promoter in Burkitt's Lymphoma and Hodgkin's Disease. Blood. 1996 Oct 15;88(8):3129-36. PubMed PMID: 8874213.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease. AU - Robertson,K D, AU - Manns,A, AU - Swinnen,L J, AU - Zong,J C, AU - Gulley,M L, AU - Ambinder,R F, PY - 1996/10/15/pubmed PY - 1996/10/15/medline PY - 1996/10/15/entrez SP - 3129 EP - 36 JF - Blood JO - Blood VL - 88 IS - 8 N2 - The Epstein-Barr virus (EBV) latency C promoter drives expression of a family of viral proteins commonly targeted by CD8 cytotoxic T cells. These proteins are not generally expressed in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. The failure to express these proteins is almost certainly an important factor in the evasion of immunosurveillance by EBV-associated tumors. In a previous study, we have shown that transcriptional activation of the C promoter is inhibited by methylation of a particular CpG site upstream of the promoter that prevents binding of a cellular protein (CBF2), and we have shown that this and adjacent CpG sites are methylated in a Burkitt's lymphoma cell line. In the present study, we show that CpG sites in the CBF2 binding region are predominantly methylated in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. In addition, we present the first direct evidence that the C promoter is transcriptionally silent in Burkitt's lymphoma. In contrast, we show a complete absence of methylation in the CBF2 binding region in a case of reversible EBV-associated B-cell lymphoma arising in an immunocompromised patient whose tumor shows C promoter transcriptional activity. By inhibiting expression of highly antigenic viral proteins, methylation of transcriptional control sequences may veil the presence of virus in tumor tissue from CD8(+) cytotoxic T-cell immune surveillance and thus facilitate viral tumorigenesis. SN - 0006-4971 UR - https://www.unboundmedicine.com/medline/citation/8874213/CpG_methylation_of_the_major_Epstein_Barr_virus_latency_promoter_in_Burkitt's_lymphoma_and_Hodgkin's_disease_ L2 - http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=8874213 DB - PRIME DP - Unbound Medicine ER -