In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4643-4643
Abstract:
Background: Lymphomagenicity of EBV in the setting of HIV infection has been widely accepted. However, the underlying carcinogenic mechanism of EBV is largely unknown and warrants further study. We sought to investigate the hypothesis that EBV infection is associated with expression of specific B-cell oncogenic markers in HIV+ DLBCL. Methods: HIV+ DLBCL cases diagnosed between 1996-2007 within the Kaiser Permanente California Health Plan were identified. Archived tumor specimens were retrieved and H & E slides were reviewed to identify representative tumor blocks for tissue microarray (TMA) construction. Immunohistochemistry staining was performed on TMA cores to analyze the expression of selected B-cell oncogenic markers in the following categories: (1) mutagenic molecule (that induce mutation/translocation), (2) cell cycle promoter, (3) B-cell activator and (4) anti-apoptotic protein. Percent of DLBCL cells with visible marker staining was scored on a scale from 0-4 (0-9%, 10-24%, 25-49%, 50-74% and ≥75%). EBV infection was determined by in situ hybridization of EBV encoded RNA and was considered positive if ≥10% of the DLBCL cells had detectable EBV. Correlations between EBV and marker expression were examined using Spearman's correlation coefficient. Results: We identified 194 HIV+ DLBCL cases. Of these, 117 lacked sufficient tissue; another 7 had undetermined EBV status; and 70 were included in the study. Marker expressions are shown in the table: Conclusion: There was a suggestion that Cyclin E and PKC-β2 were more commonly expressed in EBV+ DLBCL, and that FOXP1, BCL2, and Survivin were more commonly expressed in EBV- DLBCL. However, none of these associations reached statistical significance. These findings provide limited support that the underlying carcinogenic mechanism of EBV involves the mediation of the expression of oncogenic markers examined here. However, our study power was limited, thus requiring confirmation in larger studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4643. doi:10.1158/1538-7445.AM2011-4643
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2011-4643
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2011
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
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