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| Funder | NATIONAL CANCER INSTITUTE |
|---|---|
| Recipient Organization | University of North Carolina Chapel Hill |
| Country | United States |
| Start Date | Sep 10, 2024 |
| End Date | Aug 31, 2029 |
| Duration | 1,816 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | NIH (US) |
| Grant ID | 11001649 |
ABSTRACT Epstein-Barr Virus (EBV) is the etiological agent of several hematopoietic malignancies including multiple types of non-Hodgkin lymphoma (NHL). These EBV-positive NHL subtypes are comprised of post-transplant lymphoproliferative disease (PTLD), diffuse large B cell lymphomas (DLBCL), T cell lymphomas, Natural killer
(NK)/T cell lymphoma (NKTL), and Burkitt's lymphoma (BL). Our studies have found that FAM72A is highly expressed in EBV-positive lymphomas and contributes to EBV-mediated lymphomagenesis, which gives rise to EBV-positive NHL. In response to PAR-21-348, we propose to address how EBV’s upregulation of FAM72A
contributes to the development of EBV-driven NHL.
University of North Carolina Chapel Hill
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