# Therapy for Non-Hodgkin lympoma

> **NIH NIH R01** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2024 · $435,506

## Abstract

Abstract
Viruses are the etiological agents of a number of different human cancers. Epstein-Barr virus (EBV) is a
ubiquitous pathogen infecting over 95% of the human population worldwide. EBV is the etiological agent of
several malignancies including Hodgkin lymphoma (HL), and multiple types of non-Hodgkin lymphoma (NHL)
including post-transplant lymphoproliferative disease (PTLD), diffuse large B cell lymphomas (DLBCL), T cell
lymphomas, NK/T cell lymphoma (NKTL), and Burkitt's lymphoma (BL). In addition, EBV is also associated
with nasopharyngeal carcinoma (NPC) and gastric cancer.
There is an increased incidence of EBV-associated NHL in HIV-infected patients. HIV-positive individuals
have a 10–20% lifetime risk of developing Burkitt lymphoma and EBV-positive NKTL is seen with increased
frequency in HIV infection as well as transplant recipients. HIV-infected EBV-positive NKTL patients are also
at a higher risk for death when compared to NKTL patients without HIV.
We propose to understand how EBV is associated with multiple types of NHL in the HIV-infected population.
EBV is present in each and every lymphoma cell, which implies that EBV contributes to the initiation,
development, and maintenance of the tumor. Several of these EBV-associated lymphomas e.g. NKTL and
BL are highly aggressive and NKTL show resistance to chemotherapeutics. Hence, new therapies are needed
to target these NHL. We have found that EBV-associated NHL display high expression of a cell cycle whose
expression is upregulated following EBV infection of naïve B cells. We hypothesize that EBV activates this
kinase to drive tumor growth and survival. In this proposal, we aim to identify how EBV upregulates this kinase
and the viral genes that may be responsible for this phenomenon. We will investigate the mechanisms by
which EBV, a causal agent of human cancer, modulates cellular processes that contribute to the early events
in the carcinogenesis of EBV-associated lymphomas. We will also determine whether inhibiting this kinase
can hinder EBV-driven lymphomagenesis in vitro and in vivo, and we will investigate whether inhibitors of this
kinase can function as a novel therapeutic target to hinder the development and pathology of EBV-driven
lymphomas. The identification of novel therapeutic targets will help overcome the morbidity and mortality of
EBV-associated lymphomas around the globe and may also be relevant to non-viral cancers.

## Key facts

- **NIH application ID:** 11020542
- **Project number:** 1R01CA291437-01A1
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **Principal Investigator:** BLOSSOM A DAMANIA
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $435,506
- **Award type:** 1
- **Project period:** 2024-09-01 → 2029-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11020542

## Citation

> US National Institutes of Health, RePORTER application 11020542, Therapy for Non-Hodgkin lympoma (1R01CA291437-01A1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/11020542. Licensed CC0.

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