# EPSTEIN-BARR VIRUS AND TUMOR PROMOTION

> **NIH NIH R01** · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCI · 1988 · $122,711

## Abstract

We request support of our studies on the role of Epstein-Barr virus (EBV)
in tumor promotion.  We postulated that EBV functions as a tumor promoter
by inducing uncontrolled proliferation of chemically- or otherwise -
initiated cells, thereby allowing selection of neoplastic cells.  To study
this function of EBV, we have developed new experimental model systems in
which the interaction between EBV and target cells in vitro is separated
into two pathways:  a) the cell-transformation pathway (related to the
process of tumor promotion in vivo), and b) the non-transforming (lytic)
pathway (unrelated to tumorigenesis).

Using these model in vitro systems, we began to test our working hypothesis
that the role of EBV in carcinogenesis involves a virally-induced increase
in viral and/or cellular gene product(s) that block(s) viral lytic cycle
and activate(s) the mechanisms responsible for cell transformation.  We
have found that EBV-induced nuclear antigen EBNA-1 may play a role in
suppression of the viral lytic cycle.  We have also shown that the other
nuclear antigen, EBNA-2, may induce cell proliferation.  Finally, we have
demonstrated that some chemical carcinogens, such as benzo(a)pyrene, act
synergistically with EBV in the process of stimulating cell growth.

The goal is to continue and to extend our studies on the molecular
mechanism of cell transformation by EBV and role of chemical carcinogens in
the process.  Specifically, we propose:  1) Study expression of EBV
regulatory and transformation-related functions following infection of new
host cells with the virus; 2) Identify EBV subgenomic fragments containing
the regulatory genes; and 3) Continue our attempts to modify the virus-cell
interaction, in order to determine the role of chemical carcinogens and
cellular transforming genes as cofactors in EBV-induced cell transformation.

New methods, such as recombinant DNA, Southern, Northern and dot-blotting
and nucleic acid hybridization, Western blotting, and others, will be
utilized in this project, together with previously-established procedures
of EBV receptor-implantation and RSVE-mediated gene transfer.  The proposed
studies will help to elucidate the role of EBV in the multi-step process of
carcinogenesis.

## Key facts

- **NIH application ID:** 3171288
- **Project number:** 5R01CA033386-07
- **Recipient organization:** ST. LUKE'S-ROOSEVELT INST FOR HLTH SCI
- **Principal Investigator:** DAVID J VOLSKY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $122,711
- **Award type:** 5
- **Project period:** 1987-07-01 → 1990-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171288

## Citation

> US National Institutes of Health, RePORTER application 3171288, EPSTEIN-BARR VIRUS AND TUMOR PROMOTION (5R01CA033386-07). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171288. Licensed CC0.

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