# RNA-TUMOR VIRUS--HEMATOPOIETIC CELL INTERACTION

> **NIH NIH R01** · TUFTS UNIVERSITY BOSTON · 1991 · $152,521

## Abstract

Many retroviruses induce tumors when injected into appropriate hosts and
thus are useful tools to study the events controlling the oncogenic
process.  Rapidly transforming viruses are particularly well suited to such
studies because they seem to cause tumors by directly interfering with
normal growth and differentiation.  Generally, these viruses have lost most
or all of the genes of replication competent retroviruses and acquired
sequences closely related to normal cellular DNA called on cosequences or
onc genes.  Although formal proof is lacking in many cases, the expression
of these viral onc genes appears to be responsible for the virus' ability
to induce tumors and transform cells.  Although the products of onc genes
were originally identified by their ability to induce tumors and transform
cells, recent evidence indicates that expression of the same "transforming"
protein in different cell types can have different effects.  For example,
although Abelson virus infection of some hematopoietic cells induces
transformation of lymphoid cells, infection of hematopoietic cells derived
from early embryonic tissues induces growth and differentiation of
erythroid cells.  In addition, although A-MuLV transforms some
fibroblastoid cell lines, the virus is lethal to others.  The mode of
action of viral onc genes and the role the normal sequences from which they
were derived may play in growth and differentiation are presently unclear.
Examination of this question is an important step toward achieving an
understanding of the mechanism of oncogenesis by rapidly transforming
retroviruses.  In addition, an understanding of the mechanism(s) by which
normal cellular information is subverted, leading to the development of
malignancy, has implication beyond retrovirus-cell interaction.  To address
this question, we have chosen to study a hematopoietic cell model system
and examine the consequences of expression of two unrelated onc proteins,
P160 v-ab1, encoded by Abelson murine leukemia virus and P21 v-ras, encoded
by Harvey murine sarcoma virus.

## Key facts

- **NIH application ID:** 3171578
- **Project number:** 5R01CA033771-09
- **Recipient organization:** TUFTS UNIVERSITY BOSTON
- **SAM.gov UEI:** C1F5LNUF7W86
- **Principal Investigator:** NAOMI ROSENBERG
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $152,521
- **Award type:** 5
- **Project period:** 1983-06-01 → 1993-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171578

## Citation

> US National Institutes of Health, RePORTER application 3171578, RNA-TUMOR VIRUS--HEMATOPOIETIC CELL INTERACTION (5R01CA033771-09). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171578. Licensed CC0.

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