# REGULATION OF MMTV IN T-CELL TUMORS

> **NIH NIH R01** · UNIVERSITY OF TEXAS AT AUSTIN · 1990 · $122,161

## Abstract

Additional integrated MMTV proviruses are found in many murine
T-cell lymphomas.  Athough acquisition of MMTV proviruses also
occurs in MMTV-induced mammary carcinomas, a variety of
features distinguish the two tumor types.  (i) The additional
MMTV copies in lymphomas often originate from endogenous
MMTV rather than exogenous virus.  (ii) Most newly acquired
MMTV proviruses in lymphomas contain an LTR deletion which
involves the glucocorticoid regulatory element (GRE) or enhancer
and the LTR open reading frame (orf).  (iii) T-cell tumors with
additional MMTV proviruses lack MMTV particle production.  The
objective of this study is to determine the mechanism of MMTV
acquisition, including deletion formation, and to assess the
involvement of LTR changes in determining MMTV disease
specificity.  The ubiquity of the MMTV LTR alterations in
lymphomas suggests that there is a common mechanism for
generation and/or selection.  Selection for altered
promoter/enhancer activity will be tested using MMTV-driven
chloramphenicol acetyl transferase (CAT) constructs.  Changes in
the distribution and function of orf in lymphomas and mammary
cells will be assessed with antiseral against a trpE-orf fusion
protein.  The requirement of MMTV amplification in T-cells for
intact env gene expression (and thus extracellular virus
production) will be tested by nucleotide sequencing and molecular
constructions involving the endogenous viruses, Mtv-8, Mtv-9, and
Mtv-17.  The involvement of the LTR truncations in T-cell
lymphomagenesis will be evaluated by inserting the truncated
LTR into mammary tumor-inducing clones which are infectious in
vitro and in vivo.  Primary tumors induced by T-cell tropic
MMTVs will be examined for common sites of integration.  This
study should yield important information aobut the transmission
of endogenous viruses, the tissue-specific expression of cellular
genes, and the mechanism of MMTV-induced tumorigenesis.

## Key facts

- **NIH application ID:** 3172590
- **Project number:** 5R01CA034780-06
- **Recipient organization:** UNIVERSITY OF TEXAS AT AUSTIN
- **SAM.gov UEI:** V6AFQPN18437
- **Principal Investigator:** Jaquelin Page Dudley
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $122,161
- **Award type:** 5
- **Project period:** 1984-07-01 → 1991-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3172590

## Citation

> US National Institutes of Health, RePORTER application 3172590, REGULATION OF MMTV IN T-CELL TUMORS (5R01CA034780-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3172590. Licensed CC0.

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