# SL12 T-LYMPHOMA: A NEW MODEL FOR GENE CONTROL IN TUMORS

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 1990 · $138,400

## Abstract

Tumor cell heterogeneity is commonly observed in most
hematopoietic and solid tumors which have progressed to the
malignant state.  The heterogeneity observed is the consequence
of substantial differences in gene expression between cells
composing such tumors.  The mechanisms responsible for
heterogeneous gene expression are not well understood.  In some
lymphoproliferative diseases the heterogeneity appears to be the
consequence of cells progressing to different levels of maturation.
The proposed research plan utilizes a unique series of cloned cell
lines which differ in the kinetics of tumor development, the site
of primary organ disease, the expression of numerous surface
antigens and mRNA transcripts and the cellular response to
glucocorticoid hormones.  The applicant has developed and
extensively characterized this series of cloned cell lines to
address the mechanisms by which lymphoma cells alter their gene
expression.

From several cell clones which differ in gene expression and
tumorigenicity, cDNA libraries were constructed in lambda gt10
and 11.  cDNA clones have been isolated by subtraction
hybridization screening.  These clones represent genes which are
expressed in normal thymic lymphocytes but not in liver, brain
and other tissues.  The proposed research will investigate the
mechanism of regulation of these differentially expressed genes
and will attempt to identify some of them by DNA sequencing.
Cellular differences in sensitivity to glucocorticoid induced lysis
will be exploited to isolate hormone responsive genes implicated
in the lysis function.

The role of differentiation in the occurrence of tumor cell
heterogeneity will be further investigated using molecular probes
to genes which are sequentially expressed in thymocyte
development.  The regulation of genes encoding the T-cell antigen
receptor, the invariant T3 complex, surface glycoproteins Lyt2
and L3T4, will be examined in detail.  By comparing cell clones
representing distinct states of maturation and by inducing certain
clones to undergo maturational events, the regulation of specific
genes will be assessed.  Thymic stromal cells have induced some
SL12 clones to expressed genes necessary for T-cell maturation.
Further studies to determine the stability of the induced
alterations in gene expression and to examine their effect of
tumorigenicity are proposed.

## Key facts

- **NIH application ID:** 3175597
- **Project number:** 5R01CA037778-06
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **SAM.gov UEI:** UYTTZT6G9DT1
- **Principal Investigator:** Carol L. MacLeod
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $138,400
- **Award type:** 5
- **Project period:** 1984-06-15 → 1990-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3175597

## Citation

> US National Institutes of Health, RePORTER application 3175597, SL12 T-LYMPHOMA: A NEW MODEL FOR GENE CONTROL IN TUMORS (5R01CA037778-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3175597. Licensed CC0.

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