# EXPRESSION OF ONCOGENES & IGA GENES IN TRANSFORMED CELLS

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CAMPUS · 1988 · $161,191

## Abstract

In many Balb/c mouse myeloma cell lines, the c-myc oncogene normally
located on chromosome 15 has translocated to a H chain constant region
locus on chromosome 12.  In the majority of myelomas studied, the
translocation of c-myc is to the constant region sequence (C yield) of the
yield H chain "non-productive" gene.  The mRNA coding strand of DNA fro the
c-myc gene is on the anti-sense strand for the C yield gene.  While
unrearranged C yield alleles are transcriptionally silent, we have shown
that an excluded C yield gene element to which the c-myc oncogene has
translocated is transcriptionally active.  Several discrete cytoplasmic RNA
species hybridizing to and yield-C probe can be detected.  These are
transcribed from the C yield sense strand.  In a mouse myeloma MOPC 315
variant line (V-1), which has lost the yield-H chain gene, preliminary
results indicate that this transcription initiates within the c-myc gene,
possibly from an endogenous c-myc anti-sense promoter region(s).  The
site(s) of initiation of this transcription and the processing of these RNA
species will be characterized by S1 mapping, cDNA cloning and sequencing.
Furthermore our experiments indicate that in the murine early B-cell
lymphoma WEHI 231, which contains unrearranged c-myc genes, the growth
arrest induced by treatment with antibody against surface immunoglubulin or
with tumor promoter, is accompanied by dramatic changes in the rate of
c-myc gene transcription.  Alterations in the binding of proteins to the
c-myc (sense) promoter region(s) and in the structure of this DNA segment
will be evaluated during the growth arrest process.  Furthermore, the
effect of introduction of a translocated c-myc gene into WEHI 231 cells on
growth arrest will be monitored.  These experiments will elucidate the
mechanisms involved in normal c-myc gene regulation and evaluate the
effects of the translocation on these processes.  The results of these
studies will help define the role of these rearrangements in the neoplastic
transformation of B cells.

## Key facts

- **NIH application ID:** 3173906
- **Project number:** 5R01CA036355-05
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CAMPUS
- **SAM.gov UEI:** FBYMGMHW4X95
- **Principal Investigator:** GAIL E. SONENSHEIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $161,191
- **Award type:** 5
- **Project period:** 1984-01-01 → 1991-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3173906

## Citation

> US National Institutes of Health, RePORTER application 3173906, EXPRESSION OF ONCOGENES & IGA GENES IN TRANSFORMED CELLS (5R01CA036355-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3173906. Licensed CC0.

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