# MECHANISM OF SKIN TUMOR PROMOTION BY CHRYSAROBIN

> **NIH NIH R01** · UNIVERSITY OF TX MD ANDERSON CAN CTR · 1987 · $76,938

## Abstract

Humans are continually exposed to a wide variety of chemicals, some of
which may act as initiators, promoters, cocarcinogens and/or complete
carcinogens.  Current evidence suggests that tumor promotion plays an
important role in the etiology of human cancer.  The proposed research is
designed to investigate the mechanism of action of the anthracene-derived
mouse skin tumor promoters using 1,8-dihydroxy-3-methyl-9-anthrone
(chrysarobin) as the prototype.  Although much is known about the mechanism
of skin tumor promotion by phorbol esters, little is known about the
mechanism of action of the anthracene-derived compounds.  The specific aims
of the proposal are as follows.  The ability of chrysarobin to interact
directly or indirectly with phorbol ester bindng sites will be determined.
Our preliminary data indicates that chrysarobin does not interact
competitively with the phorbol ester receptor.  We will examine the ability
of chrysarobin to activate a partially purified protein kinase C in vitro
and/our to stimulate production of 1,2-diacylglycerol in cultures of mouse
epidermal cells.  We will also determine the ability of chrysarobin to
interact with the Ah-receptor (also called the TCDD-receptor) of mouse
epidermal cells.  A major emphasis will be to determine if specific,
saturable receptors exist for chrysarobin.  In this regard, chrysarobin
will be radioactively labeled and assayed for specific binding to mouse
epidermal particulate and soluble fractions and mouse epidermal cells in
culture.  After binding assays have been developed the affinity of other
structural analogs will be determined by competition experiments.  We will
als determine the subcellular localization and distribution of specific
binding for chrysarobin.  Finally, if appropriate, we will further
characterize the induction of epidermal ornithine decarboxylase by
chrysarobin and its relationship to skin tumor promotion by this class of
compounds.  This experimental approach will allow us to further test the
hypothesis that anthracene derived mouse skin tumor promoters work by a
mechanism different than the phorbol esters.

## Key facts

- **NIH application ID:** 3174805
- **Project number:** 5R01CA037111-05
- **Recipient organization:** UNIVERSITY OF TX MD ANDERSON CAN CTR
- **SAM.gov UEI:** S3GMKS8ELA16
- **Principal Investigator:** John DiGiovanni
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $76,938
- **Award type:** 5
- **Project period:** 1983-08-01 → 1988-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3174805

## Citation

> US National Institutes of Health, RePORTER application 3174805, MECHANISM OF SKIN TUMOR PROMOTION BY CHRYSAROBIN (5R01CA037111-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3174805. Licensed CC0.

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