# MECHANISM OF RETINOID ACTION AGAINST PROSTATE LESIONS

> **NIH NIH R01** · SOUTHERN RESEARCH INSTITUTE · 1987 · $136,615

## Abstract

Although prostate cancer is a major cause of cancer-related deaths in men
over forty years of age, its etiology remains unknown.  Previously, we have
shown that carcinogens and testosterone induce hyperplasia and anaplasia in
prostate explants and retinoids reverse these lesions.  Frequently, the
lesions induced by carcinogens are characterized as preneoplastic although
the neoplastic nature of the carcinogen-treated explants or cell lines
derived from such explants has not been demonstrated.  The major objectives
of this proposal are: first, to develop an in vitro model to demonstrate
neoplastic transformation in carcinogen-treated prostate explants; second,
to examine the prophylactic effects of all-trans-retinoic acid in cell
lines derived from prostate explants exhibiting lesions.  The neoplastic
nature of prostate lesions will be examined in cell lines derived from the
carcinogen-treated explants.  The transformed phenotypes will be
quantitated using three end points:  (a) cloning efficiency, (b)
anchorage-independent growth, and (c) tumorigenicity in syngeneic or nude
hosts.

Since the characteristics of carcinogen- and testosterone-induced lesions
in prostate explants are different, our third major objective is to define
the genesis of the lesions by elucidating for reserve and secretory cells,
cytokinetic (cell cycle growth fraction, cell turnover time, and cell loss)
and ultrastructural alterations associated with the induction and
progression of prostate lesions caused by carcinogens and androgens.

Retinoids have prophylactic and therapeutic effects against many epithelial
tumors, and since they also inhibit and reverse lesions induced by
carcinogens and testosterone in the mouse prostate organ culture, the
fourth major objective is to elucidate cytokinetic and ultrastructural
alterations associated with inhibition and reversal of prostate lesions by
retinoids.  Since sensitivities of dorsal and ventral prostate gland to
carcinogens and testosterone may vary, both glands will be examined with
respect to these alterations.

## Key facts

- **NIH application ID:** 3173192
- **Project number:** 5R01CA035593-02
- **Recipient organization:** SOUTHERN RESEARCH INSTITUTE
- **SAM.gov UEI:** CDZJAJJHJMH5
- **Principal Investigator:** DHARAM P CHOPRA
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $136,615
- **Award type:** 5
- **Project period:** 1985-08-01 → 1989-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3173192

## Citation

> US National Institutes of Health, RePORTER application 3173192, MECHANISM OF RETINOID ACTION AGAINST PROSTATE LESIONS (5R01CA035593-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3173192. Licensed CC0.

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