# MECHANISM OF PROMOTION OF CANCER IN TROUT

> **NIH NIH R01** · OREGON STATE UNIVERSITY · 1987 · $114,656

## Abstract

Preventing promotion of cancer that may already be initiated is an
attractive approach for controlling chemical carcinogenesis in humans.
However to achieve this goal mechanisms involved in promotion of cancer
need to be more cleary defined.  The long term objective of this proposal
is to characterize tumor promotion in trout and to compare processes in the
trout model with those associated with promotion in mammals.  In so doing,
we should be able to contribute new and useful information on some aspects
of promotion still poorly understood in mammals.  To achieve this goal we
propose to conduct systematic tumor studies to characterize tumor promotion
and to examine promoter-induced biochemical and cellular processes in trout.

A sub-carcinogenic dose of aflatoxin B1 (AFB1) for embryo exposure that is
promoted by subsequent dietary exposure to cyclopropene fatty acids (CPFA)
and 17-Beta-estradiol (BED) will be determined in tumor studies.  The
dose-response promotion effect of CPFA and BED and effect of time delay
between initiator and promoter stimulus will then be examined with the
sub-carcinogenic dose of AFB1.  Another tumor study will investigate the
relationship between clastogenic potency of 4 initiators, and efficacy of
3-aminobenzamide (3-AB), an inhibitor of DNA repair, to act as a promoter.

The effect of promoters on biochemical and cellular processes will be
investigated by measuring effects on cell proliferation, assayed by
[H3]-thymidine incorporation into nuclear DNA and ornithine decarboxylase
activity; on clastogenesis, measured by DNA strand breaks by alkaline
elution; and lipid peroxidation; analyzed by quantitation of diene
conjugation in nuclear lipid.  Carcinogen-induced clastogenesis with
ethylmethane sulfonate and inhibition of its repair by 3-AB will be
assessed by investigated by quantitating transfer to fluorscent labeled
RTH-149 trout cells of H3-uridine from cocultured RTH-149 cells, from
isolated trout hepatocytes and from isolated hepatocytes from trout prefed
promoter.

This approach of studying promotion of carcinogenesis in the sensitive and
cost efficient trout model to provide whole animal tumor data and cellular
and biochemical data should provide basic yet economical information on the
mechanisms of promotion cancer that may apply to all species.

## Key facts

- **NIH application ID:** 3178315
- **Project number:** 5R01CA039398-03
- **Recipient organization:** OREGON STATE UNIVERSITY
- **SAM.gov UEI:** MZ4DYXE1SL98
- **Principal Investigator:** JERRY HENDRICKS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $114,656
- **Award type:** 5
- **Project period:** 1985-09-01 → 1988-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3178315

## Citation

> US National Institutes of Health, RePORTER application 3178315, MECHANISM OF PROMOTION OF CANCER IN TROUT (5R01CA039398-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3178315. Licensed CC0.

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