# IMMUNOBIOLOGY OF UVL-INDUCED TUMORS

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1991 · $177,045

## Abstract

The majority of murine skin tumors induced by ultraviolet
radiation (UVR) are immunologically rejected following their
transplantation to normal syngeneic animals.  These same
regressor (RE) phenotype tumors, however, are fully capable of
progressive growth when inoculated into UVR-exposed recipients.
Gaining insight into the cellular and molecular mechanisms
responsible for the immunomodulatory influences of UVR has
attracted a considerable degree of research attention over the
past decade.  In fact, much of our current appreciation of the
immunobiology of skin, and the entire field of photoimmunology
evolved from these early studies in experimental
photocarcinogenesis.  It is now apparent that an elucidation of the
molecular characteristics which differentiate RE tumors from
those capable of progressive growth in immunologically normal
animals represents an important and unresolved issue in this
model system.  We recently have determined that all RE-
phenotype tumors increase their surface expression of MHC Class
I molecules in response to stimulation with gamma -interferon
(gamma IFN).  This is consistent with the reported effects of
gamma IFN on normal cell types.  Most progressor (PRO)
phenotype UVR-tumors, however, lack this response to gamma
IFN and do not increase their surface expression of MHC Class I
molecules.  This simple observation may represent an essential
and unappreciated component of the host-tumor interrelationship
associated with UVR carcinogenesis.  This is especially important
considering that Class I molecules serve as restriction elements
for T-lymphocytes.  We believe that this same finding may also
prove to have direct clinical relevance in human host-tumor
interrelationships.  We have proposed in this application to a) test
the hypothesis that a lack of responsiveness to gamma IFN can be
directly related to tumor virulence, b) determine the underlying
mechanisms responsible for gamma IFN sensitivity and investigate
possible means of pharmacologic intervention, and c) determine
whether RE-phenotype tumors gain their advantage in UVR-
exposed recipients because of a depressed capacity by these hosts
to promote a functional MHC Class I enhancing response.  This
will be accomplished experimentally by a) analyzing a number of
distinct RE and PRO tumors as well as PRO greater than RE
variants and RE greater than PRO variants, b) thoroughly
evaluating the biochemical differences between RE and PRO
tumors following gamma IFN stimulation, and c) determining
whether UVR-exposed animals are capable of stimulating gamma
IFN or IFN responses normally.

## Key facts

- **NIH application ID:** 3171000
- **Project number:** 5R01CA033065-10
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** RAYMOND A DAYNES
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $177,045
- **Award type:** 5
- **Project period:** 1982-08-01 → 1993-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171000

## Citation

> US National Institutes of Health, RePORTER application 3171000, IMMUNOBIOLOGY OF UVL-INDUCED TUMORS (5R01CA033065-10). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171000. Licensed CC0.

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