# IMMUNOBIOLOGY OF UVL-INDUCED TUMORS

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1987 · $156,078

## Abstract

Ultraviolet light (UVL)-induced carcinogenesis in mice represents an
excellent model to study tumor immunology.  The majority of primary
neoplasms induced with this physical agent are immunologically rejected
when transplanted to normal syngeneic recipients but capable of progressive
growth when transplanted to UVL-exposed animals.  This observation has been
extensively investigated and appears to be due, at least in part, to
effects mediated by UVL directly on the immunological apparatus.  To date,
UVL-induced tumors have mainly served as a tool to study this biological
phenomenon.  The aim of our study is to address a number of questions
crucial to the development of this model, using a reversal of the tack
taken in past investigations.  Employing tumor-specific immunity as a tool,
we propose:  (1)\to question the clonal nature of UVL-induced tumors;
(2)\to question the possibility that tumor-tumor or tumor-somatic cell
hybridization may represent an integral component of normal tumor
progression; (3)\to further analyze the tumorigenic heterogeneity of cells
within primary UVL-induced regressor phenotype tumors; (4)\to determine
whether the gene(s) which encodes for UVL-mediated transformation and the
gene(s) which encodes for a particular TSTA are identical or at least
linked; and (5)\to investigate further the phenomenon that cloned lines
derived from UVL-regressor phenotype tumors can be converted with normal
splenocytes (induction, selection, or both) to a virulent progressor which
expresses a TSTA identical to the original cell line.  The facilities and
technical expertise needed to conduct these studies are unique in that a
basic understanding of contemporary cellular immunology, tumor immunology,
photobiology, somatic cell genetics, and molecular genetics is essential.
It is obvious that many aspects of experimental photocarcinogenesis have
important human implications.  UVL represents a well-recognized and
documented human carcinogen, and its ability to modify certain human immune
responses is just beginning to be appreciated.  (M)

## Key facts

- **NIH application ID:** 3170997
- **Project number:** 5R01CA033065-06
- **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:** 1987
- **Award amount:** $156,078
- **Award type:** 5
- **Project period:** 1982-08-01 → 1988-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3170997

## Citation

> US National Institutes of Health, RePORTER application 3170997, IMMUNOBIOLOGY OF UVL-INDUCED TUMORS (5R01CA033065-06). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3170997. Licensed CC0.

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