# CELLULAR IMMUNE RESPONSE MECHANISMS IN BLADDER CANCER

> **NIH NIH R01** · MOUNT SINAI SCHOOL OF MEDICINE OF CUNY · 1987 · $147,546

## Abstract

We previously demonstrated enhanced lymphocyte natural cytotoxicity by
interferon (IF) in vitro and after poly I:C treatment in vivo in animal
models of carcinogen-induced and transplantable bladder cancer.  This was
associated with inhibition of tumor growth in both models by poly I:C.
Even greater inhibition was seen after treatment with both poly I:C and
indomethacin, a prostaglandin synthetase inhibitor.  Observations in this
instance were correlated with a possible role of macrophages in immune
response manipulation and tumor inhibition in these models.

The intricacy of these interactions and their effect on tumor development
in each model prompted the present proposal to explore the immunologic
effects of poly I:C both regionally and in a metastatic model in which
immune response manipulation and its effects on tumor at selected sites
would be assessed both in intact animals and in animals deficient in
selected immune response components.  C3H mice naturally deficient in
T-cell function (homozygous nudes), macrophage function (HeJ vs HeN), or
natural killer cell function (beige), as well as animals treated with
silica, carrageenan, cimetidine, and/or specific anti-interferon antisera
would be used for study of tumor development in both the carcinogen-induced
and metastatic models.  Immunologic effects of poly I:C would be assessed
by examination of lymphocyte and macrophage cytotoxicity (51Chromium
release assay using NK- and T-cell sensitive cell lines), lymphocyte
response in mixed lymphocyte- and mixed lymphocyte/tumor cell culture, and
changes in lymphocyte subpopulations (immunofluorescent labelling of
specific surface markers).  Each of these in vitro assessments would be
correlated with tumor development and progression in each model.

Specific aims of these studies are to characterize further the role of
different components of immune response expression on primary regional and
systemic tumor development, effects of deficiencies of selected
compartments on tumor progression, and effects of poly I:C in the
immunologic manipulation of these components on both tumor growth and
progression.  The relevance of these animal models to both superficially
invasive and metastatic disease as seen clinically suggest our long-term
objectives which are to determine suitable regimens for adaptation in the
treatment of both regional and metastatic bladder cancer in man.

## Key facts

- **NIH application ID:** 3177936
- **Project number:** 5R01CA039187-04
- **Recipient organization:** MOUNT SINAI SCHOOL OF MEDICINE OF CUNY
- **Principal Investigator:** Michael J. Droller
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $147,546
- **Award type:** 5
- **Project period:** 1984-07-01 → 1988-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3177936

## Citation

> US National Institutes of Health, RePORTER application 3177936, CELLULAR IMMUNE RESPONSE MECHANISMS IN BLADDER CANCER (5R01CA039187-04). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3177936. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*