# EFFECTS OF PROSTATE CANCER ON SKELETAL TISSUE

> **NIH NIH R01** · MCGILL UNIVERSITY · 1987 · $14,256

## Abstract

Adenocarcinoma of the prostate exhibits a marked propensity to metastasize
to the skeleton, where it commonly produces osteoblastic rather than
osteolytic lesions.  Although such bone-producing lesions may be due to
inhibition of bone resorbing cells (directly or via stimulation of
osteoclast-inhibiting agents such as calcitonin), most evidence suggests
that osteoblast numbers and activity are directly enhanced.  Preliminary
evidence indicates this might be due to the production by prostate cancer
of osteoblast-stimulating humoral factors.  The proposed studies are
directed at isolating and chemically purifying such humoral factors from
freshly isolated human prostate tissue (normal, hyperplastic and
neoplastic), from human prostate cancer cell lines, from transplantable rat
prostate cancers grown in vivo and in vitro, and from conditioned tissue
culture medium.  As bioassays for osteoblast-stimulating activity,
proliferation and function of isolated fetal or neonatal rat calvarial
cells grown in monolayer culture, will be examined.  As indices of cell
proliferation, [H3] thymidine incorporation, and cell numbers will be
assessed; as indices of cell function, [14C] proline incorporation into
collagenase-digestible protein, synthesis of type I collagen, alkaline
phosphatase activity, and production of Gamma-carboxyglutamic acid
containing protein will be determined.  Additionally, rat osteogenic
sarcoma cell lines (osteoblast in origin) will be employed as an alternate
bioassay system, and similar indices followed.  Tissue and medium will be
extracted in hydrophobic and hydrophilic solvents.  Hydrophilic stimulatory
extracts will be purified by gel filtration and reversed-phase liquid
chromatography and/or iron exchange chromatography.  Lipophilic stimulatory
extracts will be purified by gel chromatography and normal phase high
pressure liquid chromatography.  Sufficient purification for development of
a radioimmunoassay and for structural analysis (amino acid analysis and
ultimately sequence analysis for a peptide factor) will be attempted.
Additionally skeletal lesions produced by transplantable rat tumors in vivo
will be examined histologically and for their capacity to alter osteoclast
numbers and osteoclast binding by calcitonin.  The studies therefore seek
to examine the mechanisms whereby metastatic prostatic adenocarcinoma alter
skeletal function, and aim to chemically characterize humoral factors which
may mediate effects on the skeleton.

## Key facts

- **NIH application ID:** 3174816
- **Project number:** 3R01CA037126-03S1
- **Recipient organization:** MCGILL UNIVERSITY
- **SAM.gov UEI:** VJ62F6V2LE48
- **Principal Investigator:** DAVID GOLTZMAN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $14,256
- **Award type:** 3
- **Project period:** 1984-09-30 → 1988-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3174816

## Citation

> US National Institutes of Health, RePORTER application 3174816, EFFECTS OF PROSTATE CANCER ON SKELETAL TISSUE (3R01CA037126-03S1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3174816. Licensed CC0.

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