# CALCIUM-GROWTH IN NEOPLASTIC-NONNEOPLASTIC FIBROBLASTS

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 1990 · $162,168

## Abstract

The long-term objective of our work is to discover growth-regulatory
differences between neoplastic and nonneoplastic cells that can be
exploited in chemotherapy.  One aspect of growth regulation in
nonneoplastic cells that has been intensively investigated recently is
the role of increases in free intracellular calcium (Cai) and pH (pHi).
Our previous grant award has helped develop the technology to measure Cai
and pHi in individual cells.

The short-term objective of our studies is to utilize this technology to
determine how the increases in Cai and/or pHi are correlated with -- and,
in certain instances, required for -- growth stimulation of quiescent
nonneoplastic fibroblasts (BALB/c 3T3 and human cells).

The specific aims include:  1) Examination of the role of ionic signals
in the growth stimulation of nonneoplastic cells in monolayer culture.
For competence factors, we will focus on platelet-derived growth factor
(PDGF), fibroblast growth factor (FGF) and comitogens, such as tumor
promoters (TPA) or calcium ionophore (A23187).  Our studies have already
indicated that a transient Cai increase is required for PDGF-stimulated
DNA synthesis in quiescent BALB/c 3T3 cells.  The present application
focuses on defining what other intracellular signals (e.g., DAG)
potentiate this mitogenic effect of Cai increase and what early genes are
activated by these specific signals.  For progression factors, we will
study and compare EGF, insulin, IGF-1 and plasma.  We will concentrate on
determining the signalling pathways involved in the dependence of
progression events on extracellular Ca2+.  2) Definition of the role of
ionic signals in the growth-resistance of nonneoplastic cells in
suspension culture.  We will determine which of the intracellular signals
induced by growth factors does not occur in suspended cells.  3)
Examination of ionic signals and gene activation in neo-plastic cells.
We will determine which of the early intracellular signals are absent or
constitutively activated in neoplastic cells (e.g., 3T12, ras-
transformants, sis-transformants).  These tests will help us to determine
whether gene activation stimulated by ionic signals (Cai and pH1) is an
important aspect of the normal growth regulation that is controlled by
exogenous growth factors and attachment to substratum, and whether
deregulation of these signals results in the unrestrained growth of
neoplasms.

## Key facts

- **NIH application ID:** 3172201
- **Project number:** 5R01CA034472-05
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **SAM.gov UEI:** FTMTDMBR29C7
- **Principal Investigator:** ROBERT W TUCKER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $162,168
- **Award type:** 5
- **Project period:** 1984-08-01 → 1992-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3172201

## Citation

> US National Institutes of Health, RePORTER application 3172201, CALCIUM-GROWTH IN NEOPLASTIC-NONNEOPLASTIC FIBROBLASTS (5R01CA034472-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3172201. Licensed CC0.

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