# CELLULAR AND HUMORAL MODULATION OF HEMOPOIESIS

> **NIH NIH R01** · STANFORD UNIVERSITY · 1988 · $112,300

## Abstract

We will evaluate factors involved in the humoral and cellular
modulation of hemopoiesis in normal individuals and those with
hemopoietic diseases, including acute myeloid leukemia (AML) and
myelodysplastic syndromes (MDS).  Major emphasis will be placed on
evaluating (1) the in vitro interactions between purified
recombinant human polypeptide hemopoietic growth:  factors (HGFs)
and human hemopoietic cells, and (2) the roles of enriched
populations of accessory marrow and blood cells in generating HGFs
under the influence of interleukin 2 (IL2) and other immune
modulators.  We are using a library of recombinant HGFs and
monoclonal antibodies and have developed a variety of cell
separation techniques, ligand binding procedures and serum-free
cell proliferation, differentiation and clonogenic assays to
perform these studies.  Specific objectives regarding (1) hormonal
interactions, are to determine, at the level of specific cell
surface receptors, the role of the mesodermal stimulatory hormones
insulin and insulin-like growth factors (IGFI & II) for modulating
hemopoietic cell proliferation and differentiation, either directly
or via alteration of receptor binding action for colony stimulating
factor (GM-CSF) or erythropoietin.  We will evaluate the hypothesis
that multiple growth factors, including insulin and IGFs, interact
in situ to provide cellular competence and progression factors for
hemopoiesis. As hemopoietic progenitor cell (HPC) survival is
partly mediated through HGF effects on glucose transport and ATP
generation, we will examine the interactions between the
metabolically active mitogenic hormones insulin, IGFs and CSFs to
probe mechanisms of hemopoietic regulation.  Studies using
supplemented serum-free medium will be performed with human myeloid
and erythroid cell lines and enriched HPCs as target cells to more
precisely determine the functional effects and relationships
between HGFs.  Further, we will assess production of IGFs by these
cells to evaluate the possible autocrine or paracrine roles of
these hormones for leukemic vs normal cell growth.  (2) We will
examine the role of IL2 in enhancing provision of HGFs by enriched
T and non T- cell subsets, with particular emphasis on the effector
function of natural killer (NK) cells.  We will assess production
of proliferative (GM-CSF, BPA) and differentiative factors (G-CSF,
DF) by resting T and NK cells (which lack TAC+ IL2 receptors) vs
such activated Tac+) cells to evaluate the role of IL2 receptors
in generating HGFs.  After standardizing techniques to define HGF
production, binding and responsiveness by normal myeloid cells and
leukemic cell lines, we will (3) evaluate these parameters for
cells from our patients with hemopoietic diseases, particularly AML
and MDS, and will classify these disorders according to such basic
cellular defects in growth regulation.

## Key facts

- **NIH application ID:** 3174554
- **Project number:** 2R01CA036915-04A1
- **Recipient organization:** STANFORD UNIVERSITY
- **SAM.gov UEI:** HJD6G4D6TJY5
- **Principal Investigator:** PETER L GREENBERG
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $112,300
- **Award type:** 2
- **Project period:** 1984-03-01 → 1990-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3174554

## Citation

> US National Institutes of Health, RePORTER application 3174554, CELLULAR AND HUMORAL MODULATION OF HEMOPOIESIS (2R01CA036915-04A1). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3174554. Licensed CC0.

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