# BIOCHEMICAL PATHOLOGY OF IRON STORAGE IN LIVER CANCER

> **NIH NIH R01** · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · 1987 · $120,416

## Abstract

Hepatocellular carcinoma cells, unlike adjacent normal liver cells, resist
the accumulation of extra storage iron when confronted with parental iron
overload.  The cause and consequences of this biochemical pathology of iron
storage in neoplastic cells is unknown; moreover, the relationship between
this abnormal iron metabolism and the correlated presence of
inappropriately increased amounts of the iron-storage protein, ferritin, is
not understood.  The hypothesis that neoplasia causes abnormal iron
metabolism will be tested by the proposed experiments.  Both in vivo
approaches with human and murine hepatoma systems will be utilized.  The
relative amounts of different types of storage iron formed before and after
experimental iron overload in transplantable hepatomas and host liver will
be measured with light microscope histochemistry, immunochemistry, and
analytical chemistry.  Immunocytochemistry will be used to compare the
relative levels of ferritin in these same samples with and without iron
overload.  The actual uptake of injected iron-dextran and its resultant
subcellular processing into ferritin and hemosiderin will be measured in
hepatoma and liver cells by electron microscopy.  The major possibility
that hepatoma cells have defective uptake of iron from the iron-transport
protein, transferrin, will be tested by biochemical assays; analogous
measurements will examine the subsequent movement of iron from transferrin
into ferritin, and the ability of the tumor cells to release their
internalized iron to extracellular transferrin.  Corresponding experimental
investigations also will be conducted with induced hepatocarcinogenesis, to
evaluate the capacity for iron storage within the very earliest stages in
the progression to hepatocellular neoplasia; the formation of increased
ferritin and the coordinate presence of other normal or cancer-associated
proteins (albumin, alpha-fetoprotein) will be examined in these very early
tumor cells.  The results obtained will provide important new information
about the biochemical pathology of iron storage and iron proteins in liver
cancer and hepatocarcinogenesis, and should be of value for new clinical
approaches to its detection, diagnosis, and therapy.  (W)

## Key facts

- **NIH application ID:** 3177706
- **Project number:** 5R01CA039040-03
- **Recipient organization:** UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL
- **Principal Investigator:** WILLIAM H MASSOVER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $120,416
- **Award type:** 5
- **Project period:** 1985-02-01 → 1989-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3177706

## Citation

> US National Institutes of Health, RePORTER application 3177706, BIOCHEMICAL PATHOLOGY OF IRON STORAGE IN LIVER CANCER (5R01CA039040-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3177706. Licensed CC0.

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