# Comprehensive Cancer Center Support Grant

> **NIH NIH P30** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2024 · $185,625

## Abstract

ABSTRACT
This application is being submitted in response to the Notice of Special Interest (NOSI) identified as
NOT-CA-21-100.
 This proposal seeks to support Dr. Laura Stafman, a pediatric surgeon-scientist with both
research and clinical interests in pediatric solid tumors. This proposal builds upon her previous basic
science work while also deviating into the disparate field of metabolomics to allow her to establish herself as an
independent surgeon-scientist.
 Neuroblastoma is the most common pediatric solid tumor outside the brain. It has a poor prognosis and
for those who do survive, high morbidity. Those with high-risk disease have a survival rate around 50%. However,
there is a subset of tumors that are more differentiated and occur in younger patients. Some of these require no
treatment at all and either regress or differentiate into benign tumors spontaneously. These patients have been
shown to express more differentiation genes. Within neuroblastoma there are varying degrees of differentiation;
patients with undifferentiated disease have the worst prognosis. Treatment aimed to induce differentiation is
used in neuroblastoma given its ability to progress cells from a stem cell-like state to a more mature, differentiated
state. Cancer stem cells are a small subset of cells responsible for tumor initiation, recurrence, and drug
resistance. Differentiation, stemness, and metabolism are all linked together as metabolism controls stemness
and differentiation. If we can reprogram the cell metabolism from patients with undifferentiated neuroblastoma
or cancer stem cells (poor prognosis) to behave more like the patients with low-risk disease (better prognosis),
we may be able to more effectively treat neuroblastoma. It has been found that lipid metabolism in particular
plays a role in differentiation in neuroblastoma. PIM1 is a kinase that has been shown to play a role in
neuroblastoma differentiation as well; blocking PIM1 promotes differentiation. How this occurs is unknown, but
PIM kinases play a role in lipid metabolism in non-cancer cells.
 Therefore, the goal of this project is twofold: 1) to determine the aspects of lipid metabolism affected by
PIM1 and which of these regulates differentiation in neuroblastoma, and 2) to define the lipidomics landscape in
neuroblastoma cancer stem cells to determine vulnerabilities in this subpopulation of cells responsible for relapse
and recurrence. The findings hold promise for better understanding lipid metabolism in neuroblastoma in order
to determine potential novel therapeutics to target high-risk neuroblastoma.

## Key facts

- **NIH application ID:** 10994775
- **Project number:** 3P30CA013148-51S1
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** Barry P Sleckman
- **Activity code:** P30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $185,625
- **Award type:** 3
- **Project period:** 1997-03-28 → 2027-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10994775

## Citation

> US National Institutes of Health, RePORTER application 10994775, Comprehensive Cancer Center Support Grant (3P30CA013148-51S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10994775. Licensed CC0.

---

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