# Novel Therapy to Inhibit IPMN Progression

> **NIH NIH R01** · H. LEE MOFFITT CANCER CTR & RES INST · 2024 · $74,401

## Abstract

PROJECT SUMMARY/ABSTRACT
Despite advances in therapeutic strategies, pancreatic ductal adenocarcinoma (PDAC) remains one of the
deadliest malignancies. An opportunity exists to impact mortality from PDAC by preventing the development of
the disease through preventing progression of one of its most important precursors, intraductal papillary
mucinous neoplasm (IPMN). IPMN is a significant health problem with a high prevalence with an estimate of 6%
of MRI studies obtained for other indications demonstrating IPMN(s). Although most IPMNs are quiescent, they
represent a source of great anxiety for patients because of the fear of developing PDAC. Since 30% of PDACs
arise from IPMNs, these lesions also represent an opportunity to intercept the development of PDAC. Therefore,
is an unmet need to develop biomarkers that predict IPMN progression and strategies to intercept IPMN
progression to PDAC. We have made substantial progress in developing strategies to intercept IPMN
progression as illustrated in the parent grant of this supplement application which is translating discoveries from
our laboratory regarding the role of a micronutrient (delta-tocotrienol (DT3)) in preventing IPMN progression in a
Phase 2 prospective randomized double-blind placebo-controlled trial. Emerging studies suggest that the IPMN
Tumor Immune Microenvironment (TIME) may play a critical role in a crosstalk with pancreatic ductal epithelial
cells in promoting the progression of IPMN to PDAC. However, the role of specific immune cells and the
underlying mechanisms driving TIME mediated IPMN progression is poorly understood. To address this
knowledge gap, we propose to test the central hypothesis that crosstalk between specific immune cells
and pancreatic ductal cells influence the switch from quiescent (low-grade) IPMN to aggressive (high-
grade) IPMN leading to invasive PDAC. Using a combination of human patient samples and genetically
engineered mouse models, as well as in vivo, in vitro, and in silico approaches, we propose to map immune cell
populations and functional status around normal pancreatic duct, low-grade IPMN, high-grade IPMN, and
invasive PDAC in humans (Aim 1); and define the function of immune cells at different stages of carcinogenesis
in human and mouse (Aim 2). The supplement will allow Mrs. Krystal Villalobos-Ayala to receive further training
in conducting basic and translational research. Her results will assist in defining the role of TIME in PDAC
evolution ultimately contributing to further insights into novel immunological strategies to intercept IPMN
progression to PDAC.

## Key facts

- **NIH application ID:** 11063689
- **Project number:** 3R01CA263575-03S1
- **Recipient organization:** H. LEE MOFFITT CANCER CTR & RES INST
- **Principal Investigator:** Surinder K. Batra
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $74,401
- **Award type:** 3
- **Project period:** 2022-06-08 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11063689

## Citation

> US National Institutes of Health, RePORTER application 11063689, Novel Therapy to Inhibit IPMN Progression (3R01CA263575-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/11063689. Licensed CC0.

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