# Bidirectional interaction of platelets and tumor cells in patients with glioblastoma

> **NIH NIH R01** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2020 · $490,666

## Abstract

PROJECT SUMMARY
Glioblastoma is among the most lethal of all cancers and the most common primary malignant brain tumor,
typically lethal by 15 months. After initial tumor resection, we rely on an imperfect measure of disease response,
namely magnetic resonance brain imaging, as obtaining tumor tissue at recurrence is often dangerous or fails to
impact survival and is rarely performed. Indeed, many patients rely only on a tiny biopsy for initial diagnosis with
no ability for subsequent deep molecular analyses, let alone monitoring of disease over time. The current
proposal will address a fundamental gap in the field of GBM, i.e. the lack of predictors not dependent on the
availability of tumor tissue and those that can provide real-time, tissue-free tumor monitoring, which is particularly
critical in monitoring treatment response and assessing disease progression longitudinally. Blood-based
biomarkers such as circulating tumor cells and cell free DNA are attractive, but have yet to provide meaningful
results in GBM (compared to other cancers) and have yet to become clinical diagnostics. Tumor educated
platelets (TEPs) has recently been reported and shown to contain tumor-specific gene expression signatures
that are associated with outcome for several tumor types, but the clinical value and the mechanisms of
enrichment of TEPs are unknown. The overall goals of this proposal are to elucidate the mechanism underlying
the tumor cell–platelet interaction that leads to TEPs and to develop a TEP-based liquid biopsy platform for
longitudinal monitoring of disease in patients with GBM. In this project, we will test the hypothesis that platelet
numbers are increased in response to tumor signaling in the bone marrow and that platelets take up tumor-
derived extracellular vesicles containing RNA cargo in a PDPN dependent manner. TEP RNA signatures reflect
underlying tumor biology, growth, and treatment resistance, and will be utilized as biomarkers.
 In Aim 1, we will test the hypothesis that pro-inflammatory cytokine-mediated paraneoplastic
thrombocytosis promotes formation of TEP signatures in GBM. In Aim 2, we will test the hypothesis that PDPN
interaction with the CLEC2 receptor contributes to transfer of RNA from tumor cells to platelets. In Aim 3, we will
test the hypothesis that TEP RNA signatures can be used to monitor disease burden longitudinally in patients
with GBM.

## Key facts

- **NIH application ID:** 9832183
- **Project number:** 5R01CA225963-03
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Krishna PL Bhat
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $490,666
- **Award type:** 5
- **Project period:** 2018-12-05 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9832183

## Citation

> US National Institutes of Health, RePORTER application 9832183, Bidirectional interaction of platelets and tumor cells in patients with glioblastoma (5R01CA225963-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9832183. Licensed CC0.

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