# Targeting OSCC cells with a lozenge to treat oral cancer

> **NIH NIH R41** · SENTRIMED, INC. · 2022 · $322,833

## Abstract

Abstract/Summary
 Oral cancer kills over 8,000 people in the USA and 120,000 people worldwide every year. Over 90% of
oral cancers are caused by oral squamous cell carcinoma (OSCC), and these cells are notoriously resistant to
chemotherapeutic agents. Radiation and surgery are used to treat oral cancer patients, but cause
disfigurations and sequelae that drastically decrease the quality of life for survivors.
 The vast majority of OSCC cells express PDPN, which is a transmembrane mucin receptor that
promotes oral cancer progression. Precancerous oral lesions (e.g. leukoplakia) that express high levels of
PDPN are several times more likely to become oral cancers than lesions that do not express PDPN. Thus,
PDPN presents a functionally relevant target that can be used to detect and treat oral cancer. We found that
Maackia amurensis seed lectin (MASL) targets PDPN to kill OSCC cells. Moreover, MASL is nontoxic and can
be administered orally to inhibit tumor growth and vascularization in mice.
 We propose 3 Specific Aims to evaluate the effects of MASL on OSCC cells ex vivo and in a Phase 1
human clinical trial. In Aim 1, we will evaluate OSCC morphology, PDPN expression, vascularization, and T-
cell infiltration in oral cancer patients by IHC. Patients with lesions containing OSCC cells that express robust
levels of PDPN will be considered for treatment. In Aim 2, we will evaluate effects of MASL on OSCC
morphology, PDPN expression, angiogenesis, and T-cell infiltration in oral cancer lesions taken from patients
by biopsy or resections. In Aim 3, we will evaluate the effects of MASL on PDPN expression, motility, and
growth of OSCC cells cultured from oral cancer patients examined in Aims 1 and 2.
 We will produce oral lozenges containing MASL that will dissolve in the mouths of oral cancer patients
for direct and systemic administration to treat oral lesions that express PDPN as defined in Aim 1. We will
analyze OSCC morphology, PDPN expression, angiogenesis, and T-cell infiltration in samples taken from
these excisions. We hypothesize that MASL will decrease OSCC dysplasia, PDPN expression, and
vascularization in these patients. We also suspect that MASL will increase T-cell tumor infiltration since PDPN
has been identified as an inhibitory receptor on effector T-cells. These data will also determine how PDPN
expression and MASL sensitivity in actual patients compares to their ex vivo cell culture studies from Aim 2.
 Positive results from this project will change the clinical paradigm currently used to treat oral cancer.
Benign oral lesions are currently “watched and waited”, while OSCC is treated by surgery and radiation. Our
new paradigm will use MASL to target PDPN, which enables benign cells to develop into OSCC. Therefore,
this work should improve our ability to treat oral cancer, and other malignancies that express PDPN including
breast, glioma, lung, and skin cancer.

## Key facts

- **NIH application ID:** 10479625
- **Project number:** 1R41CA268160-01A1
- **Recipient organization:** SENTRIMED, INC.
- **Principal Investigator:** Gary Goldberg
- **Activity code:** R41 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $322,833
- **Award type:** 1
- **Project period:** 2022-08-01 → 2024-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10479625

## Citation

> US National Institutes of Health, RePORTER application 10479625, Targeting OSCC cells with a lozenge to treat oral cancer (1R41CA268160-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10479625. Licensed CC0.

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