# Artemin overexpression in oral cancer pain and carcinogenesis

> **NIH NIH R01** · NEW YORK UNIVERSITY · 2021 · $490,586

## Abstract

Oral cancer patients suffer severe chronic and mechanically-induced pain. Opioids are initially
effective, but dose escalation is required and side effects reduce quality of life. The long-term
goal is to improve management of oral cancer and oral cancer pain. Oral cancer pain is initiated
and maintained in the cancer microenvironment. Some overexpressed cancer genes,
oncogenes, can function in an autocrine manner to promote cancer and in a paracrine manner
as cancer pain mediators. The ensemble of altered genes/pathways in a cancer dictates
response to treatment, which motivates the use of combinatorial therapies tailored to the
individual (precision medicine) to both treat the cancer and pain. The overall objectives of this
application are to determine (a) whether artemin (ARTN), a gene overexpressed in oral cancer
is an oral cancer oncogene, (b) whether ARTN is an oral cancer pain mediator and (c) whether
antagonizing ARTN stops oral cancer and alleviates oral cancer pain. The central hypothesis is
that there are oral cancer oncogenes that promote cancer and induce oral cancer pain. The
rationale for this project is that proalgesic oncogenes could be targeted to treat cancer and pain.
The central hypothesis will be tested by pursuing three specific aims: (1) Determine if ARTN is a
proalgesic oncogene in human cancer; (2) Determine whether ARTN is an oncogene and a
nociceptive mediator; and (3) Determine the potential to stop oral cancer and alleviate oral
cancer pain by antagonizing proalgesic oncogenes. In the first aim, expression of ARTN will be
assessed by immunohistochemistry in archival specimens from patients who completed the
UCSF Oral Cancer Pain Questionnaire (UCSFOCPQ) to determine if expression is correlated
with pain. The second aim will evaluate the function of ARTN as an oncogene by manipulating
expression in cultured cells in vitro and in human xenograft mouse models. Whether ARTN is a
pain mediator will be assessed by measuring nociception induced by manipulating expression of
ARTN in animal models in the absence of cancer growth. For the third aim, the potential of
antagonizing ARTN to stop cancer and cancer pain will be evaluated by anti-ARTN treatment of
mouse xenograft and carcinogenesis models. The proposed research is innovative in the
applicants' opinion, because it uses information gained from genomic analysis of oral cancers to
identify putative oral cancer proalgesic oncogenes. The research is significant because it is
expected to lay the foundation for future clinical trials assessing the utility of targeting ARTN for
cancer treatment and attenuation of cancer pain. The work will motivate identification of
additional proalgesic oncogenes to improve precision cancer pain management.

## Key facts

- **NIH application ID:** 10242843
- **Project number:** 5R01CA228525-03
- **Recipient organization:** NEW YORK UNIVERSITY
- **Principal Investigator:** Donna G Albertson
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $490,586
- **Award type:** 5
- **Project period:** 2019-09-01 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10242843

## Citation

> US National Institutes of Health, RePORTER application 10242843, Artemin overexpression in oral cancer pain and carcinogenesis (5R01CA228525-03). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10242843. Licensed CC0.

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