Evidence map›Paper›PMID 39660489›Full record

ArticleCurrent neuropharmacology2025

Programmed Cell Death Protein 1 Contributes to Oral Cancer Pain via Regulating Tumor Necrosis Factor Alpha in the Spinal Trigeminal Nucleus Caudalis.

Runyi Mao, Sufang Liu, John C Dolan, Brian L Schmidt, Feng Tao

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In one paragraph

Article in Current neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Runyi MaoDepartment of Biomedical Sciences, Texas A&M University School of Dentistry, Dallas, Texas, USA.
Sufang LiuDepartment of Biomedical Sciences, Texas A&M University School of Dentistry, Dallas, Texas, USA.
John C DolanNYU Dentistry Translational Research Center, New York University College of Dentistry, New York, NY, USA.
Brian L SchmidtNYU Dentistry Translational Research Center, New York University College of Dentistry, New York, NY, USA.
Feng TaoDepartment of Biomedical Sciences, Texas A&M University School of Dentistry, Dallas, Texas, USA.

Funding

Cancer Prevention & Research Institute of Texas RP220626NIH HHS R01DE031255, R01DE032061, R01DE026806
6 · The paper itself

Abstract

backgroundOral cancer causes intense pain at the primary site, and such pain can impair oral functions. However, the underlying mechanisms for oral cancer pain are still not fully understood. In the present study, it is investigated whether programmed cell death protein 1 (PD-1) is involved in the development of oral cancer pain.

methodsRMP1-14, a specific anti-PD-1 antibody, was injected into spinal trigeminal nucleus caudalis (Sp5C) and measured pain behaviors using von Frey filaments and dolognawmeter. Western blotting and immunofluorescence staining were performed to analyze the expression of PD-1 and tumor necrosis factor alpha (TNFα) in the Sp5C.

resultsIt was observed that the PD-1 antibody significantly inhibited mechanical hypersensitivity and functional allodynia in our oral cancer pain mouse model. Moreover, we found that TNFα was highly upregulated in the Sp5C following the induction of oral cancer pain and that intra-Sp5C injection of the PD-1 antibody diminished the upregulation of TNFα. It was found that genetic deletion of TNFα or its receptor antagonism synergized the analgesic effect of PD-1 antibody on oral cancer pain.

conclusionOur results suggest that PD-1 in the Sp5C contributes to oral cancer pain by altering TNFα signaling in the trigeminal nociceptive system, and PD-1 could be targeted to develop a novel approach for oral cancer pain management.

Indexed as

Cancer PainMouth NeoplasmsProgrammed Cell Death 1 ReceptorTrigeminal Nucleus, SpinalTumor Necrosis Factor-alphaAnimalsDisease Models, AnimalHyperalgesiaMaleMiceMice, Inbred C57BLPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorTumor Necrosis Factor-alphafunctional allodyniahypersensitivityOral cancer painprogrammed cell death protein 1spinal trigeminal nucleus caudalistumor necrosis factor-alpha.

Identifiers

PMID39660489
PMCPMC12163463

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