Evidence map›Paper›PMID 41403289›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2026

Pattern-based p53 and p16 Immunohistochemistry as a Potential Alternative to Loss of Heterozygosity Testing for Progression Risk of Oral Epithelial Dysplasia.

Kelly Yi Ping Liu, Yen Chen Kevin Ko, Catherine F Poh

Abstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

What it found

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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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

1 citing paper in PubMed.

  1. Review
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

3 authors.

Kelly Yi Ping LiuDepartment of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, Vancouver, Canada.ORCID 0000-0003-4067-6913
Yen Chen Kevin KoDepartment of Pathology, BC Cancer, Vancouver, Canada.ORCID 0000-0001-6081-5971
Catherine F PohDepartment of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, Vancouver, Canada.ORCID 0000-0003-2867-9580

Funding

BC Cancer FoundationCanadian Institutes of Health Research (CIHR)University of British Columbia (UBC)
6 · The paper itself

Abstract

Oral epithelial dysplasia (OED) is the precursor to oral squamous cell carcinoma, but histologic grading alone lacks reproducibility and prognostic power. This study evaluates whether pattern-based p53 and p16 immunohistochemistry (IHC) can serve as alternative markers to genomic loss of heterozygosity (LOH) testing in predicting OED progression. From a previously characterized LOH cohort, 64 patients were assessed with IHC for p53 and p16 using defined abnormal staining patterns (overexpression, cytoplasmic, or null). Abnormal p53 expression occurred in 19% of cases, with 93% specificity, and was significantly associated with reduced progression-free survival (PFS; 8-year PFS, 25% vs. 74%; P = 0.0011). Abnormal p16 expression was observed in 56% of cases with 95% sensitivity and was significantly associated with 8-year PFS (42% vs. 96%; P < 0.0001). Combined p53/p16-abnormal IHCs identified 95% of the progressing lesions and yielded superior risk discrimination (log-rank P < 0.0001), particularly at the 3-year follow-up mark. Concordance analysis revealed moderate agreement between p16 IHC and 9p LOH (κ = 0.39) and fair agreement between p53 IHC and 17p LOH (κ = 0.21), indicating that IHC and LOH detect related but distinct molecular disruptions. Chronologic evaluation of serial biopsies supported a sequential model in which p16 alteration precedes p53 alteration during malignant progression. Taken together, these findings highlight the potential of a pattern-based approach with combined p53/p16 IHC as a feasible, scalable, and clinically accessible tool to guide surveillance intensity and timely clinical intervention, thereby reducing progression risks. PREVENTION RELEVANCE: In this study, we demonstrate that p53/p16 pattern-based IHC provides a practical and sensitive tool for predicting progression in OED. Its clinical accessibility may facilitate early detection of high-risk lesions, optimizing triage, surveillance, and preventative treatment strategies to reduce the incidence of high-grade lesions or oral cancer.

Indexed as

Biomarkers, TumorCyclin-Dependent Kinase Inhibitor p16Mouth NeoplasmsPrecancerous ConditionsTumor Suppressor Protein p53AdultAgedDisease ProgressionFemaleFollow-Up StudiesHumansImmunohistochemistryLoss of HeterozygosityMaleMiddle AgedMouth MucosaBiomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID41403289
PMCPMC13012246

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.