ArticleHead and neck pathology2025
Loss of Heterozygosity in Oral Potentially Malignant Disorders and Oral Squamous Cell Carcinoma - A Scoping Review.
Article in Head and neck pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
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Who cites it
2 citing papers in PubMed.
- Molecular and microenvironmental drivers of malignant transformation from oral potentially malignant disorders to oral squamous cell carcinoma.Frontiers in oncology · 2026Review
- Salivaomic Biomarkers-An Innovative Approach to the Diagnosis, Treatment, and Prognosis of Oral Cancer.Biology · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThis scoping review was conducted to ascertain the loss of heterozygosity (LOH) signatures reported in Oral Potentially Malignant Disorders (OPMD) and Oral Squamous Cell Carcinoma (OSCC), in the literature in the last fifty years.
methodsThe Joanna Briggs Institute recommendations (2023) for scoping review were used to extract, analyze, and present the results. The review was reported according to the PRISMA guidelines for Scoping Reviews (PRISMA-ScR). The most commonly reported genes associated with LOH in OPMD and OSCC are discussed. The Gene Ontology functional enrichment analysis gives the significance of the protein-protein interactions (PPI) of these genes using the STRING database.
resultsAn exhaustive database search of the title, abstract, and full-text screening consistent with the eligibility criteria yielded 277 studies. LOH commonly studied in OPMD and OSCC include p53 gene, p16 gene, adenomatous polyposis coli gene, retinoblastoma (Rb) gene, fragile histidine triad (FHIT) gene and phosphatase and tensin homolog (PTEN) gene. Chromosome loci involving 17p, 9p, 5q, 13q, 3p, and 10q were frequently reported in OPMD and OSCC. PPI analysis demonstrated strong evidence of p53 interaction with p16, FHIT, and Rb.
conclusionDistinctive signatures of LOH are seen in OPMD and OSCC. The LOH patterns identified in this scoping review underline the significance of advanced molecular techniques and the need for long-term prospective cohorts to understand LOH pathophysiology in oral carcinogenesis to enable their usefulness as biomarkers in early diagnosis, treatment, and prognostication of oral cancer.
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Registered trials
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