Evidence map›Paper›PMID 41898813›Full record

ArticleGenes2026

Multi-Omics Analysis of CDKN2A (p16INK4a) in Cervical Carcinoma in the Context of Human Papillomavirus and in Endometrial Carcinoma.

Rasha Elsayim, Heba W Alhamdi, Nihal Almuraikhi, Mariam Abdulaziz Alkhateeb, Taghreed Mohamed Osman Derar, Sami Habiballa Abdalla Mohamed, Esra'a Abudouleh

Abstract read
In one paragraph

Article in Genes, 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

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

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. Article
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

7 authors.

Rasha ElsayimDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Heba W AlhamdiDepartment of Biology, College of Sciences, King Khalid University, P.O. Box 960, Abha 61413, Saudi Arabia.ORCID 0000-0002-1908-9469
Nihal AlmuraikhiStem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.ORCID 0000-0003-4996-7565
Mariam Abdulaziz AlkhateebDepartment of Biology, College of Science, Princess Nourah bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.ORCID 0000-0001-8019-616X
Taghreed Mohamed Osman DerarHealth Sciences Department, College of Applied Studies, King Saud University, Riyadh 12372, Saudi Arabia.
Sami Habiballa Abdalla MohamedHealth Sciences Department, College of Applied Studies, King Saud University, Riyadh 12372, Saudi Arabia.
Esra'a AbudoulehDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-8922-0143

Funding

This work is expected to be funded by King Saud University upon acceptance of the manuscript. The funder will have no role in the study design, data acquisition, analysis, interpretation, or manuscript preparation 0000
6 · The paper itself

Abstract

backgroundCDKN2A (p16^INK4a^) is integral to the regulation of the RB-E2F cell-cycle checkpoint and is widely acknowledged as a surrogate marker for high-risk human papillomavirus (HPV)-related cervical neoplasia. Nevertheless, its diagnostic and prognostic significance in uterine corpus endometrial carcinoma (UCEC), a predominantly HPV-independent malignancy, remains inadequately characterized. This study utilized an integrated multi-omics approach to examine CDKN2A dysregulation in cervical squamous cell carcinoma (CESC) and UCEC.

methodsPan-cancer and tumor-normal differential expression analyses were performed using TIMER2.0 and GEPIA2 (TCGA/GTEx). Clinicopathological correlations were assessed with UALCAN. Protein expression patterns were analyzed using immunohistochemistry data from the Human Protein Atlas (HPA). Prognostic significance and immune-infiltration associations were evaluated using TCGA survival data and TIMER modules. Independent transcriptomic validation and diagnostic classification performance were assessed using GEO datasets GSE9750 (CESC) and GSE63678 (UCEC), including ROC-AUC analysis with cross-validation.

resultsIntegrated analyses revealed elevated CDKN2A expression in both CESC and UCEC across multiple transcriptomic cohorts, with pronounced tumor-specific protein expression on immunohistochemistry. TCGA-only tumor-normal RNA comparisons were non-significant, likely due to limited normal sample representation. In independent GEO cohorts, CDKN2A exhibited excellent tumor-normal discrimination in CESC (AUC = 0.982) and moderate discrimination in UCEC (AUC = 0.761). Survival analysis indicated tumor-specific patterns, with limited prognostic stratification in CESC and context-dependent associations in UCEC. Immune-infiltration analysis suggested tumor-type-specific interactions between CDKN2A expression and immune cell subsets.

conclusionsCDKN2A exhibits strong diagnostic performance in HPV-associated cervical cancer and moderate, cohort-dependent discriminatory ability in endometrial carcinoma. These findings reinforce its established diagnostic role in CESC and propose adjunctive utility in UCEC, underscoring the importance of tumor-contextual interpretation of CDKN2A expression in gynecologic malignancies.

Indexed as

Carcinoma, Squamous CellCyclin-Dependent Kinase Inhibitor p16Endometrial NeoplasmsPapillomavirus InfectionsUterine Cervical NeoplasmsBiomarkers, TumorFemaleGene Expression Regulation, NeoplasticHuman Papillomavirus VirusesHumansMultiomicsPrognosisBiomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16CDKN2Acervical squamous cell carcinomaendometrial carcinomahuman papillomavirustranscriptomic and proteomic evidence

Identifiers

PMID41898813
PMCPMC13025831

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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.