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<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">DH</journal-id><journal-title-group><journal-title>Dermatological Health</journal-title></journal-title-group><issn>3083-4775</issn><eissn>2981-8206</eissn><publisher><publisher-name>Bio-Byword Scientific Publishing Pty. Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.26689/dh.v2i3.8494</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>Exploring the Role of CDKN2A in Human Cancers Using an Integrative Pan-Cancer Approach</title><url>https://artdesignp.com/journal/DH/2/3/10.26689/dh.v2i3.8494</url><author>RazaSyed Hussain,AliAkbar</author><pub-date pub-type="publication-year"><year>2024</year></pub-date><volume>2</volume><issue>3</issue><history><date date-type="pub"><published-time>2024-10-15</published-time></date></history><abstract>This study aims to investigate the expression variation, biological significance, and prognostic value of cyclin-dependent kinase inhibitor 2A (CDKN2A) as a common biomarker across 33 malignancies. Various bioinformatics tools, including UALCAN, GEPIA2, OncoDB, cBioPortal, TIMER2, STRING, DAVID, and the GSCA database, were employed for this pan-cancer analysis. The results revealed significant up-regulation of CDKN2A in 24 major human cancer subtypes (P &amp;lt; 0.05). This up-regulation was strongly associated with poor overall survival and tumor dissemination, particularly in uterine corpus endometrial carcinoma (UCEC), colon adenocarcinoma (COAD), and liver hepatocellular carcinoma (LIHC), highlighting its potential as a prognostic biomarker. Moreover, CDKN2A overexpression was linked to diverse clinicopathological characteristics of patients. Genetic alterations recorded via cBioPortal indicated minimal mutation rates in COAD, LIHC, and UCEC. Additionally, promoter methylation, drug sensitivity, and enrichment analyses were performed to explore associations with CDKN2A expression. 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