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Since its role in PTC is not fully understood, we conducted a pooled analysis of genomic characteristics and clinical correlates in 1094 primary tumors from four published PTC genomic studies. The majority of PTC cases with 22qDEL exhibited arm-level loss of heterozygosity (86%); nearly all PTC cases with 22qDEL had losses in 22q12 and 13, which together constitute 70% of the q arm. Our analysis confirmed that 22qDEL occurs more frequently with RAS point mutations (50.4%), particularly HRAS (70.3%), compared with other PTC drivers (9.3%), supporting the conclusion that 22qDEL is unlikely to be a solitary driver of PTC but possibly an important co-factor in carcinogenesis, particularly in PTCs with RAS driver mutations. Differential RNA expression analyses revealed downregulation of most genes located on chromosome 22 in cases with 22qDEL compared to those without 22qDEL. Many differentially expressed genes are drawn from immune response and regulation pathways. These findings highlight the value of further investigations into the contributions of 22qDEL events to PTC, perhaps mediated through immune perturbations.<\/jats:p>","DOI":"10.1530\/etj-24-0235","type":"journal-article","created":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T13:42:46Z","timestamp":1736257366000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-17","source":"Crossref","is-referenced-by-count":2,"title":["Somatic copy number deletion of chromosome 22q in papillary thyroid carcinoma"],"prefix":"10.1530","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5389-6267","authenticated-orcid":true,"given":"Olivia W","family":"Lee","sequence":"first","affiliation":[{"name":"Laboratory of Genetic Susceptibility, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 1 , , ,","place":["Bethesda, Maryland, USA"]},{"name":"Integrative Tumor Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 2 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle M","family":"Karyadi","sequence":"additional","affiliation":[{"name":"Laboratory of Genetic Susceptibility, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 1 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen W","family":"Hartley","sequence":"additional","affiliation":[{"name":"Laboratory of Genetic Susceptibility, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 1 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weyin","family":"Zhou","sequence":"additional","affiliation":[{"name":"Cancer Genomics Research Laboratory, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research 3 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitchell J","family":"Machiela","sequence":"additional","affiliation":[{"name":"Integrative Tumor Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 2 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahriar A","family":"Zamani","sequence":"additional","affiliation":[{"name":"Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health 4 , , ,","place":["Bethesda, Maryland, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liudmyla Yu","family":"Zurnadzhy","sequence":"additional","affiliation":[{"name":"Laboratory of Morphology of the Endocrine System, V.P. 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