{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T23:19:33Z","timestamp":1791674373257,"version":"4.3.4"},"reference-count":21,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,6,28]],"date-time":"2019-06-28T00:00:00Z","timestamp":1561680000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Histopathology"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:sec><jats:title>Aim<\/jats:title><jats:p>To further characterise the thin variant of high\u2010grade squamous intraepithelial lesions (HSILs) of the cervix defined by the World Health Organization as full\u2010thickness HSILs with nine or fewer cell layers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>We examined 31 excisional cervical specimens featuring exclusively p16<jats:sup>INK4a<\/jats:sup>\u2010overexpressing thin HSILs with respect to size, location at the squamocolumnar junction or endocervical mucosa, human papilloma virus (HPV) subtypes (pretherapeutic clinical HPV tests and HPV genotyping on lesional tissue after excision), and somatic mutations in 50 cancer genes. Thin HSILs were typically solitary lesions, located at the squamocolumnar junction (20\/31; 65%), in the endocervical columnar epithelium (6\/31; 19%), and in both locations (5\/31; 16%). The horizontal extension of thin HSILs ranged from 100\u00a0\u00b5m to 8\u00a0mm, with 30% being &lt;1\u00a0mm. HPV data were available for 27 specimens. Twenty of 27 (74%) thin HSILs showed high\u2010risk HPV subtypes: HPV16 (<jats:italic>n<\/jats:italic>\u00a0=\u00a08), HPV16 with coinfection (<jats:italic>n<\/jats:italic>\u00a0=\u00a02), HPV18 (<jats:italic>n<\/jats:italic>\u00a0=\u00a01), HPV31 (<jats:italic>n<\/jats:italic>\u00a0=\u00a01), HPV33 (<jats:italic>n<\/jats:italic>\u00a0=\u00a02), HPV52\/58 (<jats:italic>n<\/jats:italic>\u00a0=\u00a02), and \u2018other\u2019 high\u2010risk HPV genotypes (<jats:italic>n<\/jats:italic>\u00a0=\u00a04). Five of 27 (19%) thin HSILs showed possibly carcinogenic subtypes: HPV53 (<jats:italic>n<\/jats:italic>\u00a0=\u00a03), HPV73 (<jats:italic>n<\/jats:italic>\u00a0=\u00a01), and HPV82 (<jats:italic>n<\/jats:italic>\u00a0=\u00a01). One thin HSIL was induced by low\u2010risk HPV6 and one by the unclassified subtype HPV44. Somatic gene mutations were not identified.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Thin HSILs were typically small lesions without somatic gene mutations. Two\u2010thirds of thin HSILs developed after a transforming infection with high\u2010risk HPV subtypes, and one\u2010third were induced by non\u2010high\u2010risk HPV subtypes. If cervical cancer screening relies solely on presently available clinical HPV DNA tests, a significant percentage of women with HSIL will be missed.<\/jats:p><\/jats:sec>","DOI":"10.1111\/his.13869","type":"journal-article","created":{"date-parts":[[2019,3,30]],"date-time":"2019-03-30T09:49:50Z","timestamp":1553939390000},"page":"405-412","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Thin variant of high\u2010grade squamous intraepithelial lesion \u2013 relationship with high\u2010risk and possibly carcinogenic human papilloma virus subtypes and somatic cancer gene mutations"],"prefix":"10.1111","volume":"75","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7077-578X","authenticated-orcid":false,"given":"Sigrid","family":"Regauer","sequence":"first","affiliation":[{"name":"Diagnostic and Research Institute of Pathology Medical University Graz Graz 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