Clonal Relationship Between Lichen Sclerosus, Differentiated Vulvar Intra-epithelial Neoplasia and Non HPV-related Vulvar Squamous Cell Carcinoma
Differentiated vulvar intraepithelial neoplasia (dVIN) and lichen sclerosus (LS) can give rise to vulvar squamous cell carcinoma (VSCC), but genetic evidence is currently still limited. We aimed to determine genetic abnormalities in VSCC and backtrack these abnormalities in the dVIN and LS lesions....
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| Veröffentlicht in: | Cancer genomics & proteomics 2020-03, Vol.17 (2), p.151-160 |
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| creator | Pouwer, Anne-Floor W VAN DEN Einden, Loes C G VAN DER Linden, Michelle Hehir-Kwa, Jayne Y Yu, Jiangyan Hendriks, Koen M Kamping, Eveline J Eijkelenboom, Astrid Massuger, Leon F A G Bulten, Johan VAN Tilborg, Angela A G DE Hullu, Joanne A Kuiper, Roland P |
| description | Differentiated vulvar intraepithelial neoplasia (dVIN) and lichen sclerosus (LS) can give rise to vulvar squamous cell carcinoma (VSCC), but genetic evidence is currently still limited. We aimed to determine genetic abnormalities in VSCC and backtrack these abnormalities in the dVIN and LS lesions.
DNA from VSCC and patient-matched dVIN and LS samples of twelve patients was collected. High-resolution genome-wide copy number analysis was performed and subsequently, we sequenced TP53.
Copy number alterations were identified in all VSCC samples. One dVIN lesion presented with three copy number alterations that were preserved in the paired VSCC sample. Targeted sequencing of TP53 identified mutations in five VSCCs. All five mutations were traced back in the dVIN (n=5) or the LS (n=1) with frequencies ranging from 3-19%.
Our data provide genetic evidence for a clonal relationship between VSCC and dVIN or LS. |
| doi_str_mv | 10.21873/cgp.20175 |
| format | Article |
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DNA from VSCC and patient-matched dVIN and LS samples of twelve patients was collected. High-resolution genome-wide copy number analysis was performed and subsequently, we sequenced TP53.
Copy number alterations were identified in all VSCC samples. One dVIN lesion presented with three copy number alterations that were preserved in the paired VSCC sample. Targeted sequencing of TP53 identified mutations in five VSCCs. All five mutations were traced back in the dVIN (n=5) or the LS (n=1) with frequencies ranging from 3-19%.
Our data provide genetic evidence for a clonal relationship between VSCC and dVIN or LS.</description><identifier>ISSN: 1109-6535</identifier><identifier>EISSN: 1790-6245</identifier><identifier>DOI: 10.21873/cgp.20175</identifier><identifier>PMID: 32108037</identifier><language>eng</language><publisher>Greece: International Institute of Anticancer Research</publisher><subject>Abnormalities ; Cell differentiation ; Copy number ; Deoxyribonucleic acid ; DNA ; Genetic abnormalities ; Genomes ; Lesions ; Mutation ; p53 Protein ; Sequences ; Squamous cell carcinoma</subject><ispartof>Cancer genomics & proteomics, 2020-03, Vol.17 (2), p.151-160</ispartof><rights>Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</rights><rights>Copyright International Institute of Anticancer Research Mar/Apr 2020</rights><rights>Copyright 2020, International Institute of Anticancer Research 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-3d2bff8439d4e954b50fda2afba6206b7717e6d0d3cf9c07e0fb9b4bfc3ee8763</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7078831/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7078831/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32108037$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pouwer, Anne-Floor W</creatorcontrib><creatorcontrib>VAN DEN Einden, Loes C G</creatorcontrib><creatorcontrib>VAN DER Linden, Michelle</creatorcontrib><creatorcontrib>Hehir-Kwa, Jayne Y</creatorcontrib><creatorcontrib>Yu, Jiangyan</creatorcontrib><creatorcontrib>Hendriks, Koen M</creatorcontrib><creatorcontrib>Kamping, Eveline J</creatorcontrib><creatorcontrib>Eijkelenboom, Astrid</creatorcontrib><creatorcontrib>Massuger, Leon F A G</creatorcontrib><creatorcontrib>Bulten, Johan</creatorcontrib><creatorcontrib>VAN Tilborg, Angela A G</creatorcontrib><creatorcontrib>DE Hullu, Joanne A</creatorcontrib><creatorcontrib>Kuiper, Roland P</creatorcontrib><title>Clonal Relationship Between Lichen Sclerosus, Differentiated Vulvar Intra-epithelial Neoplasia and Non HPV-related Vulvar Squamous Cell Carcinoma</title><title>Cancer genomics & proteomics</title><addtitle>Cancer Genomics Proteomics</addtitle><description>Differentiated vulvar intraepithelial neoplasia (dVIN) and lichen sclerosus (LS) can give rise to vulvar squamous cell carcinoma (VSCC), but genetic evidence is currently still limited. We aimed to determine genetic abnormalities in VSCC and backtrack these abnormalities in the dVIN and LS lesions.
DNA from VSCC and patient-matched dVIN and LS samples of twelve patients was collected. High-resolution genome-wide copy number analysis was performed and subsequently, we sequenced TP53.
Copy number alterations were identified in all VSCC samples. One dVIN lesion presented with three copy number alterations that were preserved in the paired VSCC sample. Targeted sequencing of TP53 identified mutations in five VSCCs. All five mutations were traced back in the dVIN (n=5) or the LS (n=1) with frequencies ranging from 3-19%.
Our data provide genetic evidence for a clonal relationship between VSCC and dVIN or LS.</description><subject>Abnormalities</subject><subject>Cell differentiation</subject><subject>Copy number</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Genetic abnormalities</subject><subject>Genomes</subject><subject>Lesions</subject><subject>Mutation</subject><subject>p53 Protein</subject><subject>Sequences</subject><subject>Squamous cell carcinoma</subject><issn>1109-6535</issn><issn>1790-6245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNpVUctu1TAQtRCIPmDDByBL7BBp_UqcbJBKeLTSVUEUurUcZ9zrytdO7aQVn9E_rvughdWMNGfOmTkHoTeU7DHaSr5vzqY9Rqisn6FtKjtSNUzUz0tPSVc1Na-30E7O54QIyQV5ibY4o6QlXG6j697HoD3-CV7PLoa8dhP-BPMVQMArZ9alnBgPKeYlf8CfnbWQIMxOzzDi08Vf6oSPwpx0BZOb1-BdYTuGOHmdncY6jPg4Bnz447RKtxpPWycXi97EJeMevMe9TsaFuNGv0AurfYbXD3UX_f765Vd_WK2-fzvqD1aVEaSZKz6ywdpW8G4U0NViqIkdNdN20A0jzSAlldCMZOTGdoZIIHboBjFYwwFa2fBd9PGed1qGDYwGbp_wakpuo9MfFbVT_0-CW6uzeKkkkW3LaSF490CQ4sUCeVbncUnFzKwY7zhpKResoN7fo0yxMCewjwqUqLv4VIlP3cVXwG__vekR-jcvfgNQY5n3</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Pouwer, Anne-Floor W</creator><creator>VAN DEN Einden, Loes C G</creator><creator>VAN DER Linden, Michelle</creator><creator>Hehir-Kwa, Jayne Y</creator><creator>Yu, Jiangyan</creator><creator>Hendriks, Koen M</creator><creator>Kamping, Eveline J</creator><creator>Eijkelenboom, Astrid</creator><creator>Massuger, Leon F A G</creator><creator>Bulten, Johan</creator><creator>VAN Tilborg, Angela A G</creator><creator>DE Hullu, Joanne A</creator><creator>Kuiper, Roland P</creator><general>International Institute of Anticancer Research</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20200301</creationdate><title>Clonal Relationship Between Lichen Sclerosus, Differentiated Vulvar Intra-epithelial Neoplasia and Non HPV-related Vulvar Squamous Cell Carcinoma</title><author>Pouwer, Anne-Floor W ; 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We aimed to determine genetic abnormalities in VSCC and backtrack these abnormalities in the dVIN and LS lesions.
DNA from VSCC and patient-matched dVIN and LS samples of twelve patients was collected. High-resolution genome-wide copy number analysis was performed and subsequently, we sequenced TP53.
Copy number alterations were identified in all VSCC samples. One dVIN lesion presented with three copy number alterations that were preserved in the paired VSCC sample. Targeted sequencing of TP53 identified mutations in five VSCCs. All five mutations were traced back in the dVIN (n=5) or the LS (n=1) with frequencies ranging from 3-19%.
Our data provide genetic evidence for a clonal relationship between VSCC and dVIN or LS.</abstract><cop>Greece</cop><pub>International Institute of Anticancer Research</pub><pmid>32108037</pmid><doi>10.21873/cgp.20175</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Abnormalities Cell differentiation Copy number Deoxyribonucleic acid DNA Genetic abnormalities Genomes Lesions Mutation p53 Protein Sequences Squamous cell carcinoma |
| title | Clonal Relationship Between Lichen Sclerosus, Differentiated Vulvar Intra-epithelial Neoplasia and Non HPV-related Vulvar Squamous Cell Carcinoma |
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