Hyojin Chae , Myungshin Kim , Jihyang Lim , Yonggoo Kim , Kyungja Han , Seok Lee
{"title":"B lymphoblastic leukemia with ETV6 amplification","authors":"Hyojin Chae , Myungshin Kim , Jihyang Lim , Yonggoo Kim , Kyungja Han , Seok Lee","doi":"10.1016/j.cancergencyto.2010.08.004","DOIUrl":null,"url":null,"abstract":"<div><p>We presente a case of acute lymphoblastic leukemia caused by <em>ETV6</em> amplification. Although the cytogenetic result revealed complex karyotype, multicolor fluorescence in situ hybridization and high-resolution multicolor banding supported amplification of a gene on 12p13. Fluorescence in situ hybridization with <em>ETV6</em> probe confirmed the amplification. <em>ETV6</em> generally plays as tumor-suppressor gene in leukemia. Their expression is decreased or missed by deletion or mutation. Otherwise, ETV6 protein overexpression was verified in this case by immunohistochemistry. Any translocation or mutation involving <em>ETV6</em> was not detected. This experience strongly supports the hypothesis that the amplification of <em>ETV6</em> is a possible mechanism of leukeogenesis as oncogene.</p></div>","PeriodicalId":55596,"journal":{"name":"Cancer Genetics and Cytogenetics","volume":"203 2","pages":"Pages 284-287"},"PeriodicalIF":0.0000,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cancergencyto.2010.08.004","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Genetics and Cytogenetics","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0165460810004450","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9
Abstract
We presente a case of acute lymphoblastic leukemia caused by ETV6 amplification. Although the cytogenetic result revealed complex karyotype, multicolor fluorescence in situ hybridization and high-resolution multicolor banding supported amplification of a gene on 12p13. Fluorescence in situ hybridization with ETV6 probe confirmed the amplification. ETV6 generally plays as tumor-suppressor gene in leukemia. Their expression is decreased or missed by deletion or mutation. Otherwise, ETV6 protein overexpression was verified in this case by immunohistochemistry. Any translocation or mutation involving ETV6 was not detected. This experience strongly supports the hypothesis that the amplification of ETV6 is a possible mechanism of leukeogenesis as oncogene.
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