{"title":"肾嗜瘤细胞瘤线粒体DNA中不存在hini限制性异常。","authors":"Brooks, Marshall, Isaacs, Johns","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Renal oncocytomas are characterized by bland-appearing eosinophilic cells with a profusion of mitochondria. Previous work has suggested that these tumors possess a mutation in the 16.5-kbp circular mitochondrial DNA (mtDNA) manifested by an abnormal restriction fragment pattern after digestion with HinfI (Welter et al, Genes Chromosomes Cancer 1989;1:7-82). To better characterize this mtDNA abnormality in renal oncocytomas, we amplified the entire mitochondrial genome from five paired normal and oncocytoma specimens and subjected the amplified fragments to digestion with the restriction enzyme HinfI. No somatically acquired alterations were detected in the mtDNA from any of the five renal oncocytomas. One specimen displayed a known HinfI polymorphism in the mtDNA from both the normal and oncocytoma tissues. Our data do not support the existence of somatically acquired mitochondrial genome abnormalities in renal oncocytomas.</p>","PeriodicalId":80296,"journal":{"name":"Molecular urology","volume":"3 1","pages":"1-3"},"PeriodicalIF":0.0000,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Absence of HinfI Restriction Abnormalities in Renal Oncocytoma Mitochondrial DNA.\",\"authors\":\"Brooks, Marshall, Isaacs, Johns\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Renal oncocytomas are characterized by bland-appearing eosinophilic cells with a profusion of mitochondria. Previous work has suggested that these tumors possess a mutation in the 16.5-kbp circular mitochondrial DNA (mtDNA) manifested by an abnormal restriction fragment pattern after digestion with HinfI (Welter et al, Genes Chromosomes Cancer 1989;1:7-82). To better characterize this mtDNA abnormality in renal oncocytomas, we amplified the entire mitochondrial genome from five paired normal and oncocytoma specimens and subjected the amplified fragments to digestion with the restriction enzyme HinfI. No somatically acquired alterations were detected in the mtDNA from any of the five renal oncocytomas. One specimen displayed a known HinfI polymorphism in the mtDNA from both the normal and oncocytoma tissues. Our data do not support the existence of somatically acquired mitochondrial genome abnormalities in renal oncocytomas.</p>\",\"PeriodicalId\":80296,\"journal\":{\"name\":\"Molecular urology\",\"volume\":\"3 1\",\"pages\":\"1-3\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1999-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular urology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular urology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
肾嗜酸性细胞瘤的特征是嗜酸性细胞呈淡色,并有大量线粒体。先前的研究表明,这些肿瘤具有16.5 kbp环状线粒体DNA (mtDNA)突变,表现为用hini消化后出现异常的限制性片段模式(Welter等,Genes chromosome Cancer 1989;1:7-82)。为了更好地表征肾癌细胞瘤中的mtDNA异常,我们从5对正常和癌细胞瘤标本中扩增了整个线粒体基因组,并用限制性内切酶HinfI消化扩增片段。在五种肾嗜瘤细胞瘤的mtDNA中未检测到体细胞获得性改变。一个标本在正常和癌细胞瘤组织的mtDNA中显示出已知的hini多态性。我们的数据不支持肾嗜瘤细胞瘤中存在体细胞获得性线粒体基因组异常。
Absence of HinfI Restriction Abnormalities in Renal Oncocytoma Mitochondrial DNA.
Renal oncocytomas are characterized by bland-appearing eosinophilic cells with a profusion of mitochondria. Previous work has suggested that these tumors possess a mutation in the 16.5-kbp circular mitochondrial DNA (mtDNA) manifested by an abnormal restriction fragment pattern after digestion with HinfI (Welter et al, Genes Chromosomes Cancer 1989;1:7-82). To better characterize this mtDNA abnormality in renal oncocytomas, we amplified the entire mitochondrial genome from five paired normal and oncocytoma specimens and subjected the amplified fragments to digestion with the restriction enzyme HinfI. No somatically acquired alterations were detected in the mtDNA from any of the five renal oncocytomas. One specimen displayed a known HinfI polymorphism in the mtDNA from both the normal and oncocytoma tissues. Our data do not support the existence of somatically acquired mitochondrial genome abnormalities in renal oncocytomas.