精原细胞瘤
生物
癌症研究
基因复制
外显子
PDGFRA公司
基因
肿瘤进展
原癌基因蛋白质c-kit
生殖细胞
癌变
生殖细胞肿瘤
分子生物学
遗传学
干细胞因子
干细胞
造血
主旨
化疗
间质细胞
作者
Alan McIntyre,Brenda Summersgill,Beata Grygalewicz,Ad Gillis,J. Stoop,Ruud J. H. L. M. van Gurp,Nening M. Dennis,Cyril Fisher,Robert Huddart,Colin Cooper,Jeremy Clark,J. Wolter Oosterhuis,Leendert H. J. Looijenga,Janet Shipley
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2005-09-15
卷期号:65 (18): 8085-8089
被引量:158
标识
DOI:10.1158/0008-5472.can-05-0471
摘要
Abstract We have previously identified amplification at 4q12 in testicular germ cell tumors of adolescents and adults centered around the KIT gene encoding a tyrosine kinase transmembrane receptor. Analysis of primary testicular germ cell tumors totaling 190 cases revealed 21% of the seminoma subtype with an increased copy number of KIT whereas this change was rarely found in the nonseminomas. In most cases, gain of KIT did not include the immediately flanking noncoding DNA or the flanking genes KDR and PDGFRA. Increased copy number of KIT was not found in the putative precursor lesion, carcinoma in situ (CIS), adjacent to tumor with this change. KIT overexpression was found independent of gain and KIT immunostaining was stronger in selected cases with gain of KIT compared to those without. Taken together with activating mutations of KIT in exon 17 identified in 13% of seminomas, this suggests that the KIT gene product plays a role in the progression of CIS towards seminoma, the further understanding of which may lead to novel less toxic therapeutic approaches.
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