...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Oncogene >High-resolution array CGH analysis of salivary gland tumors reveals fusion and amplification of the FGFR1 and PLAG1 genes in ring chromosomes
【24h】

High-resolution array CGH analysis of salivary gland tumors reveals fusion and amplification of the FGFR1 and PLAG1 genes in ring chromosomes

机译：唾液腺肿瘤的高分辨率阵列CGH分析显示环染色体中FGFR1和PLAG1基因的融合和扩增

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We have previously identified a subgroup of pleomorphic salivary gland adenomas with ring chromosomes of uncertain derivation. Here, we have used spectral karyotyping (SKY), fluorescence in situ hybridization (FISH) and high-resolution oligonucleotide array-CGH to determine the origin and content of these rings and to identify genes disrupted as a result of ring formation. Of 16 tumors with rings, 11 were derived from chromosome 8, 3 from chromosome 5 and 1 each from chromosomes 1, 6 and 9. Array-CGH revealed that 10/11 r(8) consisted of amplification of a 19?Mb pericentromeric segment with recurrent breakpoints in FGFR1 in 8p12 and in PLAG1 in 8q12.1. Molecular analyses revealed that ring formation consistently generated novel FGFR1–PLAG1 gene fusions in which the 5′-part of FGFR1 is linked to the coding sequence of PLAG1. An alternative mechanism of PLAG1 activation was found in tumors with copy number gain of an intact PLAG1 gene. Rings derived from chromosomes 1, 5, 6 or 9 did not result in gene fusions, but rather resulted in losses indicative of the involvement of putative tumor suppressor genes on 8p, 5p, 5q and/or 6q. Our findings also reveal a novel mechanism by which FGFR1 contributes to oncogenesis and further illustrate the versatility of the FGFR1 and PLAG1 genes in tumorigenesis.
机译：我们之前鉴定了具有不确定衍生的环染色体的亲主唾液腺腺瘤的亚组。在这里，我们使用光谱核型（天空），原位杂交（鱼）和高分辨率寡核苷酸阵列-CGH以确定这些环的起源和含量，并鉴定由于环形成而被破坏的基因。具有环的16个肿瘤，11来自染色体5，3来自染色体5和1，来自染色体1,6和9.阵列-CGH显示10/11 r（8）组成的19αMB蠕虫大分子段的扩增在8P12和8Q12.1中的FGFR1和PLAG1中的复发断点。分子分析显示，环形成始终如一地产生新的FGFR1-PLAG1基因融合，其中FGFR1的5'部分与PLAG1的编码序列连接。在具有完整PLAG1基因的拷贝数增益的肿瘤中发现了PLAG1活化的替代机制。源自染色体1,5,6或9的环并未导致基因融合，而是导致损耗，指示推定肿瘤抑制基因对8P，5P，5Q和/或6Q的累积。我们的研究结果还揭示了一种新的机制，FGFR1有助于肿瘤发生，进一步说明肿瘤发生中FGFR1和PLAG1基因的多功能性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号