...
首页> 外文期刊>Neuropathology and applied neurobiology >Tumour necrosis and microvascular proliferation are associated with 9p deletion and CDKN2A alterations in 1p/19q-deleted oligodendrogliomas.
【24h】

Tumour necrosis and microvascular proliferation are associated with 9p deletion and CDKN2A alterations in 1p/19q-deleted oligodendrogliomas.

机译:肿瘤坏死和微血管增生与1p / 19q缺失的少突胶质细胞瘤中9p缺失和CDKN2A改变有关。

获取原文
获取原文并翻译 | 示例

摘要

A subset of oligodendrogliomas and oligoastrocytomas has been associated with 1p/19q deletion. Subsequently, this genetic alteration was linked to chemosensitivity and classic histology of oligodendrogliomas. Tumoural progression includes deletions of 9p, 10q and alterations of CDKN2A. However, these (epi)genetic changes have not been associated with specific histological features. In a series of 45 gliomas including oligodendrogliomas, oligoastrocytomas and astrocytomas, deletions of chromosomal regions implied in these tumours (1p, 9p, 10, 17p13, 19q and 22) were looked for by microsatellite analysis. Tumours that were deleted for 1p and 19q were selected. Subsequently, presence of deletions in the other studied regions, (epi)genetic changes in p14ARF, CDKN2A and CDKN2B, as well as histological features, were associated to these tumours. 1p/19q deletion was observed in 22 tumours. Twenty-one of them presented regions of classic histology of oligodendroglioma. A deletion of 9p was found in eight of them, always in association with tumour necrosis and/or microvascular proliferation. In addition, (epi)genetic alterations of CDKN2A were observed in 71% of these tumours. Presence of regions of classic histology of oligodendroglioma in a tumour sample is predictive of 1p/19q deletions. Necrosis and/or microvascular proliferation are signs of an additional 9p deletion. Finally, as CDKN2A (epi)genetic alterations were found in 71% of the 1p/19q/9p-deleted oligodendrogliomas, CDKN2A may have a role in oligodendroglioma-associated microvascular proliferation.
机译:少突胶质细胞瘤和少突星形细胞瘤的一个子集已与1p / 19q缺失相关。随后,这种遗传改变与少突胶质细胞瘤的化学敏感性和经典组织学有关。肿瘤进展包括9p,10q的缺失和CDKN2A的改变。但是,这些(表观)遗传变化尚未与特定的组织学特征相关联。在包括少突胶质细胞瘤,少突星形细胞瘤和星形细胞瘤在内的一系列45个神经胶质瘤中,通过微卫星分析寻找这些肿瘤中隐含的染色体区域的缺失(1p,9p,10、17p13、19q和22)。选择1p和19q被删除的肿瘤。随后,在其他研究区域中缺失的存在,p14ARF,CDKN2A和CDKN2B的(epi)遗传变化以及组织学特征与这些肿瘤相关。在22个肿瘤中观察到1p / 19q缺失。其中二十一个介绍了少突胶质细胞瘤的经典组织学区域。他们中的八个发现9p缺失,通常与肿瘤坏死和/或微血管增生有关。另外,在这些肿瘤的71%中观察到CDKN2A的(表观)遗传改变。肿瘤样品中少突胶质细胞瘤的经典组织学区域的存在可预测1p / 19q缺失。坏死和/或微血管增生是另外9p缺失的迹象。最后,由于在1p / 19q / 9p缺失的少突胶质细胞瘤中发现了71%的CDKN2A(epi)遗传改变,因此CDKN2A可能在少突胶质细胞瘤相关的微血管增生中起作用。

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