Neuroblastoma consensus deletion maps to 1p36.1–2
Neuroblastoma consensus deletion maps to 1p36.1–2
复制标题
神经母细胞瘤共有缺失映射到 1p36.1–2
作者：
A. Weith;T. Martinsson;C. Cziepluch;S. Brüderlein;L. Amler;F. Berthold;M. Schwab
至少70%的人类神经母细胞瘤在1号染色体短臂上显示细胞遗传学上可见的畸变。我们使用了一组探针来检测多态性DNA位点，其中大部分来自微解剖的远端1p染色体片段文库，以比较9种不同肿瘤和相应正常组织的DNA杂交模式。在8个神经母细胞瘤中，至少用两个探针观察到等位基因丢失。这些缺失的大小不同。由于所有8个肿瘤的一致缺失包括1p36.1-2片段，我们得出结论，与神经母细胞瘤肿瘤发生相关的遗传信息位于这个大约10兆碱基的片段中。先前的研究显示MYCN在神经母细胞瘤中扩增。我们的研究没有提供证据证明MYCN扩增和1p缺失之间的相关性，这表明这两种遗传改变是由分子机制引起的，彼此之间没有直接关系。
At least 70% of human neuroblastomas display cytogenetically visible aberrations in the short arm of chromosome 1. We have used a panel of probes detecting polymorphic DNA loci, most of which were derived from a library of microdissected distal 1p chromosome fragments, to compare the hybridization pattern of DNA on nine different tumors and the corresponding normal tissue. In eight of the neuroblastomas allelic loss was observed with at least two probes. The deletions were of different size. Since a consensus deletion in all eight tumors included the segment 1p36.1–2, we conclude that genetic information related to neuroblastoma tumorigenesis is located within this approximately 10 megabase segment. Previous studies have revealed the amplification of MYCN in neuroblastomas. Our study did not provide evidence for a correlation between MYCN amplification and the 1p deletion, suggesting that the two genetic alterations result from molecular mechanisms that are not directly related to each other.
影响因子：
56.9
作者：
FEARON, ER;HAMILTON, SR;VOGELSTEIN, B
通讯作者：
VOGELSTEIN, B
影响因子：
56.9
作者：
BAKER, SJ;FEARON, ER;VOGELSTEIN, B
通讯作者：
VOGELSTEIN, B
DOI：
10.1073/pnas.86.10.3753
发表时间：
1989-05-01
影响因子：
11.1
作者：
FONG, CT;DRACOPOLI, NC;BRODEUR, GM
通讯作者：
BRODEUR, GM