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神经母细胞瘤中miR-34a水平降低并非由TP53结合位点的突变所致。

Reduced levels of miR-34a in neuroblastoma are not caused by mutations in the TP53 binding site.

作者信息

Feinberg-Gorenshtein Galina, Avigad Smadar, Jeison Marta, Halevy-Berco Gili, Mardoukh Jacques, Luria Drorit, Ash Shifra, Steinberg Ran, Weizman Avraham, Yaniv Isaac

机构信息

Molecular Oncology, Felsenstein Medical Research Center, Petah Tikva, Israel.

出版信息

Genes Chromosomes Cancer. 2009 Jul;48(7):539-43. doi: 10.1002/gcc.20662.

Abstract

Neuroblastoma (NB) is the most common extracranial solid tumor in children below the age of 5 years. miR-34a, located in chromosome band 1p36, has been recently implicated as a tumor suppressor gene in NB. In addition, it has been shown that miR-34a is activated by TP53 by binding to a TP53 binding site upstream to the mature miR-34a. We studied NB tumors from 57 patients for miR-34a expression levels, 1p status, mutations in the TP53 coding region and mutations of the TP53 binding site. Reduced expression levels of miR-34a were identified in tumors harboring 1p36.3 Loss (P = 0.028). No mutations were identified in the coding region of TP53, or in the TP53 binding site. Thus, mutations in the binding site are not an additional mechanism for the inactivation of miR-34a in NB. Other regulatory mechanisms controlling miR-34a expression and its relationship to TP53 should be further explored.

摘要

神经母细胞瘤(NB)是5岁以下儿童最常见的颅外实体瘤。位于染色体1p36带的miR-34a最近被认为是NB中的一种肿瘤抑制基因。此外,研究表明miR-34a通过与成熟miR-34a上游的TP53结合位点结合而被TP53激活。我们研究了57例患者的NB肿瘤中miR-34a的表达水平、1p状态、TP53编码区突变以及TP53结合位点突变。在存在1p36.3缺失的肿瘤中发现miR-34a表达水平降低(P = 0.028)。在TP53的编码区或TP53结合位点未发现突变。因此,结合位点突变不是NB中miR-34a失活的额外机制。应进一步探索控制miR-34a表达的其他调控机制及其与TP53的关系。

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