应用FISH-TSA技术检测急性髓性白血病(AML)多发内分泌肿瘤1型(MEN1)基因等位基因缺失。

Hasan Acar, Murat Kaynak, Tahsin Yakut, Fahri Uçar, Unal Egeli
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引用次数: 4

摘要

我们采用单色和双色荧光原位杂交(FISH)技术,结合新的检测系统酪酰胺信号扩增(TSA),利用多内分泌肿瘤1型(MEN1)基因和11号染色体特异性α卫星DNA探针,对MEN1基因的等位基因缺失进行了研究。MEN1基因是一个新的肿瘤抑制基因,最近被克隆到染色体11q13上。对22例急性髓性白血病(AML)患者骨髓间期核进行FISH联合TSA检测。FISH-TSA分析显示,22例患者中有4例(18.18%)、9例AML-M2患者中有2例(22.2%)、6例AML-M4患者中有1例(16.6%)、4例AML-M5患者中有1例(25.0%)存在MEN1基因的单等位基因缺失。我们的研究表明,尽管11号染色体的长臂(q13区域)涉及AML的染色体重排,但MEN1基因的等位基因缺失并不是AML肿瘤发生的主要原因或主要事件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Determination of allelic deletion of multiple endocrine neoplasm type 1 (MEN1) gene in acute myeloid leukemia (AML) by application of FISH-TSA technique.

We have used the single and dual color fluorescence in situ hybridization (FISH) technique combined with a new detection system, tyramide signal amplification (TSA), by using the multiple endocrine neoplasm type 1 (MEN1) gene and chromosome 11 specific alpha satellite DNA probes for the study of the allelic deletion of the MEN1 gene. The MEN1 gene is a new tumor suppressor gene and has been recently cloned on chromosome 11q13. FISH combined with the TSA detection system was performed on bone marrow interphase nuclei of 22 patients with acute myeloid leukemia (AML). The FISH-TSA analysis revealed the mono allelic deletion of the MEN1 gene in 4 out of 22 patients (18.18%), 2 of 9 AML-M2 patients (22.2%), 1 of 6 AML-M4 patients (16.6%), and 1 of 4 AML-M5 patients (25.0%). Our study indicates that allelic deletion of the MEN1 gene is not a major cause or a primary event in tumorigenesis of AML, although the long arm (q13 region) of chromosome 11 involves a chromosomal rearrangement in AML.

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