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通过聚合酶链反应分析及N-myc扩增对48例神经母细胞瘤中假定的肿瘤抑制基因位点1p36缺失情况进行研究:德国神经母细胞瘤研究组的结果

Loss of the putative tumor suppressor-gene locus 1p36 as investigated by a PCR-assay and N-myc amplification in 48 neuroblastomas: results of the German Neuroblastoma Study Group.

作者信息

Christiansen H, Delattre O, Fuchs S, Theobald M, Christiansen N M, Berthold F, Lampert F

机构信息

Universitäts-Kinderklinik, Giessen.

出版信息

Prog Clin Biol Res. 1994;385:19-25.

PMID:7972212
Abstract

48 primary neuroblastomas have been examined for an amplified N-myc and loss of the putative tumor suppressor-gene locus 1p36 by loss of heterozygosity studies (LOH 1p36). In 25% of these tumors N-myc amplification and/or a LOH 1p36 was detected, and these patients had a bad prognostic clinical outcome. 75% of the tumors neither had an amplified N-myc nor a LOH 1p36, and these patients had a much better prognosis. Thus, tumor genetic changes can subdivide two types of neuroblastoma with profound different clinical behavior. Detection of these genetic changes at diagnosis could help in front-line risk adapted therapy stratifications in neuroblastoma.

摘要

通过杂合性缺失研究(1p36杂合性缺失,LOH 1p36)对48例原发性神经母细胞瘤进行了检测,以确定N-myc是否扩增以及假定的肿瘤抑制基因位点1p36是否缺失。在这些肿瘤中,25%检测到N-myc扩增和/或1p36杂合性缺失,这些患者的临床预后较差。75%的肿瘤既没有N-myc扩增也没有1p36杂合性缺失,这些患者的预后要好得多。因此,肿瘤基因改变可将神经母细胞瘤分为两种具有截然不同临床行为的类型。诊断时检测到这些基因改变有助于神经母细胞瘤的一线风险适应性治疗分层。

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