Gain of chromosome arm 17q predicts unfavourable outcome in neuroblastoma patients

被引:80
作者
Lastowska, M
Cotterill, S
Pearson, ADJ
Roberts, P
McGuckin, A
Lewis, I
Bown, N
机构
[1] UNIV NEWCASTLE UPON TYNE, INST CHILD HLTH, NEWCASTLE UPON TYNE NE1 7RU, TYNE & WEAR, ENGLAND
[2] ST JAMES UNIV HOSP, CYTOGENET UNIT, LEEDS LS9 7TF, W YORKSHIRE, ENGLAND
[3] UNIV NEWCASTLE UPON TYNE, DEPT PATHOL, NEWCASTLE UPON TYNE NE2 4AA, TYNE & WEAR, ENGLAND
[4] ST JAMES UNIV HOSP, DEPT PAEDIAT ONCOL, LEEDS LS9 7TF, W YORKSHIRE, ENGLAND
[5] INST PAEDIAT, CLIN PAEDIAT HAEMATOL & ONCOL, POZNAN, POLAND
关键词
chromosome 17q gain; neuroblastoma primary tumours; prognosis;
D O I
10.1016/S0959-8049(97)00282-7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Gain of chromosome arm 17q has recently been reported in neuroblastoma tumours. We analysed 17q status in relation to other known prognostic features and clinical outcome in a series of 45 tumours. Chromosome 17 status was detected by cytogenetic analysis, fluorescence in situ hybridisation (FISH) and comparative genomic hybridisation (CGH) and correlated with other clinical and genetic factors. Survival analysis was calculated by the Kaplan-Meier estimation. Twenty-eight out of 45 tumours showed 17q gain, and this was associated with established indicators of poor prognosis; stage 4 disease (P<0.001), age above 1 year at diagnosis (P<0.001), Ip deletion (P<0.01), MYCN amplification (P=0.03) and diploidy/tetraploidy (P=0.04). 17q gain was associated with poor outcome: 3-year survival was 13.5% compared with 100% for tumours without 17q gain (P=0.0001); and progression-free survival (PFS) was 8.1% after 3 years compared with 83% for 17q normal tumours (P=0.0001). PFS in 28 MYCN non-amplified patients indicated that 17q status has discriminatory power within this group: PFS 0% for 17q gain (n=14) versus 100% for normal 17q (n=14) (P=0.0001). This study indicates that 17q changes have prognostic significance in neuroblastoma and should be a target for molecular cytogenetic detection at diagnosis. (C) 1997 Elsevier Science Ltd.
引用
收藏
页码:1627 / 1633
页数:7
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