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施-戴二氏综合征发展为骨髓增生异常综合征/急性髓系白血病的途径:衰老、核型不稳定性及获得性染色体异常的作用

The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.

作者信息

Maserati Emanuela, Pressato Barbara, Valli Roberto, Minelli Antonella, Sainati Laura, Patitucci Francesco, Marletta Cristina, Mastronuzzi Angela, Poli Furio, Lo Curto Francesco, Locatelli Franco, Danesino Cesare, Pasquali Francesco

机构信息

Biologia e Genetica, Dipartimento di Scienze Biomediche Sperimentali e Cliniche, Università dell'lnsubria, Varese, Italy.

出版信息

Br J Haematol. 2009 Apr;145(2):190-7. doi: 10.1111/j.1365-2141.2009.07611.x. Epub 2009 Feb 17.

Abstract

An investigation of 22 new patients with Shwachman-Diamond syndrome (SDS) and the follow-up of 14 previously reported cases showed that (i) clonal chromosome changes of chromosomes 7 and 20 were present in the bone marrow (BM) of 16 out of 36 cases, but if non-clonal changes were taken into account, the frequency of anomalies affecting these chromosomes was 20/36: a specific SDS karyotype instability was thus confirmed; (ii) the recurrent isochromosome i(7)(q10) did not include short arm material, whereas it retained two arrays of D7Z1 alphoid sequences; (iii) the deletion del(20)(q11) involved the minimal region of deletion typical of myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML); (iv) only one patient developed MDS, during the rapid expansion of a BM clone with a chromosome 7 carrying additional material on the short arms; (v) the acquisition of BM clonal chromosome anomalies was age-related. We conclude that karyotype instability is part of the natural history of SDS through a specific mutator effect, linked to lacking SBDS protein, with consequent clonal anomalies of chromosomes 7 and 20 in BM, which may eventually promote MDS/AML with the patients' ageing.

摘要

对22例新诊断的施瓦茨曼-戴蒙德综合征(SDS)患者的调查以及对14例先前报道病例的随访显示:(i)36例中的16例骨髓(BM)中存在7号和20号染色体的克隆性染色体改变,但如果将非克隆性改变考虑在内,影响这些染色体的异常频率为20/36:因此证实了SDS存在特定的核型不稳定性;(ii)反复出现的等臂染色体i(7)(q10)不包括短臂物质,而保留了两组D7Z1α卫星序列;(iii)缺失del(20)(q11)涉及骨髓增生异常综合征(MDS)和急性髓系白血病(AML)典型的最小缺失区域;(iv)只有1例患者在一个带有短臂额外物质的7号染色体的BM克隆快速扩增期间发生了MDS;(v)BM克隆性染色体异常的获得与年龄相关。我们得出结论,核型不稳定性是SDS自然病程的一部分,通过一种特定的诱变效应,与缺乏SBDS蛋白有关,导致BM中7号和20号染色体出现克隆性异常,随着患者年龄增长,这最终可能促进MDS/AML的发生。

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