Zhang Su-Jiang, Shi Jing-Yi, Li Jian-Yong
Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Leuk Res. 2009 Aug;33(8):1141-3. doi: 10.1016/j.leukres.2009.02.025. Epub 2009 Mar 21.
Chronic myeloid leukemia (CML) progression is characterized by occurrence of new cytogenetic and molecular abnormalities. In the previous study, we have shown the important role of GATA-2 L359 V mutation in CML progression. To further ascertain the truth of transcription factor GATA-2 in hematological malignancies, we expanded our study to GATA-2 full length by directly sequencing and applied MassARRAY assay into GATA-2 L359 V mutation analysis. Finally, no GATA-2 L359 V mutation was found in 270 acute myeloid leukemia, 30 myelodysplastic syndrome, 50 acute lymphoblastic leukemia, 12 chronic lymphocytic leukemia, 40 CML chronic phase and 286 BCR/ABL negative myeloproliferative disorders except CML blast crisis. A new variation of GATA-2 resulted in P250A change was identified, which was not found to have statistical difference between patients with hematological malignancies and healthy control. Hence, we concluded GATA-2 L359 V is exclusively associated with CML progression but not other hematological malignancies and P250A is a new single nucleotide polymorphism.
慢性髓性白血病(CML)进展的特征是出现新的细胞遗传学和分子异常。在先前的研究中,我们已经表明GATA-2 L359V突变在CML进展中起重要作用。为了进一步确定转录因子GATA-2在血液系统恶性肿瘤中的真实情况,我们通过直接测序将研究扩展到GATA-2全长,并将MassARRAY分析应用于GATA-2 L359V突变分析。最后,在270例急性髓性白血病、30例骨髓增生异常综合征、50例急性淋巴细胞白血病、12例慢性淋巴细胞白血病、40例CML慢性期以及286例除CML急变期外的BCR/ABL阴性骨髓增殖性疾病中均未发现GATA-2 L359V突变。鉴定出一种导致P250A改变的GATA-2新变异,发现其在血液系统恶性肿瘤患者与健康对照之间无统计学差异。因此,我们得出结论,GATA-2 L359V仅与CML进展相关,而与其他血液系统恶性肿瘤无关,且P250A是一种新的单核苷酸多态性。