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目的 探讨p16基因、蛋白失活在小儿急性淋巴细胞白血病 (ALL)中的临床意义。方法应用免疫细胞化学方法检测 5 2例初治小儿ALLP16蛋白的表达水平。差异PCR技术检测 42例初治小儿ALLp16基因的纯合缺失。结果 p16基因总的纯合缺失率 38% (16 /4 2 ) ,p16基因缺失与T系表型、高白细胞总数 (>2 5× 10 9/L)、高肿瘤负荷、髓外浸润等影响预后的高危临床特征显著相关。高危型ALLp16基因缺失率 (6 7% )远高于标危型ALL(10 % ) ,P <0 .0 1。在预后好者中 ,p16基因纯合缺失率为 10 % (2 /19) ;在预后差者中 ,p16基因纯合缺失率为 5 4% (6 /11) ,二组差异有显著性 ,P <0 .0 5。P16蛋白表达缺失率为 5 8% (30 /5 2 ) ,P16蛋白缺失者除多见髓外浸润外 ,与其它临床高危因素及预后无关。结论 p16基因、蛋白失活在小儿ALL的发病过程中起重要作用。p16基因缺失者预后不良 ,与ALL复发可能有关 ,可作为评估预后 ,指导治疗的指标之一。
Objective To investigate the clinical significance of p16 gene and protein inactivation in children with acute lymphoblastic leukemia (ALL). Methods The expression of ALLP16 protein in 52 untreated infants was detected by immunocytochemistry. Differential PCR was used to detect homozygous deletion of ALLp16 gene in 42 newly diagnosed children. Results The overall deletion rate of p16 gene was 38% (16/42). The deletion of p16 gene was associated with T phenotype, total leukocyte count (> 25 × 10 9 / L), high tumor burden and extramedullary infiltration Prognostic high-risk clinical features were significantly associated. The high-risk ALLp16 gene deletion rate (67%) was much higher than the standard-hazard ALL (10%), P <0.01. The percentage of homozygous deletion in p16 gene was 10% (2/19) in those with good prognosis, 54% (6/11) in homozygous deletion in p16 gene, and the difference was significant between the two groups P <0. 0 5. The deletion rate of P16 protein was 58% (30/5 2). P16 protein deletion was not related to other clinical risk factors and prognosis except extra-infiltration extramedullary infiltration. Conclusion p16 gene and protein inactivation plays an important role in the pathogenesis of childhood ALL. The poor prognosis of p16 gene deletion may be related to the relapse of ALL and may be used as one of the indicators to evaluate the prognosis and guide the treatment.