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目的 探讨p16和p15基因第二外显子HapⅡ位点在成人急性髓性白血病 (AML)中的突变。方法 用甲基敏感和甲基非敏感限制性内切酶切消化基因组DNA后 ,经PCR扩增和琼脂糖电泳研究 3 1例AML中无p16/p15基因第二外显子缺失的患者中HapⅡ位点的突变情况。结果 在 3 1例成人AML样本中 ,p16E2 的 4个HapⅡ位点和p15E2 的 6个HapⅡ位点均未发生突变。结论 本研究提示p16和p15基因第二外显子中因甲基化而引起的CCGG位点的突变在成人AML患者中不是主要失活方式。
Objective To investigate the mutations of the second exon HapⅡ locus of p16 and p15 genes in adult acute myeloid leukemia (AML). Methods After digestion of genomic DNA with methyl-sensitive and non-sensitive methyl-sensitive restriction endonucleases, 31 cases of AML without the second exon of p16 / p15 gene were studied by PCR amplification and agarose gel electrophoresis. Site mutation. Results In 31 adult AML samples, no mutation was found in 4 Hap II sites of p16E2 and 6 Hap II sites of p15E2. Conclusions This study suggests that mutations in the CCGG site due to methylation in exon 2 of p16 and p15 genes are not major inactivation modalities in adult AML patients.