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作 者:董华丽[1] 吕楠[2] 李大启[3] 陈萍[3] 邵建华[3] 董学斌[3]
机构地区:[1]山东潍坊医学院研究生处,261041 [2]山东大学附属济南市中心医院中心实验室 [3]山东大学附属济南市中心医院血液科
出 处:《白血病.淋巴瘤》2014年第6期350-353,共4页Journal of Leukemia & Lymphoma
摘 要:目的 探讨非霍奇金淋巴瘤(NHL)患者骨髓垂体瘤转化基因(PTTG)与c-myc基因的表达及其临床意义.方法 采用反转录聚合酶链反应(RT-PCR)法检测38例NHL患者骨髓及10例慢性淋巴结炎患者骨髓单个核细胞(BMMNC)中PTTG及c-myc基因的表达.结果 NHL患者骨髓中PTTG和c-myc基因的表达水平均明显高于慢性淋巴结炎组,差异有统计学意义(PTTG:0.567 7±0.270 7比0.071 2±0.020 1,t=4.706,P<0.05; c-myc:0.352 6±0.185 4比0.107 3±0.043 5,t=3.303,P=0.002).外周T细胞淋巴瘤和弥漫大B细胞淋巴瘤患者PTTG及c-myc基因表达水平差异均无统计学意义(PTTG:0.556 8±0.211 3比0.602 8±0.244 6,t=0.640,P=0.527;c-myc:0.350 1±0.177 6比0.361 0±0.190 2,t=0.302,P=0.765).PTTG基因的表达与NHL骨髓浸润、国际预后指数(IPI)评分呈正相关(r=0.422,r=0.387;均P<0.05).c-myc基因的表达与NHL骨髓浸润、IPI评分呈正相关(r=0.431,r=0.344,均P<0.05).NHL患者骨髓PTTG基因和c-myc基因的表达呈正相关(r=0.490,P<0.05).结论 NHL中PTTG、c-myc呈高表达状态,PTTG可能通过直接或间接途径促进c-myc的高表达.Objective To explore the expression of pituitary tumor transforming gene (PTTG) and c-myc gene in patients with non-Hodgkin lymphoma (NHL),its relationship with NHL and its clinical significance.Methods PTTG mRNA and c-myc mRNA levels in bone marrow mononuclear cell (BMMNC) isolated from 38 NHL patients and 10 chronic lymphadenitis patients were quantified by reverse transcriptionpolymerase chain reaction (RT-PCR).Results mRNA expression of PTTG and c-myc gene in BMMNC was significantly higher in NHL patients than those in normal controls (PTTG:0.567 7±0.270 7 vs 0.071 2± 0.020 1,t =4.706,P 〈 0.05; c-myc:0.352 6±0.185 4 vs 0.107 3±0.043 5,t =3.303,P =0.002).The expression of PTTG and c-myc gene in peripheral T cell lymphoma and diffuse large B cell lymphoma showed no significant difference (PTTG:0.556 8±0.211 3 vs 0.602 8±0.244 6,t =0.640,P =0.527; c-myc:0.350 1± 0.177 6 vs 0.361 0±0.190 2,t =0.302,P =0.765).Both expression of PTTG and c-myc were positively related to NHL clinical stage and IPI.Expression of PTTG mRNA was positively related to the expression of c-myc mRNA.Conclusion There was overexpression of PTTG and c-myc in NHL,which indicates that PTTG might be involved in tumorigenesis of NHL through direct or indirect activation of c-myc oncogene.
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