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71.
目的探讨结外鼻型NK/T细胞淋巴瘤(NKTCL)根据发病部位分为鼻源和鼻外的临床特征和免疫组化特点、疗效的比较,并分析其预后因素。方法收集2004年1月至2008年12月我院收治的44例NKTCL患者的临床资料。从年龄、性别、Ann Arbor分期、临床症状、体征及免疫组化、TCR基因重排、EBV-DNA检测和治疗方案等几方面进行回顾性分析。结果 38例鼻源和6例鼻外患者在Ann Arbor分期Ⅲ、Ⅳ期所占比例,结外侵犯≥2个,PS评分≥2分三方面,鼻外均高于鼻源。在免疫组化方面,鼻源和鼻外肿瘤细胞均不表达CD20、CD79、Pax-5,而CD2、CD3ε、CD56、LAT、CD7及细胞毒素相关抗原(GRB、TIA-1、Perf)表达阳性。TCR克隆性重排均有33.3%的患者表达阳性,EBV-DNA检测鼻源25.0%、鼻外33.3%的患者表达阳性。治疗结果显示,44例患者,总完全缓解(CR)率72.5%,3年和5年总生存率(OS)分别为56.12%和44.90%。中位生存时间为47个月(1～105个月)。鼻源的CR率显著高于鼻外(P=0.034),复发率显著低于鼻外(P=0.027)。但生存率差异无统计学意义... 相似文献
72.
Objective: To explore the effects of dexamethasone (DXM) and vincristine (VCR) on cytosine arabinoside (Ara-C) induced apoptosis and activation of nuclear factor-κ-gene binding (NF-κB) in leukemic cell line HL60-n. Methods: Apoptosis of HL60-n cells was analysed by TdT-mediated X-dUTP nick and end labeling (TUNEL) and DNA electrophoresis. NF-κB activity of HL60-n cells was detected by electrophoretic mobility shift assay (EMSA). Results: There was slight activation of NF-κB in HL60-n cells without drug induction. Ara-C at 1 μmol/L significantly enhanced the activation of NF-κB in HL60-n cells. The level of NF-κB activation induced by DXM at 1 μmol/L or VCR at 0.1 μmol/L had no significant difference compared with that of the control group. However, in HL60-n cells pre-treated with 1 μmol/L of DXM or 0.1 μmol/L of VCR, the activation of NF-κB induced by 1 μmol/L of Ara-C was significantly suppressed with inhibition rates of 31.0% and 47.0%, respectively. The apoptosis rates of HL60-n cells induced by 1.0 μmol/L, 10 μmol/L and 100 μmot/L Ara-C were 45.00±3.16%, 61.88±3.40% and 77.62±4.75%, respectively. The apoptotic rates of HL60-n cells induced by DXM at 1 μmol/L or VCR at 0.1 μmol/L were similar to that of the control group. However, either DXM at 1 μmol/L or VCR at 0.l μmol/L could enhance the apoptosis of HL60-n cells induced by Ara-C at 1 μmol/L with rates of 39.1% and 59.2%, respectively. Conclusion: Ara-C can induce apoptosis and activation of NF-κB in HL60-n cells. The mechanism of increased apoptosis of HL60-n cells by DXM or VCR may be related to suppression of NF-κB activation. 相似文献
73.
目的 研究微小残留白血病的治疗新方法。方法 采用重组人白细胞介素-2（rhIL-2）和苦参碱单独或联合治疗小鼠多药耐药微小残留白血病。 DBA小鼠接种P388／VCR-G细胞（1×106／只）后第3天,用环磷酰胺（Cy）35 mg／kg一次腹腔注射,24 h 后实验分4组。对照组：腹腔注射生理盐水0.2 ml／次,2次／d,连续5 d。rhIL-2组：腹腔注射rhIL-2 1×105U／次,2次／d,连续5 d。苦参碱组：腹腔注射苦参碱25 mg／kg,1次／d,连续5 d。rhIL-2＋苦参碱组：腹腔注射rhIL-2 1×105U／次,2次／d,连续5 d;苦参碱25 mg／kg,1次／d,连续5 d。结果 对照组小鼠平均生存期（25.2±1.10）d,rhIL-2治疗组平均生存期分别延长至（36.25±1.26）d,按回归方程y天数= -1.98x细胞数+28.61推算,相当于杀灭了1×103左右的白血病细胞。苦参碱治疗组平均生存期分别延长至（37.8±13.7）d,亦相当于杀灭了1×103左右的白血病细胞。rhIL-2联合苦参碱治疗组平均生存期为（37.0±1.87）d,与单用比较无统计学差异（P＞0.05）。结论 rhIL-2和苦参碱单独应用均有显著抑制微小残留白血病细胞增生的作用,但两者联合应用无明显协同作用 相似文献