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染色体异常对硼替佐米治疗初治多发性骨髓瘤疗效及预后的影响

发布时间:2019-08-12 10:26
【摘要】:目的:探讨染色体异常对硼替佐米治疗初治多发性骨髓瘤(MM)疗效及预后的影响。方法:收集本院2008年1月至2011年12月收治的152例初治MM患者资料,对患者均采用以硼替佐米为主的多药联合化疗方案治疗并于4个用期后分析疗效;同时制备染色体标本,分别采用R显带技术和DNA序列探针进行核型和基因(RB1缺失、D13S319缺失、P53缺失、IgH重排和1q21扩增)分析,分析总体疗效及染色体异常患者的疗效和远期生存情况,采用Kaplan-Meier法进行生存分析,COX风险比例模型进行多因素分析。结果:152例MM患者中检出核型异常者47例(30.92%),RB1异常者43例(28.29%),D13S319异常者49例(32.24%),P53异常者30例(19.74%),IgH异常者58例(38.16%),1q21异常者33例(21.71%)。全组152例患者的疗效均可以评价,其中获CR、nCR、PR、MR和PD者分别为24、54、21、14和39例,总有效率为74.34%,显效率为50.66%;核型、D13S319、P53及IgH异常者的总有效率和显效率均低于相应正常者(P0.05),RB1、1q21异常者的显效率均低于相应正常者(P0.05);全组随访22-72个月,中位随访52.0个月,截至随访日期,中位生存期(OS)尚未达。不同染色体异常者的中位OS均低于正常者(P0.05);经COX多因素模型分析发现,染色体异常均为影响MM预后的独立因素,如核型、RB1、D13S319、P53、IgH和1q21异常相对于正常者的风险分别提高了3.124、1.177、2.639、6.552、2.045和7.264倍,差异均有统计学意义。结论:染色体异常可影响硼替佐米治疗初治MM的疗效及预后,检测染色体异常对初治MM的治疗有一定参考价值。
[Abstract]:Objective: to investigate the effect of chromosome abnormality on the efficacy and prognosis of bortezomib in the treatment of (MM) in patients with multiple myeloma. Methods: the data of 152 patients with MM treated in our hospital from January 2008 to December 2011 were collected. All the patients were treated with bortezomib combined chemotherapy regimen and the curative effect was analyzed after 4 periods of use. At the same time, chromosome specimens were prepared and karyotype and gene (RB1 deletion, D13S319 deletion, p53 deletion, IgH rearrangement and 1q21 amplification) were analyzed by R banding technique and DNA sequence probe, respectively. the overall curative effect and the curative effect and long-term survival of patients with chromosome abnormality were analyzed. Kaplan-Meier method was used for survival analysis and COX risk ratio model was used for multivariate analysis. Results: abnormal karyotype was found in 47 cases (30.92%), abnormal RB1 in 43 cases (28.29%), abnormal D13S319 in 49 cases (32.24%), abnormal p53 in 30 cases (19.74%) in 58 cases (38.16%), abnormal 1q21 in 33 cases (21.71%), and abnormal karyotype in 47 cases (30.92%), abnormal RB1 in 43 cases (28.29%), abnormal D13S319 in 49 cases (32.24%), abnormal p53 in 58 cases (38.16%) and abnormal 1q21 in 33 cases (21.71%). The total effective rate and effective rate of CR,nCR,PR,MR and PD were 24, 54, 21, 14 and 39, respectively, the total effective rate was 74.34%, the effective rate was 50.66%, the total effective rate and effective rate of abnormal p53 and IgH were lower than those of the corresponding normal group (P 0.05), and the effective rate of abnormal RB1,1q21 was lower than that of the corresponding normal group (P 0.05). The follow-up period was 22 鈮,

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