Tuominen Rainer, Jewell Rosalyn, van den Oord Joost J, Wolter Pascal, Stierner Ulrika, Lindholm Christer, Hertzman Johansson Carolina, Lindén Diana, Johansson Hemming, Frostvik Stolt Marianne, Walker Christy, Snowden Helen, Newton-Bishop Julia, Hansson Johan, Egyházi Brage Suzanne
Department of Oncology and Pathology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Int J Cancer. 2015 Jun 15;136(12):2844-53. doi: 10.1002/ijc.29332. Epub 2014 Nov 24.
To investigate the predictive and prognostic value of O(6) -methylguanine DNA methyltransferase (MGMT) inactivation by analyses of promoter methylation in pretreatment tumor biopsies from patients with cutaneous melanoma treated with dacarbazine (DTIC) or temozolomide (TMZ) were performed. The patient cohorts consisted of Belgian and Swedish disseminated melanoma patients. Patients were subdivided into those receiving single-agent treatment with DTIC/TMZ (cohort S, n = 74) and those treated with combination chemotherapy including DTIC/TMZ (cohort C, n = 79). Median follow-up was 248 and 336 days for cohort S and cohort C, respectively. MGMT promoter methylation was assessed by three methods. The methylation-related transcriptional silencing of MGMT mRNA expression was assessed by real-time RT-PCR. Response to chemotherapy and progression-free survival (PFS) and overall survival were correlated to MGMT promoter methylation status. MGMT promoter methylation was detected in tumor biopsies from 21.5 % of the patients. MGMT mRNA was found to be significantly lower in tumors positive for MGMT promoter methylation compared to tumors without methylation in both treatment cohorts (p < 0.005). DTIC/TMZ therapy response rate was found to be significantly associated with MGMT promoter methylation in cohort S (p = 0.0005), but did not reach significance in cohort C (p = 0.16). Significantly longer PFS was observed among patients with MGMT promoter-methylated tumors (p = 0.002). Multivariate Cox regression analysis identified presence of MGMT promoter methylation as an independent variable associated with longer PFS. Together, this implies that MGMT promoter methylation is associated with response to single-agent DTIC/TMZ and longer PFS in disseminated cutaneous melanoma.
通过分析接受达卡巴嗪(DTIC)或替莫唑胺(TMZ)治疗的皮肤黑色素瘤患者预处理肿瘤活检组织中的启动子甲基化,来研究O(6)-甲基鸟嘌呤-DNA甲基转移酶(MGMT)失活的预测和预后价值。患者队列包括比利时和瑞典的播散性黑色素瘤患者。患者被分为接受DTIC/TMZ单药治疗的患者(队列S,n = 74)和接受包括DTIC/TMZ在内的联合化疗的患者(队列C,n = 79)。队列S和队列C的中位随访时间分别为248天和336天。MGMT启动子甲基化通过三种方法进行评估。通过实时逆转录聚合酶链反应评估MGMT mRNA表达的甲基化相关转录沉默。化疗反应、无进展生存期(PFS)和总生存期与MGMT启动子甲基化状态相关。在21.5%的患者肿瘤活检组织中检测到MGMT启动子甲基化。在两个治疗队列中,与无甲基化的肿瘤相比,MGMT启动子甲基化阳性的肿瘤中MGMT mRNA显著更低(p < 0.005)。在队列S中发现DTIC/TMZ治疗反应率与MGMT启动子甲基化显著相关(p = 0.0005),但在队列C中未达到显著水平(p = 0.16)。在MGMT启动子甲基化肿瘤患者中观察到显著更长的PFS(p = 0.002)。多变量Cox回归分析确定MGMT启动子甲基化的存在是与更长PFS相关的独立变量。总之,这意味着MGMT启动子甲基化与播散性皮肤黑色素瘤对单药DTIC/TMZ的反应以及更长的PFS相关。