Paré L, Marcuello E, Altés A, del Río E, Sedano L, Salazar J, Cortés A, Barnadas A, Baiget M
Department of Genetics, Hospital de la Santa Creu i Sant Pau, Universitat Autonoma de Barcelona [corrected] Barcelona 08025, Spain.
Br J Cancer. 2008 Oct 7;99(7):1050-5. doi: 10.1038/sj.bjc.6604671. Epub 2008 Sep 16.
To determine whether molecular parameters could be partly responsible for resistance or sensitivity to oxaliplatin (OX)-based chemotherapy used as first-line treatment in advanced colorectal cancer (CRC). We studied the usefulness of the excision repair cross-complementing 1 (ERCC1), xeroderma pigmentosum group D (XPD), XRCC1 and GSTP1 polymorphisms as predictors of clinical outcome in these patients. We treated 126 CRC patients with a first-line OX/5-fluorouracil chemotherapeutic regimen. Genetic polymorphisms were determined by real-time PCR on an ABI PRISM 7000, using DNA from peripheral blood. Clinical response (CR), progression-free survival (PFS) and overall survival (OS) were evaluated according to each genotype. In the univariate analysis for CR, ERCC1-118 and XPD 751 polymorphisms were significant (P=0.02 and P=0.05, respectively). After adjustment for the most relevant clinical variables, only ERCC1-118 retained significance (P=0.008). In the univariate analysis for PFS, ERCC1-118 and XPD 751 were significant (P=0.003 and P=0.009, respectively). In the multivariant analysis, only the XPD 751 was significant for PFS (P=0.02). Finally, ERCC1-118 and XPD 751 polymorphisms were significant in the univariate analysis for OS (P=0.006 and P=0.015, respectively). Both genetic variables remained significant in the multivariate Cox survival analysis (P=0.022 and P=0.03). Our data support the hypothesis that enhanced DNA repair diminishes the benefit of platinum-based treatments.
为了确定分子参数是否可能部分导致晚期结直肠癌(CRC)一线治疗中对奥沙利铂(OX)为基础的化疗产生耐药或敏感。我们研究了切除修复交叉互补基因1(ERCC1)、着色性干皮病D组(XPD)、XRCC1和谷胱甘肽S-转移酶P1(GSTP1)基因多态性作为这些患者临床结局预测指标的实用性。我们用一线OX/5-氟尿嘧啶化疗方案治疗了126例CRC患者。使用外周血DNA,通过ABI PRISM 7000上的实时PCR确定基因多态性。根据每种基因型评估临床缓解(CR)、无进展生存期(PFS)和总生存期(OS)。在CR的单因素分析中,ERCC1 - 118和XPD 751基因多态性具有显著性(分别为P = 0.02和P = 0.05)。在对最相关临床变量进行校正后,只有ERCC1 - 118仍具有显著性(P = 0.008)。在PFS的单因素分析中,ERCC1 - 118和XPD 751具有显著性(分别为P = 0.003和P = 0.009)。在多因素分析中,只有XPD 751对PFS具有显著性(P = 0.02)。最后,在OS的单因素分析中,ERCC1 - 118和XPD 751基因多态性具有显著性(分别为P = 0.006和P = 0.015)。在多因素Cox生存分析中,这两个基因变量均保持显著性(P = 0.022和P = 0.03)。我们的数据支持这样的假设,即增强的DNA修复会降低铂类治疗的获益。