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血浆脂联素水平与不同分子亚型乳腺癌发生风险的相关性研究

Association Between Plasma Adiponectin and Risk of Breast Cancer by Molecular Subtypes

  • 摘要:
      目的  探讨血浆脂联素水平与不同分子亚型乳腺癌发生风险的相关性。
      方法  本研究采用病例对照设计,选择2014年4月至2015年5月经组织病理学诊断确诊的乳腺癌新发病例437例作为病例组,选择同期健康体检女性469例作为对照组。采用统一编制的结构化调查问卷收集研究对象基本信息并采集血样,采用酶联免疫吸附试验(ELASA)测定血浆脂联素浓度。按绝经状态分层后,采用方差分析比较对照组与不同分子亚型乳腺癌血浆脂联素水平的分布差异,并用无序多分类logistic回归分析血浆脂联素水平与不同分子分型乳腺癌发生风险的相关性。
      结果  乳腺癌患者中有310例Luminal型、83例HER-2过表达型和44例基底型。对照组血浆脂联素水平中位数(P25,P75)为14.85(9.69, 21.35) μg/mL;病例组上述各分子亚型血浆脂联素水平中位数(P25,P75)分别为11.74(8.15, 16.14) μg/mL、12.02(8.43, 16.96) μg/mL和12.67(8.25, 17.27) μg/mL,与对照组相比差异有统计学意义(P0.001)。无序多分类logistic回归显示,调整了混杂因素后,与对照组比,血浆脂联素水平越高,绝经前Luminal型乳腺癌发生风险越低(OR绝经前Luminal=0.50,95%CI:0.27~0.92,P趋势=0.001),绝经后Luminal型和HER-2过表达型乳腺癌发生风险越低(OR绝经后Luminal=0.06,95%CI:0.02~0.23,P趋势 < 0.001;OR绝经后HER-2+=0.06,95%CI:0.01~0.62,P趋势=0.001),其余亚组无统计学意义。
      结论  低血浆脂联素水平将导致绝经前、绝经后Luminal型和绝经后HER-2过表达型乳腺癌的发生风险增高。

     

    Abstract:
      Objective  To explore the relationships between plasma adiponectin levels and risk of breast cancer by molecular subtype.
      Methods  A case-control study including 437 histopathologic confirmed primary breast cancer cases and 469 healthy female controls was conducted between April 2014 and May 2015. Basic information of the participants were collected using a structured questionnaire. Blood samples were collected and the plasma adiponectin levels were measured by enzyme-linked immunosorbent assay (ELASA). Analysis of variance (ANOVA) was used to compare the differences of plasma adiponectin levels among the control group and the breast cancer groups with different molecular subtypes. Multinomial logistic regression was used to investigate the association between plasma adiponectin levels and risk of breast cancer by molecular subtypes. All the statistical analyses were stratified by menopausal status.
      Results  Among the 437 breast cancer cases, there were 310 Luminal breast cancer cases, 83 HER-2-enriched breast cancer cases and 44 basal-like breast cancer cases. The median (P25, P75) of plasma adiponectin level of the controls was 14.85 (9.69, 21.35) μg/mL. The medians (P25, P75) of plasma adiponectin levels of the cases were 11.74 (8.15, 16.14) μg/mL, 12.02(8.43, 16.96) μg/mL and 12.67(8.25, 17.27) μg/mL for Luminal, HER-2-enriched and basal-like subtype respectively, which were statistically different from the controls (P < 0.001). Multinomial logistic regression showed that, after adjustment for the confounders, the higher levels of plasma adiponectin were associated with the lower risks of pre-menopausal Luminal breast cancer (ORpre-menopausal Luminal=0.50, 95%CI: 0.27-0.92, Ptrend=0.001), post-menopausal Luminal breast cancer (ORpost-menopausal Luminal=0.06, 95%CI: 0.02-0.23, Ptrend < 0.001) and post-menopausal HER-2-enriched breast cancer (ORpost-menopausal HER-2-enriched=0.06, 95%CI: 0.01-0.62, Ptrend=0.001).
      Conclusion  Lower levels of plasma adiponectin may increase the risk of pre-menopausal and post-menopausal Luminal breast cancer and post-menopausal HER-2-enriched breast cancer.

     

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