Differential prognostic impact of the cyclins E and B in premenopausal and postmenopausal women with lymph node-negative breast cancer
Differential prognostic impact of the cyclins E and B in premenopausal and postmenopausal women with lymph node-negative breast cancer
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DOI：
10.1002/ijc.11132
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发表时间：
2003-07-10
影响因子：
6.4
通讯作者：
Parwaresch, R
中科院分区：
文献类型：
--
作者：
Rudolph, P;Kühling, H;Parwaresch, R
为了寻找新的预后因素，我们研究了细胞周期蛋白表达对乳腺癌预后的影响。对273例pT 1/pT 2 NO乳腺癌患者的存档肿瘤标本进行细胞周期蛋白E、A和B的免疫染色。结果被评估为无转移（MFS）和疾病特异性生存期（DSS），中位观察期为99个月。在绝经后妇女中，细胞周期蛋白E显著预测DSS，而在绝经前患者中，细胞周期蛋白B显著预测DSS。细胞周期蛋白A无统计学意义。当在多变量分析中比较细胞周期蛋白与标准预后指标的预后影响时，细胞周期蛋白E和细胞周期蛋白B分别被选为绝经后和绝经前患者生存的独立预测因子。在模型中加入Ki-67后，细胞周期蛋白E失去了意义，而细胞周期蛋白B仍然是唯一的独立预后因素，肿瘤相关死亡的风险比为4.5（p = 0.026）。因此，如果考虑到与绝经状态的关系，对细胞周期蛋白表达的评估可能会完善目前的预后模型。细胞周期蛋白的预后相关性可能归因于对增殖、细胞存活和遗传不稳定性的影响。了解导致细胞周期蛋白表达失调的分子机制可能会指导风险适应性治疗方案的决策。
Searching for new prognostic factors, we investigated the influence of cyclin expression on breast cancer prognosis. A total of 273 archival tumor specimens from patients with pT1/pT2 NO breast cancers treated by surgery and local irradiation were immunostained for cyclins E, A and B. Outcome was evaluated as metastasis-free (MFS) and diseasespecific survival (DSS) over a median observation period of 99 months. In postmenopausal women, DSS was significantly predicted by cyclin E, and in premenopausal patients by cyclin B. No statistical significance was found for cyclin A. When the prognostic impact of cyclins was compared to that of standard prognostic indicators in a multivariate analysis, both cyclin E and cyclin B were selected as independent predictors of survival in postmenopausal and premenopausal patients, respectively. After inclusion of Ki-67 in the model, cyclin E lost its significance, whereas cyclin B remained the only independent prognostic factor with a hazard ratio of 4.5 (p = 0.026) for tumor-related death. Assessment of cyclin expression may, therefore, refine current prognostic models if considered in relation to menopausal status. The prognostic relevance of cyclins is likely attributable to an influence on proliferation, cell survival and genetic instability. Awareness of the molecular mechanisms leading to deregulated cyclin expression may guide decisions for risk-adapted therapy regimens.