de la Monte S M, Moore G W, Hutchins G M
Cancer. 1986 Aug 15;58(4):985-93. doi: 10.1002/1097-0142(19860815)58:4<985::aid-cncr2820580432>3.0.co;2-i.
The responsiveness of prostate cancer to treatment with estrogen has been recognized for over 40 years, but whether the effect is mediated by diminished tumor growth or reduction in metastatic spread is not known. To answer this question the authors reviewed the clinical and pathologic features of 89 patients with metastatic prostate cancer after autopsy. Sixty-three percent of the patients studied were black. Patients treated with estrogen survived somewhat longer (0.05 less than P less than 0.10), but they had significantly greater numbers of metastatic sites (P less than 0.001) and greater overall tumor burden (P less than 0.001), with significantly increased frequencies of metastases to the liver, adrenal gland, bone, lymph nodes, large bowel, lungs, serosal surfaces, ureters, and central nervous system (CNS) (all P less than 0.05 or lower) compared with patients who had not been treated with estrogen. However, patients not treated with estrogen more frequently died from other causes (P less than 0.001). When the patients who died from other causes were excluded from the data analysis, there were no significant differences in the number of metastatic sites between patients who received estrogen therapy and those who did not, and the only remaining significant difference in the distribution of metastases was that patients who received estrogen treatment had more frequent metastases to the adrenal cortex and CNS (P less than 0.05). These observations were corroborated by cluster analysis of the metastatic patterns. Cluster analysis also identified a subset of predominantly (67%) black patients who developed distant metastases without much local spread of tumor. This suggests that tumor behavior in this group was less predictable than for the other patients in whom disease appeared to progress from Stage A to Stage D as expected. The authors conclude that estrogen therapy may prolong survival by slowing the rate of tumor growth rather than by inhibiting the metastatic progression of prostate cancer or destroying selective populations of tumor cells.
前列腺癌对雌激素治疗的反应性在40多年前就已得到认可，但这种效应是由肿瘤生长减缓还是转移扩散减少介导的尚不清楚。为了回答这个问题，作者回顾了89例转移性前列腺癌患者尸检后的临床和病理特征。研究的患者中有63%是黑人。接受雌激素治疗的患者存活时间稍长一些（0.05＜P＜0.10），但他们的转移部位明显更多（P＜0.001），总体肿瘤负荷更大（P＜0.001），与未接受雌激素治疗的患者相比，转移至肝脏、肾上腺、骨骼、淋巴结、大肠、肺、浆膜表面、输尿管和中枢神经系统（CNS）的频率显著增加（所有P＜0.05或更低）。然而，未接受雌激素治疗的患者更常死于其他原因（P＜0.001）。当将死于其他原因的患者排除在数据分析之外时，接受雌激素治疗的患者和未接受雌激素治疗的患者在转移部位数量上没有显著差异，转移分布中唯一剩下的显著差异是接受雌激素治疗的患者肾上腺皮质和CNS转移更频繁（P＜0.05）。这些观察结果通过转移模式的聚类分析得到了证实。聚类分析还确定了一个主要为（67%）黑人的患者亚组，他们发生远处转移时肿瘤局部扩散较少。这表明该组患者的肿瘤行为比其他患者更难以预测，在其他患者中疾病似乎按预期从A期进展到D期。作者得出结论，雌激素治疗可能通过减缓肿瘤生长速度而非抑制前列腺癌的转移进展或破坏肿瘤细胞的选择性群体来延长生存期。
