TY - JOUR
T1 - Metastatic behavior of prostate cancer
T2 - Cluster analysis of patterns with respect to estrogen treatment
AU - De la Monte, S. M.
AU - Moore, G. W.
AU - Hutchins, G. M.
PY - 1986
Y1 - 1986
N2 - 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 <P <0.10), but they had significantly greater numbers of metastatic sites (P <0.001) and greater overall tumor burden (P <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 <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 <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 <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.
AB - 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 <P <0.10), but they had significantly greater numbers of metastatic sites (P <0.001) and greater overall tumor burden (P <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 <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 <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 <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.
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M3 - Article
C2 - 3719562
AN - SCOPUS:0022449953
SN - 0008-543X
VL - 58
SP - 985
EP - 993
JO - Cancer
JF - Cancer
IS - 4
ER -