ABSTRACT
Compelling evidence points to an estrogen receptor independent mechanism of action of tamoxifen in the extracellular matrix, in addition to its action via the estrogen receptors. We retrospectively studied 380 patients who underwent curative resection for primary breast cancer in our institution from January 1994 to December 1998, of which 227 received tamoxifen in the perioperative period and the remaining 153 never received tamoxifen or delayed the initiation of treatment for at least two weeks following the operation. The administration of tamoxifen in the perioperative period resulted in the prolongation of axillary drainage (mean 10.07 SD 4.18 days vs mean 8.33 SD 2.85 days), which was statistically significant for patients younger than 70 years. There was no difference in the duration of fluid drainage in relation to the number of positive nodes, except in cases of more than 9 nodes involved by the tumor. We assumed that tamoxifen causes a delay in would healing through the secretion of active transforming growth factor beta(TGF-beta), which is the principle negative growth modulator and which can be secreted from epithelial and stromal elements, independently of hormonal receptor status.
