Abstract
Tamoxifen (TAM) is known to have a dual mechanism of action: (1) to compete with 17β-estradiol (E2) at the receptor site and to block the promotional role of E2 in breast cancer; and (2) to bind DNA after metabolic activation and to initiate carcinogenesis. Recent large clinical trials indicate that TAM is also an effective chemopreventive agent against breast cancer. The mechanism is unknown. Because E2 requires activation by epoxidation to bind DNA forming DNA adducts [1], and the same is true for TAM [2], the question is whether this preventive effect of TAM against breast cancer is contributory to the possibility that TAM, as an effective competitor for epoxidation, prevents the formation of E2 epoxide and consequently breast cancer. Evidence will be presented to show that, indeed, when incubated together with E2 for epoxidation, TAM was able to dramatically reduce the formation of E2 epoxide as measured by both the loss of the ability of E2 to inhibit nuclear RNA synthesis, and the reduced binding of [3H]labeled E2 to nuclear DNA. Identical results were obtained when TAM and estrone (E1) were used. These results suggest that the breast cancer preventive effect of TAM is through a competitive epoxidation mechanism with E1/E2.
Highlights
Lymph node biopsy is important as a prognostic factor, and influences therapy
In this study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis
This study was undertaken to determine the effect of wound healing drainages and postsurgical sera obtained from breast carcinoma (BC) patients on proliferation of dormant BC cells and to assess the role of HER2 oncoprotein in this proliferation
Summary
Lymph node biopsy is important as a prognostic factor, and influences therapy. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma, the net growth of epithelial cells results from a growth imbalance in favour of proliferation. The objective of this study was to assess the efficacy of hyperbaric oxygen therapy in symptomatic patients after breast cancer treatment. Conclusion: Hyperbaric oxygen therapy should be considered as a treatment option for patients with persisting symptomatology following breast-conserving therapy. We hypothesized that COX-2 expression was associated with that of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) in human breast cancer. Conclusion: COX-2 expression is significantly associated with increased cellular proliferation and angiogenesis in invasive breast cancer. Recent studies have demonstrated that the sentinel node biopsy (SNB) is a reliable and minimally invasive method for determining the axillary node status in patients with breast cancer. Conclusion: Overexpression of episialin strongly inhibits fat secretion, and critically affects timing of involution of the lactating mammary gland
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