Abstract
Objective: to determine a possible correlation between the tumor response in patients suffering from breast cancer, initially treated with tamoxifen, and plasma concentration of this drug.Methods: we studied 27 elderly patients (age range: 62 to 82 y) with advanced breast carcinoma who were treated with a daily dose of 20 mg of oral tamoxifen, for 3 mo. Responders were followed-up for 19 mo, and nonresponders for 21 mo. We measured plasma tamoxifen citrate levels in order to determine their possible correlation with objective remission of the disease.Results: the correlation was found to be significant among responders (37%), whose median plasma tamoxifen level was 187.40ng. ml-1, when comparing to non-responders, whose median plasma tamoxifen level was 99.52ng. ml-1. The frequency distribution of patients in both groups with concentration of tamoxifen lower and higher than 182.60ng. ml-1 was significant (fisher’s test p-value<0,0011).Conclusion: considering the results herein, we suggest that patients whose plasma tamoxifen levels reach 182.60ng. ml-1 after 3 mo of treatment, with no tumor response, may not benefit from this treatment, and an alternative therapy should be regarded.
Highlights
Hormonal manipulation was one of the first modalities of palliative treatment among the therapies for breast cancer
One of the major additive treatments is based on the use of tamoxifen, which belongs to a group of compounds structurally different from estrogens because of their ability to interact with estrogen receptors, acting either as estrogen agonists or antagonists depending on the target tissue and the hormonal medium
A total of 35 blood samples were obtained from the 27 patients; 8 of them obtained as a control before treatment, and the remaining 27 after 3 mo of treatment
Summary
Hormonal manipulation was one of the first modalities of palliative treatment among the therapies for breast cancer. One of the major additive treatments is based on the use of tamoxifen, which belongs to a group of compounds structurally different from estrogens because of their ability to interact with estrogen receptors, acting either as estrogen agonists or antagonists depending on the target tissue and the hormonal medium. There is no doubt that its role as a blocker of estrogen-binding to its receptor by its own binding to the receptor promotes an antagonistic antiestrogen effect. Another mechanism of its antiproliferative action is the induction of growth factors (TGF-β), which acts as a negative intracellular regulator by an autocrine action when produced intracellularly, or by a paracrine action when produced by mammary tissue stroma [3]
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