Acquired tamoxifen resistance in human breast cancer--potential mechanisms and clinical implications

Anti-cancer Drugs
S R Johnston

Abstract

The widespread use of the antiestrogen tamoxifen in the management of breast cancer has resulted in more patients eventually developing acquired resistance to the drug. Tumors may often retain sensitivity to further endocrine therapies despite resistance to tamoxifen. The basis for this partial form of acquired resistance in vivo has been the subject of several recent investigations and the likely mechanisms are reviewed in this article. Ineffective antiestrogen blockade could result from metabolic tolerance and inadequate intra-tumoral concentrations of the drug. Alternatively, there is experimental evidence that tamoxifen's partial agonist activity may be responsible for stimulation of tumor re-growth. Studies of the estrogen receptor (ER) have shown that in many cases expression of a fully functional wild-type receptor continues at relapse. Experimental evidence that mutant or variant forms of the receptor may account for resistance have not been confirmed by recent in vivo studies. There is some evidence for re-modeling of ER expression at relapse and it remains to be determined if there is enhanced sensitivity of ER+ cells to hormonal stimuli at relapse. Clonal selection of an ER- phenotype may occur in some instances, esp...Continue Reading

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