Abstract
Several major defects in the estrogen receptor pathway have been evidenced in most human breast cancers by an immunofluorescence tracing of estradiol receptor complexes at the single cell level. Endogenous peroxidase seems a reliable postreceptor marker for estrogen-sensitive breast cancer cells. Since almost all human breast cancers appear to include both hormone-sensitive and autonomous cell populations, a combined use of endocrine and cytotoxic regimens is urged. The hormonal regulation of tumor growth parameters could be exploited in order to achieve a maximum recruitment of synchronized tumor cells at risk to chemotherapy.
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