Mechanisms of hormone resistance in breast cancer.
At least half of all advanced breast cancers are positive for estrogen receptor (ER) and progesterone receptor (PR), but many nevertheless fail to respond to endocrine therapy. Studies of breast cancer cell lines and breast tumor specimens are beginning to reveal molecular heterogeneity of the receptors in subpopulations of these cells, leading to altered receptor function and sometimes to hormone resistance. Here we will review the data on molecular and cellular heterogeneity involving ER and PR, and possible underlying mechanisms of resistance to tamoxifen and progestins.
Horwitz
K B
KB
Dept. of Medicine, University of Colorado Health Sciences Center, Denver 80262.
D000595:Amino Acid Sequence; D001943:Breast Neoplasms / Q000737:chemistry / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D002455:Cell Division / Q000187:drug effects; D004351:Drug Resistance; D005260:Female; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D011372:Progestins / Q000627:therapeutic use*; D011960:Receptors, Estrogen / Q000032:analysis / Q000235:genetics*; D011980:Receptors, Progesterone / Q000187:drug effects / Q000235:genetics*; D013629:Tamoxifen / Q000494:pharmacology / Q000627:therapeutic use*; D014407:Tumor Cells, Cultured
D011372:Progestins; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013629:Tamoxifen