Hypothesis: Dehydroepiandrosterone sulfate (DHEA-S) comediates breast cancer progression via estrogen receptors (ERs) and androgen receptors (ARs).
Design: Breast cancer cells that were ER positive-AR positive or ER negative-AR positive were pretreated with anastrozole, tamoxifen citrate, or bicalutamide, then stimulated with 228 microM DHEA-S.
Setting: University Surgical Oncology Research Laboratory.
Background: Patterns of elevated serum peptides may reveal additional markers and permit better classification of tumors based on (secondary) peptide secretion.
Methods: Fasting peptide profiles were obtained from 31 carcinoid patients. vasoactive intestinal peptide (VIP), pancreatic polypeptide (PP), neurotensin, substance P, gastrin-releasing polypeptide (GRP), calcitonin, gastrin, and pancreastatin were measured.
Background: We investigated the stimulatory potential of dehydroepiandrosterone sulfate (DHEA-S) on tamoxifen-treated cells and assessed its effect on cancer progression in the adjuvant setting.
Methods: Mean serial serum levels of sex hormones from 44 patients receiving tamoxifen were correlated with follow-up status. T-47D (ER+/PR+) and HCC1937 (ER-/PR-) breast cancer cells were pretreated with 100 microM anastrozole, with or without tamoxifen, and stimulated with 22.
Hypothesis: Patients who receive hormone replacement therapy (HRT) and subsequently develop breast cancer are more likely to be diagnosed by palpation than mammography and have a higher stage of cancer at initial diagnosis.
Design: Retrospective case series.
Setting: University hospital.