Understanding the biologic mechanisms responsible for breast-cancer progression during tamoxifen or fulvestrant treatment.

Background: Dehydroepiandosterone sulfate (DHEAS) causes breast-cancer proliferation, even during tamoxifen or fulvestrant blockade. The purpose of this study was to determine possible mechanisms for this treatment failure.

Methods: T-47D cells (estrogen receptor [ER] and progesterone receptor [PR] positive) were treated with fulvestrant (10 micromol/L), tamoxifen (10 mmol/L or 0.

DNA fingerprints provide a patient-specific breast cancer marker.

Background: Detection of systemic breast cancer recurrence is limited by lack of universally expressed tumor cell markers. We hypothesized that a test that detects genetic alterations specific to breast cancer cells of an individual patient would provide a superior cancer marker.

Methods: DNA was extracted from blood, primary tumor, and axillary lymph nodes of 33 breast cancer patients and normal breast tissue of 12 control patients.

Relationships among delay of diagnosis, extent of disease, and survival in patients with abdominal carcinoid tumors.

Background: A correlation between delay in diagnosis of carcinoid and extent of disease and survival was investigated.

Methods: In all, 115 patients with carcinoid were interviewed. Data collected included symptoms, delay of diagnosis, incorrect diagnoses given, extent of disease at diagnosis, and survival.

Estrogen and androgen receptors as comediators of breast cancer cell proliferation: providing a new therapeutic tool.

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.

Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant.

Hypothesis: Dehydroepiandrosterone sulfate (DHEA-S) causes a proliferation of estrogen receptor (ER)-positive breast cancer cells, even with tamoxifen citrate blockade. The ER antagonist ICI 182780 (fulvestrant) will more effectively stop the proliferative effect of DHEA-S on breast cancer cells.

Design: Examination of in vitro breast cancer cell growth in the presence of fulvestrant and DHEA-S.

Serum peptide profiles in patients with carcinoid tumors.

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.

The effect of high dehydroepiandrosterone sulfate levels on tamoxifen blockade and breast cancer progression.

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.

A new score for the evaluation of palpable breast masses in women under age 40.

Background: The purpose of this study was to develop a rapid and accurate diagnostic test for palpable breast masses in women under age 40.

Methods: Masses were evaluated utilitzing a modified triple test score (MTTS), which assigned scores of 1 point for benign, 2 points for suspicious, or 3 points for malignant findings from physical examination, ultrasonography, and fine needle aspiration. The MTTS was the sum of the three scores and was correlated with biopsy or follow-up.

The impact of hormone replacement therapy on the detection and stage of breast cancer.

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.

Proliferation of rhesus ovarian surface epithelial cells in culture: lack of mitogenic response to steroid or gonadotropic hormones.

Ovarian cancer is the most lethal gynecological cancer, and approximately 90% of ovarian cancers derive from the ovarian surface epithelium (OSE), yet the biology of the OSE is poorly understood. Factors associated with increased risk of non-hereditary ovarian cancer include the formation of inclusion cysts, effects of reproductive hormones and the number of ovulations experienced in a woman's lifetime. Distinguishing between these factors is difficult in vivo, but cultured OSE cells are viable tools for some avenues of research.