Some properties of the ecdysteroid receptor in the salivary gland of the ixodid tick, Amblyomma hebraeum.

Salivary gland degeneration in ixodid ticks is triggered by an ecdysteroid hormone. We used [3H]ponasterone A (PoA) as a specific ligand to detect the ecdysteroid receptor in the salivary glands of large, partially fed female ticks (Amblyomma hebraeum Koch; Acari: Ixodidae). Binding of [3H]PoA was thermolabile and sensitive to pronase, but not to DNase or RNase, indicating that the ligand binds to a protein.

Androgen receptor in the harderian glands of the golden hamster: characterization and the effects of androgen deprivation, the pituitary, and gender.

The harderian glands of the golden hamster were found, by a competitive binding assay using [3H]mibolerone as the ligand, to have a high affinity androgen receptor. In intact male hamsters, this receptor was present in both cytosolic and nuclear KCl-extractable fractions. Castration or hypophysectomy led to 3- to 5-fold increases in the concentrations of cytosolic receptor with decreased dissociation constants.

Correlation between c-erbB-2 amplification and risk of recurrent disease in node-negative breast cancer.

Drawing upon the comprehensive population-based Northern Alberta Breast Cancer Registry containing 704 patients with histologically negative axillary lymph nodes who have been followed for 5-16 years, we have undertaken a retrospective case-control study to evaluate the utility of genomic amplification of specific protooncogenes [c-erbB-2 (nee HER-2/neu), c-erbA, c-myc, int-2, and hst-1] as predictive indicators of clinical outcome in node-negative disease. To this end, 115 women with node-negative breast cancer who had recurred at any time up to 16 years posttreatment (cases) were matched pairwise for appropriate clinicopathological variables (size of primary tumor, menopausal state, estrogen receptor status, anniversary year of treatment, and patient age) with a second group of 115 women (controls) selected from a cohort of 502 node-negative patients who had not relapsed during long-term follow-up. Tumor DNA extracted from archival formalin-fixed, paraffin-embedded tissue blocks were analyzed for protooncogene copy number by slot-blot hybridization.

Immunoassay for estrogen receptor does not detect inactivated receptor.

Accurate quantification of estrogen receptor (ER) is essential for optimal clinical characterization of individual cases of breast cancer. If breast tumors are mishandled, the relatively labile ER protein may lose its steroid-binding capacity (become inactivated) and not be measurable by the routine steroid-binding assay. We tested whether the commercial enzyme immunoassay of Abbott Laboratories could quantify inactivated ER.

The levo enantiomer of o,p'-DDT inhibits the binding of 17 beta-estradiol to the estrogen receptor.

It has been discovered previously that the known estrogenic activity of o,p'-DDT resides with the levo enantiomer. Since it has been presumed that this relatively weak estrogenic activity of o,p'-DDT is mediated by the estrogen receptor, the ability of the resolved enantiomeric forms of o,p'-DDT to inhibit the binding of 17 beta-estradiol to the receptor was investigated. Competitive binding assays including the use of double-reciprocal plots and sucrose gradient analyses revealed that the levo and not the dextro enantiomer could inhibit the estradiol binding to the estrogen receptor.