Advanced breast cancer biopsy instrumentation: a critique.

BACKGROUND: Large-core biopsies or open biopsies with needle localization have been the mainstay of treatment for evaluating nonpalpable mammographic abnormalities. The newly introduced Advanced Breast Biopsy Instrumentation (ABBI) system combines digital stereotactic imaging with a highly developed single-use biopsy device to locate and remove a radiographically discovered breast lesion to an accuracy of 1 mm. STUDY DESIGN: We conducted a review of the first 58 cases involving the use of the ABBI system. This article evaluates the accuracy of specimen targeting, the success rate of lesion removal, the operative complications, the mechanical difficulties, and patient satisfaction with the ABBI system. RESULTS: The lesion was removed successfully in 47 of the 58 cases. Nine patients were eliminated in initial screening and the procedure could not be completed in two. Although the success rate was high, 14 of the procedures required conversion to "open" ABBI procedures for completion of the biopsy. CONCLUSIONS: The ABBI system is an alternative to open biopsy with needle localization or large-core biopsy for nonpalpable mammographic abnormalities. This technique allows complete removal of the lesion in a one-step procedure. The ABBI system has certain limitations and mechanical problems, at least currently, and offers an advantage over current diagnostic modalities in a very limited number of cases only.

A novel method for rapid enrichment of lactotrophs from dispersed anterior pituitary cells of the rat.

A polyclonal antibody to the rat D2 dopamine (DA) receptor was rapidly and covalently attached to surface-activated polystyrene cultureware (MicroCEL-Lector plates). Addition of a suspension of dispersed rat anterior pituitary cells resulted in the rapid (within 1 h) selection of cells possessing D2 DA receptors (i.e. lactotrophs). Four-fold enrichment (from about 20% in the suspension to about 80%) was routinely obtained, as judged by prolactin (PRL) immunostaining. The enriched cells were virtually free of fibroblasts and were much more homogeneous in appearance than untreated cells after 3 days in culture. Lactotroph-enriched cell cultures displayed similar functional characteristics as untreated cells when assessed by determining dose-response curves for inhibition of PRL secretion by the DA agonist N-propylnorapomorphine. This method may be generally applicable for the selective enrichment and purification of desired cell types from heterogeneous mixtures in tissue dispersions.

Comparative effects of receptor inactivation, 17 beta-estradiol and pertussis toxin on dopaminergic inhibition of prolactin secretion in vitro.

Akin to receptor inactivation with phenoxybenzamine (PBZ) (1 microM, 1 hr), treatment of anterior pituitary cells with 17 beta-estradiol (10 nM, 3 days) right-shifted the dose-response curve for inhibition of prolactin (PRL) secretion by the full agonist R-(-)-N-n-propylnorapomorphine (NPA) and reduced the maximal effect [EC50 (pM) and percent maximal effect: control, 25.4 and 81.2; PBZ, 115.3 and 57.9; 17 beta-estradiol, 358 and 58.6]. PBZ treatment of 17 beta-estradiol-pretreated cultures further reduced the maximal response but did not alter the EC50. Plots of receptor occupancy vs. response indicated a large receptor reserve for NPA (approximately 60%) in control cultures but its abolition by 17 beta-estradiol. 17 beta-Estradiol pretreatment elicited identical rightward shifts (4.5-fold) and similar reductions in maximal PRL inhibition by quinpirole and (+)-3-PPP, although these drugs were partial agonists with dissimilar efficacies relative to NPA (0.61 and 0.12, respectively) at presynaptic striatal D2 receptors. However, receptor inactivation experiments with (+)-3-PPP and quinpirole, and subsequent comparison of receptor occupancy vs. response plots, demonstrated that the relative efficacies of quinpirole and (+)-3-PPP were reversed in the striatum and anterior pituitary. In striatum, half-maximal response to quinpirole and (+)-3-PPP required 6.2 and 30% receptor occupancy, respectively, whereas 25.6 and 9.6% occupancy was required in the pituitary. Pertussis toxin treatment (10 ng/ml, 24 hr) produced large shifts in the dose-response curves for all three agonists (8.4-21.9-fold), but was distinguished from the effects of both PBZ and 17 beta-estradiol by a significant (P < .001) decrease in the slope factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Receptor reserve for D2 dopaminergic inhibition of prolactin release in vivo and in vitro.

The full dopamine agonist R-(-)-N-n-propylnorapomorphine (NPA) completely suppressed (ED50 0.12 micrograms/kg) serum prolactin (PRL) levels elevated by pretreatment with gamma-butyrolactone (750 mg/kg). Pretreatment with the receptor-inactivating agent N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (1 and 2 x 6 mg/kg) progressively shifted the dose-response curve for NPA to the right, but PRL secretion was still maximally inhibited. Receptor inactivation elicited smaller (2-fold) dextral shifts in the ED50 for the partial agonists (+)- and (-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine. These results are consistent with the presence of a sizable receptor reserve at the D2 receptor regulating PRL release in the anterior pituitary. Analogous results were obtained in vitro utilizing primary cultures of anterior pituitary cells. NPA potently inhibited basal PRL release in culture (ED50 0.06 nM, maximal inhibition 83%). Receptor alkylation with phenoxybenzamine (1 microM, 1 hr) did not affect basal PRL release but right-shifted the ED50 for NPA more than 6-fold and attenuated maximal inhibition (to 68%); both effects were significant (P less than .01). The extracellular accumulation of cyclic AMP (cAMP) stimulated by a combination of forskolin (1 microM) and 3-isobutyl-1-methyl xanthine (100 microM) required higher concentrations of NPA (ED50 0.36 nM), and the maximal effect was much smaller (46%). Phenoxybenzamine treatment did not alter either basal or forskolin-stimulated cAMP accumulation, but it reduced the maximal inhibitory response to NPA (to 13%) without shifting the ED50. Plots of receptor occupancy vs. response demonstrated a 60% receptor reserve for NPA inhibition of PRL release, but none for inhibition of cAMP production.(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of spare autoreceptors regulating dopamine agonist inhibition of tyrosine hydroxylation in slices of rat striatum.

Incubation of rat striatal slices with forskolin (0.05-10 microM) elicited a dose-dependent increase in the activity of tyrosine hydroxylase (TH) assayed in subsequently solubilized extracts of the enzyme. At low concentrations (33 microM) of the cofactor (6R)-5,6,7,8-tetrahydro-L-biopterin dihydrochloride TH activity was increased 2.5 to 3-fold. Kinetic analysis of TH activity as a function of (6R)-5,6,7,8-tetrahydro-L-biopterin dihydrochloride concentration indicated that the enzyme isolated from control slices was composed of multiple species with different Km's for cofactor. Treatment with forskolin (1.5-15 microM) converted the enzyme into a single species with a low Km (28 microM) for (6R)-5,6,7,8-tetrahydro-L-biopterin dihydrochloride. The dopamine (DA) agonist R-(-)-N-n-propylnorapomorphine (0.1 microM) reversed forskolin-induced activation of TH. Concentration-response curves were obtained for inhibition of forskolin-stimulated TH by R-(-)-N-n-propylnorapomorphine and the DA autoreceptor-selective agonists (+)- and (-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine and 3-[4-(4-phenyl-1,2,3,6-tetrahydropyridyl-1)-butyl]indole. R-(-)-N-n-propylnorapomorphine maximally inhibited forskolin-stimulated activity 85%, as indicated by ALLFIT computer analysis of concentration-response curves. (+)-3-(3-hydroxyphenyl)-N-n-propylpiperidine and 3-[4-(4-phenyl-1,2,3,6-tetrahydropyridyl-1)-butyl]indole produced a lower degree of maximal inhibition (54 and 63%, respectively), whereas (-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine was inactive. The D2 DA receptor blocker sulpiride (1 microM) competitively antagonised the effects of all the agonists.(ABSTRACT TRUNCATED AT 250 WORDS)