Search

Objective: The primary objective was to quantify and compare the accuracy and failure rates of directional vacuum assisted biopsy (DVAB) and core needle biopsy (CNB) when used under stereotactic (ST) guidance to biopsy suspicious breast lesions identified with screening mammography., Methods: We performed a systematic review of the literature published from January 1996 to July 2004, reporting all-comers populations in Western-style health care systems (i.e., North America, Europe, Australia or New Zealand), referred after screening mammography for breast biopsy using DVAB or CNB under ST guidance. Meta-analyses were conducted for DVAB and CNB, using open surgical biopsy and/or long-term clinical and/or mammogram follow-up as the diagnostic reference standard. The main outcomes of interest were those of greatest clinical relevance, i.e., miss rates and underestimation rates for malignancy. Also, technical failure rate and non-diagnostic rate were assessed for each biopsy method., Results: Thirty-five studies qualified for the review. There were 12 studies with a DVAB group (n=5,119 patients), and 25 studies with a CNB group (n=6,236). There were no studies including both a DVAB and a CNB group, thus precluding any direct, within-study comparisons of accuracy. Overall agreement rate between DVAB and the reference standard was 97.3%, and between CNB and the reference standard, 93.5%. The frequency of technical failures with CNB was slightly higher than DVAB (5.7 vs. 1.5%), as was the frequency of non-diagnostic samples (2.1 vs. 0%). Of the non-diagnostic CNB samples, 23% were subsequently found to be malignant on reference standard. In multivariate analyses using four covariates (procedure type, geographic location, reference standard, and patient position), there were no significant predictors of agreement rates, but some variables were significant predictors of miss rates. For benign to malignant upgrades, study location was a significant predictor, with more upgrades in non-NA locations. For atypia to malignant upgrades, the type of procedure was a significant predictor, with more underestimations in CNB studies., Conclusion: The best available evidence suggests that, in screening populations referred for minimally invasive breast biopsy biopsy requiring ST guidance, DVAB may provide lower miss and underestimation rates for clinically relevant diagnoses than does CNB.

Renal branching morphogenesis, defined as growth and branching of the ureteric bud (UB), is a tightly regulated process controlled by growth factor-dependent tissue interactions. Previously, using in vitro models of branching morphogenesis, we demonstrated that BMP2 signals via its intracellular effectors, SMAD1 and SMAD4, to control UB cell proliferation and branching in a manner modulated by Glypican-3 (GPC3), a cell surface heparan sulfate proteoglycan. Here, we used loss-of-function genetic mouse models to investigate the functions of Bmp2 and Gpc3-Bmp2 interactions in vivo. Progressively greater increases in UB cell proliferation were observed in Bmp2+/-, Smad4+/-, and Bmp2+/-; Smad4+/- mice compared to Wt. This increased cell proliferation was accompanied by a significant increase in UB branching in Smad4+/- and Bmp2+/-;Smad4+/- mice compared to Wt. Reduction of Gpc3 gene dosage also increased UB cell proliferation, an effect that was enhanced in Gpc3+/-;Bmp2+/- mice to an extent greater than the sum of that observed in Gpc3+/- and Bmp2+/- mice. Reduction of both Gpc3 and Bmp2 gene dosage enhanced cell proliferation in the metanephric mesenchyme compared to Wt, an effect not observed in either Bmp2+/- or Gpc3+/- mice. Phosphorylation of SMAD1, a measure of SMAD1 activation, was progressively decreased in Gpc3+/- and Gpc3+/-;Bmp2+/- mice compared to Wt, suggesting that Gpc3 stimulates Bmp2-dependent SMAD signaling in vivo. These results demonstrate that BMP2-SMAD signaling, modulated by GPC3, inhibits renal branching morphogenesis in vivo.

The intracellular and extracellular glycosaminoglycans (GAGs) of peripheral leukocytes in normal subjects and leukemic patients were characterized by electrophoresis and enzyme sensitivity. Normal peripheral granulocytes (PMN) are very rich in trypsin removable surface GAGs, while none are present on the surface of leukemic cells in acute myeloid leukemia. The intracellular and extracellular GAGs have also been analysed in the pig and compared to normal pig bone marrow haematopoietic cells. Mysenchymal cells cultured in vitro from marrow matrix and peripheral endothelial cells have also been studied. The results suggest that the exposure of cell surface chondroitin sulphate A is an important step involved in the peripheralisation of PMN.

Intercellular glycosaminoglycans have been isolated from normal and neoplastic mammalian tissues. They have been characterized by cellulose acetate electrophoresis and by chemical and enzymatic degradation. The electrophoretic pattern of the intercellular glycosaminoglycans is tissue specific. Furthermore, the electrophoretic patterns of all spontaneous neoplasias analyzed differ significantly from patterns obtained from the tissues of origin.