SummaryThe transient and localized signaling events between invasive breast cancer cells and the underlying endothelial cells have remained poorly characterized. We report a novel approach integrating vascular engineering with three-dimensional time-lapse fluorescence resonance energy transfer (FRET) imaging to dissect how endothelial myosin light chain kinase (MLCK) is modulated during tumor intravasation. We show that tumor transendothelial migration occurs via both paracellular (i.e. through cell-cell junctions) and transcellular (i.e. through individual endothelial cells) routes. Endothelial MLCK is activated at the invasion site, leading to regional diphosphorylation of myosin-II regulatory light chain (RLC) and myosin contraction. Blocking endothelial RLC diphosphorylation blunts tumor transcellular, but not paracellular, invasion. Our results implicate an important role for endothelial myosin-II function in tumor intravasation.

This C-Boost radiotherapy regimen administers a substantially higher biologically effective dose compared with conventional radiation schedules. Preliminary locoregional control and survival rates are promising with no significant acute and/or late toxicities.

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Pregnancy in the setting of renal failure has higher rates of adverse events necessitating increased monitoring and treatment. Pregnant women with end-stage renal disease have higher rates of hypertension, and 50% of pregnancies are complicated by preeclampsia. We describe the case of a 32-year-old parturient with end-stage renal disease on hemodialysis with superimposed preeclampsia who developed clinically significant hyperkalemia with electrocardiographic changes after magnesium infusion. The magnesium infusion was stopped, and the patient underwent emergent hemodialysis with subsequent improvement. Hyperkalemia caused by magnesium infusion is a rare and not very well-understood phenomenon.