Publications by authors named "J R Linderman"

This article highlights key topic areas related to dietary supplements (DSs) and performance-enhancing substances. It also discusses evidence-based resources the medical community can use when discussing high-quality DSs with Servicemembers interested in taking DSs. We briefly overview how DSs are regulated in the United States, discuss problematic categories and issues related to quality, expand upon what are often considered performance-enhancing substances yet sometimes sold as DSs, and then offer solutions to counter the consequences of the dark side of the DS industry.

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Targeting signaling pathways that drive cancer cell migration or proliferation is a common therapeutic approach. A popular experimental technique, the scratch assay, measures the migration and proliferation-driven cell closure of a defect in a confluent cell monolayer. These assays do not measure dynamic effects.

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Introduction: Antibody-drug conjugates (ADCs) show significant clinical efficacy in the treatment of solid tumors, but a major limitation to their success is poor intratumoral distribution. Adding a carrier dose improves both distribution and overall drug efficacy of ADCs, but the optimal carrier dose has not been outlined for different payload classes.

Objective: In this work, we study two carrier dose regimens: 1) matching payload potency to cellular delivery but potentially not reaching cells farther away from blood vessels, or 2) dosing to tumor saturation but risking a reduction in cell killing from a lower amount of payload delivered per cell.

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Antibody-drug conjugates (ADCs) have experienced a surge in clinical approvals in the past five years. Despite this success, a major limitation to ADC efficacy in solid tumors is poor tumor penetration, which leaves many cancer cells untargeted. Increasing antibody doses or co-administering ADC with an unconjugated antibody can improve tumor penetration and increase efficacy when target receptor expression is high.

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Single cancer cells within a tumor exhibit variable levels of resistance to drugs, ultimately leading to treatment failures. While tumor heterogeneity is recognized as a major obstacle to cancer therapy, standard dose-response measurements for the potency of targeted kinase inhibitors aggregate populations of cells, obscuring intercellular variations in responses. In this work, we develop an analytical and experimental framework to quantify and model dose responses of individual cancer cells to drugs.

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