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David T. Vistica

Researcher at MedStar Washington Hospital Center

Publications -  6
Citations -  12122

David T. Vistica is an academic researcher from MedStar Washington Hospital Center. The author has contributed to research in topics: Cell growth & Sulforhodamine B. The author has an hindex of 6, co-authored 6 publications receiving 11416 citations.

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New Colorimetric Cytotoxicity Assay for Anticancer-Drug Screening

TL;DR: The SRB assay provides a sensitive measure of drug-induced cytotoxicity, is useful in quantitating clonogenicity, and is well suited to high-volume, automated drug screening.
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Feasibility of a High-Flux Anticancer Drug Screen Using a Diverse Panel of Cultured Human Tumor Cell Lines

TL;DR: A pilot-scale, in vitro, anticancer drug screen utilizing a panel of 60 human tumor cell lines organized into subpanels representing leukemia, melanoma, and cancers of the lung, colon, kidney, ovary, and central nervous system is described.
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Therapeutic vulnerability of an in vivo model of alveolar soft part sarcoma (ASPS) to antiangiogenic therapy.

TL;DR: A preclinical in vivo model for ASPS is described which will facilitate investigation into the biology of this slow growing soft tissue sarcoma and demonstrates the feasibility of using an antiangiogenic approach in the treatment of ASPS.
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New Carbon Dioxide-Independent Basal Growth Medium for Culture of Diverse Tumor and Nontumor Cells of Human and Nonhuman Origin

TL;DR: The 50% inhibitory concentration values obtained with carmustine, doxorubicin, and tamoxifen in cell lines maintained in the new medium under atmospheric CO2 were closely comparable to those obtained with these drugs against cells maintained in RPMI-1640 under a 5% CO2 environment.
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Bioinformatic Analysis of Patient-Derived ASPS Gene Expressions and ASPL-TFE3 Fusion Transcript Levels Identify Potential Therapeutic Targets

TL;DR: The identification of pathways and gene subsets characteristic of ASPS support current therapeutic strategies that target the FLT1 and MET, while also proposing additional targeting of genes found in pathways involved in the cell cycle, cell adhesion, and chemokine-related protein tyrosine kinase activity.