Andrew E. Schade
Cleveland Clinic
13 Papers
38 Citations
Andrew E. Schade is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Signal transduction & Haematopoiesis. The author has an hindex of 9, co-authored 13 publications.
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Papers
Dasatinib, a small-molecule protein tyrosine kinase inhibitor, inhibits T-cell activation and proliferation.
Andrew E. Schade,Gary L. Schieven,Robert M. Townsend,Anna M. Jankowska,Vojkan Susulic,Rosemary Zhang,Hadrian Szpurka,Jaroslaw P. Maciejewski +7 more
TL;DR: It is shown that dasatinib inhibits TCR-mediated signal transduction, cellular proliferation, cytokine production, and in vivo T-cell responses, and the effect is reversible or may be overcome by signals bypassing the TCR, such as phorbol ester.
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Phosphatidylinositol-3-phosphate kinase pathway activation protects leukemic large granular lymphocytes from undergoing homeostatic apoptosis.
TL;DR: T-LGL pathogenesis is dependent on activity of the PI3K-AKT pathway, without which the leukemic cells will begin to undergo spontaneous apoptosis, and it is proposed that novel therapeutics inhibiting thePI3K -AKT axis may provide effective treatment for T-L GL.
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An algorithm for managing warfarin resistance.
TL;DR: This review offers an algorithm for the evaluation of patients with suspected warfarin resistance who need higher-than-expected doses of warFarin to reach their target INR.
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T-large granular lymphocyte leukemia: current molecular concepts.
TL;DR: Application of new technologies, including TCR repertoire analysis by sequencing, clonotypic quantitative PCR and VB flow cytometry facilitate clinical diagnosis and may allow insights into the regulation of T CR repertoire and consequences resulting from the contraction of clonal diversity.
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Altered lipid raft composition and defective cell death signal transduction in glycosylphosphatidylinositol anchor-deficient PIG-A mutant cells.
TL;DR: It is suggested that the altered LR‐dependent signalling in PNH‐like cells may induce different responses to pro‐inflammatory cytokines from those observed in cells with intact GPI‐AP.
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