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Amedeo Amedei

Researcher at University of Florence

Publications -  262
Citations -  11307

Amedeo Amedei is an academic researcher from University of Florence. The author has contributed to research in topics: Medicine & Immune system. The author has an hindex of 52, co-authored 196 publications receiving 8838 citations. Previous affiliations of Amedeo Amedei include French Institute of Health and Medical Research & UniFi.

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Broad targeting of resistance to apoptosis in cancer.

TL;DR: This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer.
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Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

TL;DR: Natural compounds found to inhibit one or more pathways that contribute to proliferation have been found and will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression.
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Broad targeting of angiogenesis for cancer prevention and therapy

TL;DR: 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy are identified and 10 plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to cause excessive toxicity.
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Tissue invasion and metastasis: Molecular, biological and clinical perspectives.

TL;DR: This review lists the disruption of E-cadherin and tight junctions, key signaling pathways, including urokinase type plasminogen activator (uPA), phosphatidylinositol 3-kinase/v-akt murine thymoma viral oncogene (PI3K/AKT), focal adhesion kinase (FAK), β-catenin/zinc finger E-box binding homeobox 1 (ZEB
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The Helicobacter pylori Vacuolating Toxin Inhibits T Cell Activation by Two Independent Mechanisms

TL;DR: It is reported that VacA also interferes with T cell activation by two different mechanisms, one of which involves activation of intracellular signaling through the mitogen-activated protein kinases MKK3/6 and p38 and the Rac-specific nucleotide exchange factor, Vav.