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Donald L. Durden

Researcher at University of California, San Diego

Publications -  122
Citations -  6165

Donald L. Durden is an academic researcher from University of California, San Diego. The author has contributed to research in topics: PTEN & Phosphorylation. The author has an hindex of 41, co-authored 117 publications receiving 5619 citations. Previous affiliations of Donald L. Durden include Children's Hospital Los Angeles & Fred Hutchinson Cancer Research Center.

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'Pseudopalisading' necrosis in glioblastoma: A familiar morphologic feature that links vascular pathology, hypoxia, and angiogenesis

TL;DR: Vaso-occlusive and prothrombotic mechanisms in GBM could readily explain the presence of pseudopalisading necrosis in tissue sections, the rapid peripheral expansion on neuroimaging, and the dramatic shift to an accelerated rate of clinical progression resulting from hypoxia-induced angiogenesis.
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PTEN protects p53 from Mdm2 and sensitizes cancer cells to chemotherapy.

TL;DR: The PTEN tumor suppressor protein is shown to protect p53 from survival signals, permitting p53 to function as a guardian of the genome as mentioned in this paper, and it can sensitize tumor cells to chemotherapy that relies on p53 activity.
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A vascular targeted pan phosphoinositide 3-kinase inhibitor prodrug, SF1126, with antitumor and antiangiogenic activity

TL;DR: The development and antitumor activity of a novel RGDS-conjugated LY294002 prodrug, termed SF1126, which is designed to exhibit increased solubility and bind to specific integrins within the tumor compartment, resulting in enhanced delivery of the active compound to the tumor vasculature and tumor.
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PTEN controls tumor-induced angiogenesis

TL;DR: Evidence is provided that PTEN regulates tumor-induced angiogenesis and the progression of gliomas to a malignant phenotype via the regulation of phosphoinositide-dependent signals.
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PTEN and Hypoxia Regulate Tissue Factor Expression and Plasma Coagulation by Glioblastoma

TL;DR: Results show that PTEN loss and hypoxia up-regulate TF expression and promote plasma clotting by glioma cells, suggesting that these mechanisms may underlie intravascular thrombosis and pseudopalisading necrosis in glioblastoma.