A
Avi Ashkenazi
Researcher at Massachusetts Institute of Technology
Publications - 370
Citations - 48530
Avi Ashkenazi is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Receptor & Apoptosis. The author has an hindex of 98, co-authored 340 publications receiving 46279 citations. Previous affiliations of Avi Ashkenazi include University of California, San Francisco & Washington University in St. Louis.
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Journal ArticleDOI
Death receptors: signaling and modulation
Avi Ashkenazi,Vishva M. Dixit +1 more
TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
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Safety and antitumor activity of recombinant soluble Apo2 ligand
Avi Ashkenazi,Roger Pai,Sharon Fong,Susan Leung,David A. Lawrence,Scot A. Marsters,Christine Blackie,Ling Chang,Amy E. McMurtrey,Andrea Hebert,Laura DeForge,Iphigenia Koumenis,Derf Lewis,Louise A. Harris,Jeanine L. Bussiere,Hartmut Koeppen,Zahra Shahrokh,Ralph H. Schwall +17 more
TL;DR: Apo2L may have potent anticancer activity without significant toxicity toward normal tissues, and cooperated synergistically with the chemotherapeutic drugs 5-fluorouracil or CPT-11, causing substantial tumor regression or complete tumor ablation.
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Induction of Apoptosis by Apo-2 Ligand, a New Member of the Tumor Necrosis Factor Cytokine Family *
Robert M. Pitti,Scot A. Marsters,Siegfried Ruppert,Christopher J. Donahue,Alison Moore,Avi Ashkenazi +5 more
TL;DR: Results suggest that, along with other family members such as Fas/Apo-1 ligand and TNF, Apo-2L may serve as an extracellular signal that triggers programmed cell death.
Journal ArticleDOI
Control of TRAIL-Induced Apoptosis by a Family of Signaling and Decoy Receptors
James P. Sheridan,Scot A. Marsters,Robert M. Pitti,Austin L. Gurney,Maya Skubatch,Daryl T. Baldwin,Lakshmi Ramakrishnan,Christa L. Gray,Kevin P. Baker,William I. Wood,Audrey Goddard,Paul J. Godowski,Avi Ashkenazi +12 more
TL;DR: A cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli in tumor cells.
Journal ArticleDOI
Targeting death and decoy receptors of the tumour-necrosis factor superfamily
TL;DR: Cancer cells often develop resistance to chemotherapy or irradiation through mutations in the p53 tumour-suppressor gene, which prevent apoptosis induction in response to cellular damage, so agents that are designed to activate death receptors or block decoy receptors might be used to kill tumour cells that are resistant to conventional cancer therapies.