William B Mitchell, MD
- ASSOCIATE PROFESSOR | Pediatrics, Hematology/Oncology
Dr. William Beau Mitchell is an Associate Professor of Pediatric Hematology/Oncology at Kravis Children's Hospital at Mount Sinai, where he is the Director of Benign Hematology and Director of the Pediatric Hemophilia Treatment Center. His primary clinical focus is on hemophilia and other bleeding disorders, sickle cell disease, and platelet disorders. Dr. Mitchell attended Tufts University College of Medicine, completed his Pediatric Residency at Boston City Hospital, and completed his Pediatric Hematology/Oncology fellowship at Mount Sinai Hospital. His clinical experience has included directorship of the Weill Cornell Hemophilia Treatment Center. Dr Mitchell’s clinical research has focused on novel therapies for rare bleeding disorders such as hemophilia and ITP. His basic science research has focused on the production of platelets from stem cells and he remains active in that field. He has lectured nationally and internationally on his ongoing project to generate platelets from stem cells for clinical use. He has published widely, including invited reviews in both clinical and scientific journals.
Dr. Mitchell is board certified in Pediatric Hematology/Oncology by the American Board of Pediatrics.
Dr. Mitchell's areas of expertise include:
Sickle Cell Disease
Bone Marrow Failure
MD, Tufts University School of Medicine
Residency, Pediatrics, Boston University Medical Center
Fellowship, Pediatric Hem/onc, Mount Sinai Hospital
Role of Calcium Binding in Alpha IIb Biogenesis
Nair S , Li J , Mitchell WB, Mohanty D , Coller BS, French DL. Two new beta3 integrin mutations in Indian patients with Glanzmann thrombasthenia: localization of mutations affecting cysteine residues in integrin beta3. Thromb Haemost 2002 Sep; 88(3): 503-9.
Mitchell WB, Li JH, Michelson AD, Bussel J , Coller BS, French DL. Two novel mutations in the alpha IIb calcium-binding domains identify hydrophobic regions essential for alpha IIbbeta 3 biogenesis. Blood 2003 Mar; 101(6): 2268-76.
French DL, Fruchtman S , Mitchell WB, Coller BS, Peretz H . Evidence for megakaryocyte engraftment following reduced-intensity conditioning. Exp Hematol 2004 Sep; 32(9): 877-80.
Li J , Mitchell WB, Ruan J , Takagi J , Springer TA, French DL, Coller BS. Integrin beta3 regions controlling binding of murine mAb 7E3: implications for the mechanism of integrin alphaIIbbeta3 activation. Proc Natl Acad Sci U S A 2004 Sep; 101(36): 13114-20.
Avanzi M, Oluwadara O, Cushing M, Mitchell M, Fischer S, Mitchell W. A novel bioreactor and culture method drives high yields of platelets from stem cells. . Transfusion 2015 October;.
Davila J, Manwani D, Vasovic L, Avanzi M, Uehlinger J, Ireland K, Mitchell WB. A novel inflammatory role for platelets in sickle cell disease. Platelets 2015; 26(8).
Avanzi MP, Izak M, Oluwadara OE, Mitchell WB. Actin inhibition increases megakaryocyte proplatelet formation through an apoptosis-dependent mechanism. PloS one 2015; 10(4).
Mitchell WB, Pinheiro MP, Boulad N, Kaplan D, Edison MN, Psaila B, Karpoff M, White MJ, Josefsson EC, Kile BT, Bussel JB. Effect of thrombopoietin receptor agonists on the apoptotic profile of platelets in patients with chronic immune thrombocytopenia. American journal of hematology 2014 Dec; 89(12).
Avanzi MP, Mitchell WB. Ex vivo production of platelets from stem cells. British journal of haematology 2014 Apr; 165(2).
Mitchell WB, Bussel JB. Thrombopoietin Receptor Agonists: A Critical Review.. Seminars in Hematology 2015 January; 52(1): 46-52.
Avanzi M, Goldberg F, Davila J, Langhi D, Chiattone C, Mitchell W. Rho kinase inhibition drives megakaryocyte polyploidization and proplatelet formation through MYC and NFE2 downregulation. . Br J Haematol 2014 March; 164(6): 867-76.
Avanzi MP, Chen A, He W, Mitchell WB. Optimizing megakaryocyte polyploidization by targeting multiple pathways of cytokinesis. . Transfusion 2012 November; 52(11): 2406-13.
Mitchell W, Li J, Murcia M, Valentin N, Newman P, Coller B. Mapping early conformational changes in IIb and 3 during biogenesis reveals a potential mechanism for IIb3 adopting its bent conformation.. Blood 2007 May; 109(9): 3725-3732.
Mitchell W, Li J, French D, Coller B. IIb3 biogenesis is controlled by engagement of IIb in the calnexin cycle via the N15-linked glycan. . Blood 2006 April; 107(7): 2713-2719.