R
Richard Stone
Researcher at Harvard University
Publications - 1407
Citations - 70944
Richard Stone is an academic researcher from Harvard University. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 113, co-authored 1307 publications receiving 61169 citations. Previous affiliations of Richard Stone include Toronto Western Hospital & Brigham and Women's Hospital.
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Journal ArticleDOI
Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia
Brian J. Druker,François Guilhot,Stephen G. O'Brien,Insa Gathmann,Hagop M. Kantarjian,Norbert Gattermann,Michael W. Deininger,Richard T. Silver,John M. Goldman,Richard Stone,Francisco Cervantes,Andreas Hochhaus,Bayard L. Powell,Janice Gabrilove,Philippe Rousselot,Josy Reiffers,Jan J. Cornelissen,Timothy P. Hughes,Hermine Agis,Thea Kolsen Fischer,Gregor Verhoef,John D. Shepherd,Giuseppe Saglio,Alois Gratwohl,Johan Lanng Nielsen,Jerald P. Radich,Bengt Simonsson,Kerry Taylor,Michele Baccarani,Charlene So,Laurie Letvak,Richard A. Larson +31 more
TL;DR: After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients.
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Randomized Controlled Trial of Azacitidine in Patients With the Myelodysplastic Syndrome: A Study of the Cancer and Leukemia Group B
Lewis R. Silverman,Erin P. Demakos,Bercedis L. Peterson,Alice B. Kornblith,Jimmie C. Holland,Rosalie Odchimar-Reissig,Richard Stone,Douglas A. Nelson,Bayard L. Powell,Carlos M. DeCastro,John Ellerton,Richard A. Larson,Charles A. Schiffer,James F. Holland +13 more
TL;DR: Aza C treatment results in significantly higher response rates, improved quality of life, reduced risk of leukemic transformation, and improved survival compared with supportive care.
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A Tyrosine Kinase Created by Fusion of the PDGFRA and FIP1L1 Genes as a Therapeutic Target of Imatinib in Idiopathic Hypereosinophilic Syndrome
Jan Cools,Jan Cools,Daniel J. DeAngelo,Jason Gotlib,Elizabeth H. Stover,Robert D. Legare,Robert D. Legare,J. E. Cortes,Jeffrey L. Kutok,Jennifer J. Clark,Ilene Galinsky,James D. Griffin,Nicholas C.P. Cross,Ayalew Tefferi,James M. Malone,Rafeul Alam,Stanley L. Schrier,Janet L. Schmid,Michal G. Rose,Peter Vandenberghe,Gregor Verhoef,Marc Boogaerts,Iwona Wlodarska,Hagop M. Kantarjian,Peter Marynen,Steven Coutre,Richard Stone,D. Gary Gilliland +27 more
TL;DR: The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib, and data indicate that the deletion of genetic material may result in gain-of-function fusion proteins.
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Pretreatment cytogenetic abnormalities are predictive of induction success, cumulative incidence of relapse, and overall survival in adult patients with de novo acute myeloid leukemia: results from Cancer and Leukemia Group B (CALGB 8461)
John C. Byrd,Krzysztof Mrózek,Richard K. Dodge,Andrew J. Carroll,Colin G. Edwards,Diane C. Arthur,Mark J. Pettenati,Shivanand R. Patil,Kathleen W. Rao,Michael S. Watson,Prasad Koduru,Joseph O. Moore,Richard Stone,Robert J. Mayer,Eric J. Feldman,Frederick R. Davey,Charles A. Schiffer,Richard A. Larson,Clara D. Bloomfield +18 more
TL;DR: In this paper, the prognostic impact of cytogenetic abnormalities on complete remission (CR) rate, 5-year cumulative incidence of relapse (CIR), and 5-to-5-year overall survival (OS) of acute myeloid leukemia (AML) patients was investigated.
Journal ArticleDOI
Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation
Richard Stone,Sumithra J. Mandrekar,Ben L. Sanford,Kristina Laumann,Susan Geyer,Clara D. Bloomfield,Christian Thiede,Thomas W. Prior,Konstanze Döhner,Guido Marcucci,Francesco Lo-Coco,Rebecca B. Klisovic,Andrew H. Wei,Jorge Sierra,Miguel A. Sanz,Joseph Brandwein,Theo de Witte,Dietger Niederwieser,Frederick R. Appelbaum,Bruno C. Medeiros,Martin S. Tallman,Jürgen Krauter,Richard F. Schlenk,Arnold Ganser,Hubert Serve,Gerhard Ehninger,Sergio Amadori,Richard A. Larson,Hartmut Döhner +28 more
TL;DR: The addition of the multitargeted kinase inhibitor midostaurin to standard chemotherapy significantly prolonged overall and event‐free survival among patients with AML and a FLT3 mutation.