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Brian J. P. Huntly
Researcher at University of Cambridge
Publications - 168
Citations - 21295
Brian J. P. Huntly is an academic researcher from University of Cambridge. The author has contributed to research in topics: Myeloid leukemia & Leukemia. The author has an hindex of 54, co-authored 144 publications receiving 19135 citations. Previous affiliations of Brian J. P. Huntly include Cambridge University Hospitals NHS Foundation Trust & Brigham and Women's Hospital.
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Journal ArticleDOI
Early Loss of CREBBP Confers Malignant Stem Cell Properties on Lymphoid Progenitors
Brian J. P. Huntly,Sarah J. Horton,George Giotopoulos,Haiyang Yun,Shabana Vohra,Olivia Sheppard,Rachael Bashford-Rogers,Mamunur Rashid,Daniel Sasca,Faisal Basheer,Paolo Gallipoli,Jessica Okosun,Daniel J. Hodson,Jude Fitzgibbon,Ming Du,David J. Adams +15 more
TL;DR: It is demonstrated that early loss of Crebbp in hematopoietic stem and progenitor cells (HSPC) leads to increased development of hematological malignancies, particularly of the B-lymphoid lineage that mimic features of human lymphomas.
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Core outcome set measurement for future clinical trials in acute myeloid leukemia: the HARMONY study protocol using a multi-stakeholder consensus-based Delphi process and a final consensus meeting.
Katharina Lang,Kathryn L. Harrison,Paula R Williamson,Brian J. P. Huntly,Gert J. Ossenkoppele,Jan Geissler,Tamás Bereczky,Jesús M. Hernández-Rivas,Helene Chevrou-Severac,Rory Goodbody,Renate Schulze-Rath,Lars Bullinger +11 more
TL;DR: A pilot study to define a core outcome set in AML on the basis of a multi-stakeholder consensus to allow consistent comparison of future clinical trials and real-world evidence research and ensures that appropriate outcomes valued by a range of stakeholders are measured within future trials.
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The Genomic Landscape of Myeloproliferative Neoplasms: Somatic Calr Mutations in the Majority of JAK2-Wildtype Patients
Jyoti Nangalia,Charles E. Massie,E. Joanna Baxter,Francesca L. Nice,Gunes Gundem,David C. Wedge,Edward Avezov,Juan Li,Karoline Kollmann,David G. Kent,Athar Aziz,Anna L. Godfrey,Jonathan Hinton,Inigo Martincorena,Peter Van Loo,Amy V. Jones,Paola Guglielmelli,Patrick S. Tarpey,Heather P. Harding,John D Fitzpatrick,Calum T Goudie,Christina A. Ortmann,Stephen J. Loughran,Keiran Raine,David T. Jones,Adam Butler,Jon W. Teague,Sarah O’Meara,Stuart McLaren,Michele Bianchi,Yvonne Silber,Danai Dimitropolou,David Bloxham,Laura Mudie,Mark Maddison,Ben Robinson,Clodagh Keohane,Cathy MacLean,Kate Hill,Kim Orchard,Sudhir Tauro,Ming-Qing Du,Mel Greaves,David G. Bowen,Brian J. P. Huntly,Claire N. Harrison,Nicholas C.P. Cross,David Ron,Alessandro M. Vannucchi,Elli Papaemmanuil,Peter J. Campbell,Anthony R. Green +51 more
TL;DR: Novel somatic mutations in calreticulin ( CALR) were identified by exome sequencing in the majority (26/31) of JAK2 or MPL unmutated patients, and 97% of patients harbored a mutation in 1 of these 3 genes.
Journal ArticleDOI
Cdx4 Upregulates Hox Gene Expression and Generates Acute Myeloid Leukemia Alone and in Cooperation with Meis1a in a Murine Model.
Dimple Bansal,Claudia Scholl,Stefan Fröhling,Elizabeth McDowell,Benjamin H. Lee,Konstanze Döhner,Patricia Ernst,Alan Davidson,George Q. Daley,Leonard I. Zon,D. Gary Gilliland,Brian J. P. Huntly +11 more
TL;DR: It is reported here that CDX4 is normally expressed in early hematopoietic progenitors, and is aberrantly expressed in~25% of AML patient samples, and data indicate that Cdx4 regulates Hox gene expression in adult hematoiesis and may serve as an upstream regulator of Hox genes expression in the induction of acute leukemia.
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FoxO Are Critical Mediators of Hematopoietic Stem Cell Resistance to Physiologic Oxidative Stress.
Zuzana Tothova,Ramya Kollipara,Brian J. P. Huntly,Benjamin H. Lee,Diego H. Castrillon,Emmanuelle Passegué,Dana E. Cullen,Elizabeth McDowell,Suzan Lazo-Kallanian,Ifor R. Williams,Ronald A. DePinho,D. Gary Gilliland +11 more
TL;DR: Results demonstrate that, in the HSC compartment, FoxO proteins are mediators of quiescence and enhanced survival and play essential regulatory roles in the response to physiologic oxidative stress, a function that may contribute to the long-term regenerative potential of the hematopoietic stem cell compartment.