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Anthony V. Moorman
Researcher at Newcastle University
Publications - 261
Citations - 16875
Anthony V. Moorman is an academic researcher from Newcastle University. The author has contributed to research in topics: Minimal residual disease & Acute lymphocytic leukemia. The author has an hindex of 63, co-authored 236 publications receiving 14702 citations. Previous affiliations of Anthony V. Moorman include King's College London & University of Southampton.
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Journal ArticleDOI
Refinement of cytogenetic classification in acute myeloid leukemia: determination of prognostic significance of rare recurring chromosomal abnormalities among 5876 younger adult patients treated in the United Kingdom Medical Research Council trials
David Grimwade,Robert Kerrin Hills,Anthony V. Moorman,Helen Walker,S Chatters,Anthony H. Goldstone,Keith Wheatley,Christine J. Harrison,Alan Kenneth Burnett +8 more
TL;DR: Analysis of outcomes of 5876 patients treated in Medical Research Council trials allows more reliable prediction of outcome for patients with rarer abnormalities and may facilitate the development of consensus in reporting of karyotypic information in clinical trials involving younger adults with AML.
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Genetic variegation of clonal architecture and propagating cells in leukaemia
Kristina Anderson,Christoph Lutz,Frederik W. van Delft,Caroline M. Bateman,Yan-Ping Guo,Susan M. Colman,Helena Kempski,Anthony V. Moorman,Ian Titley,John Swansbury,Lyndal Kearney,Tariq Enver,Tariq Enver,Mel Greaves +13 more
TL;DR: This issue is examined in childhood acute lymphoblastic leukaemia in which the ETV6–RUNX1 gene fusion is an early or initiating genetic lesion followed by a modest number of recurrent or ‘driver’ copy number alterations.
Journal ArticleDOI
Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial
Anthony V. Moorman,Christine J. Harrison,Georgina Buck,Sue Richards,Lorna M. Secker-Walker,M Martineau,Gail H. Vance,Athena M. Cherry,Rodney R. Higgins,Adele K. Fielding,Letizia Foroni,Elisabeth Paietta,Martin S. Tallman,Mark R. Litzow,Peter H. Wiernik,Jacob M. Rowe,Anthony H. Goldstone,Gordon W. Dewald +17 more
TL;DR: The observation that Ho-Tr and, for the first time, karyotype complexity confer an increased risk of treatment failure demonstrates that cytogenetic subgroups other than the Ph chromosome can and should be used to risk stratify adults with ALL in future trials.
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Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: A meta-analysis of individual patient data from randomised controlled trials
Robert Kerrin Hills,Sylvie Castaigne,Frederick R. Appelbaum,Jacques Delaunay,Stephen H. Petersdorf,Megan Othus,Elihu H. Estey,Hervé Dombret,Sylvie Chevret,Norbert Ifrah,Jean-Yves Cahn,Christian Recher,Lucy Chilton,Anthony V. Moorman,Alan Kenneth Burnett +14 more
TL;DR: Gemtuzumab ozogamicin can be safely added to conventional induction therapy and provides a significant survival benefit for patients without adverse cytogenetic characteristics, and its licence status might need to be reviewed.
Journal ArticleDOI
Deregulated expression of cytokine receptor gene, CRLF2 , is involved in lymphoid transformation in B-cell precursor acute lymphoblastic leukemia
Lisa J. Russell,Melania Capasso,Inga Vater,Takashi Akasaka,Olivier Bernard,María José Calasanz,Thiruppavaii Chandrasekaran,Elise Chapiro,S Gesk,Mike Griffiths,David S. Guttery,Claudia Haferlach,Lana Harder,Olaf Heidenreich,Julie Irving,Lyndal Kearney,Florence Nguyen-Khac,Lee Machado,Lynne Minto,Aneela Majid,Anthony V. Moorman,Heather Morrison,Vikki Rand,Jonathan C. Strefford,Claire Schwab,Holger Tönnies,Martin J. S. Dyer,Reiner Siebert,Christine J. Harrison +28 more
TL;DR: Overexpression of CRLF2 was associated with activation of the JAK-STAT pathway in cell lines and transduced primary B-cell progenitors, sustaining their proliferation and indicating a causal role of C RLF2 overexpression in lymphoid transformation.