M
Mike Griffiths
Researcher at University of Birmingham
Publications - 27
Citations - 4205
Mike Griffiths is an academic researcher from University of Birmingham. The author has contributed to research in topics: Myeloid leukemia & Chromosomal translocation. The author has an hindex of 25, co-authored 27 publications receiving 3783 citations. Previous affiliations of Mike Griffiths include Medical Research Council & Salisbury University.
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Journal ArticleDOI
Assessment of Minimal Residual Disease in Standard-Risk AML.
Adam Ivey,Robert Kerrin Hills,Michael A. Simpson,Jelena V. Jovanovic,Amanda F. Gilkes,Angela Grech,Yashma Patel,Neesa Bhudia,Hassan Farah,Joanne Mason,Kerry Wall,Susanna Akiki,Mike Griffiths,Ellen Solomon,Frank McCaughan,David C. Linch,Rosemary E. Gale,Paresh Vyas,Sylvie D. Freeman,Nigel H. Russell,Alan Kenneth Burnett,David Grimwade +21 more
TL;DR: Although mutations associated with preleukemic clones remained detectable during ongoing remission after chemotherapy, NPM1 mutations were detected in 69 of 70 patients at the time of relapse and provided a better marker of disease status.
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Coexistence of LMPP-like and GMP-like Leukemia Stem Cells in Acute Myeloid Leukemia
Nicolas Goardon,Emanuele Marchi,Ann Atzberger,Lynn Quek,Anna Schuh,Shamit Soneji,Petter S. Woll,Adam J. Mead,Kate A. Alford,R Rout,Salma Chaudhury,Amanda F. Gilkes,Steven Knapper,Kheira Beldjord,Suriya Begum,Susan Rose,Nicola Geddes,Mike Griffiths,Graham R. Standen,Alexander Sternberg,Jamie Cavenagh,Hannah Hunter,David G. Bowen,Sally Killick,L. G. Robinson,Andrew Price,Elizabeth Macintyre,Paul Virgo,Alan Kenneth Burnett,Charles Craddock,Tariq Enver,Sten Eirik W. Jacobsen,Catherine Porcher,Paresh Vyas +33 more
TL;DR: It is shown that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients, suggesting that in most cases primaryCD34+ AML is a progenitors disease where LSCs acquire abnormal self-renewal potential.
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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.
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Azacitidine augments expansion of regulatory T cells after allogeneic stem cell transplantation in patients with acute myeloid leukemia (AML)
Oliver Goodyear,Michael Dennis,Nadira Y. Jilani,Nadira Y. Jilani,Justin Loke,Shamyla Siddique,Shamyla Siddique,Gordon B. Ryan,Jane Nunnick,Jane Nunnick,Rahela Khanum,Manoj Raghavan,Manoj Raghavan,Mark Cook,John A. Snowden,Mike Griffiths,Nigel H. Russell,John A. Liu Yin,Charles Crawley,Gordon Cook,Paresh Vyas,Paul Moss,Ram Malladi,Ram Malladi,Charles Craddock,Charles Craddock +25 more
TL;DR: Data support the further examination of AZA after transplantation as a mechanism of augmenting a GVL effect without a concomitant increase in GVHD.
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Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia
Yang Li,Claire Schwab,Sarra Ryan,Elli Papaemmanuil,Hazel M. Robinson,Patricia Jacobs,Anthony V. Moorman,Sara Dyer,Julian Borrow,Mike Griffiths,Nyla A. Heerema,Andrew J. Carroll,Polly Talley,Nick Bown,Nick Telford,Fiona M. Ross,Lorraine Gaunt,Richard J. Q. McNally,Bryan D. Young,Paul Sinclair,Vikki Rand,Manuel R. Teixeira,Olivia Joseph,Ben Robinson,Mark Maddison,Nicole Dastugue,Peter Vandenberghe,Claudia Haferlach,Philip J. Stephens,Jiqiu Cheng,Peter Van Loo,Peter Van Loo,Michael R. Stratton,Peter J. Campbell,Peter J. Campbell,Christine J. Harrison +35 more
TL;DR: It is shown that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population.