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1 of cell fate (e.g. LMO2 which is involved in acute leukaemia).
2 2(-/-)Fancd2(-/-) mice spontaneously develop acute leukaemia.
3 years or over who underwent a transplant for acute leukaemia.
4 in a T cell line derived from a childhood T-acute leukaemia.
5 have improved the outlook for patients with acute leukaemia.
6 ns in infant and secondary treatment-related acute leukaemias.
7 lving the RUNX1 gene are frequently found in acute leukaemias.
8 ocations occur in man at chromosome 11q23 in acute leukaemias.
9 erent partner genes in a proportion of human acute leukaemias.
10 slocation in T cells prior to development of acute leukaemias.
11 romosomal translocations in childhood T cell acute leukaemias.
12 fered to patients receiving chemotherapy for acute leukaemia and high dose chemotherapy for solid tum
13 ese findings identify a dependency factor in acute leukaemia and suggest a mechanistic rationale for
14 Outcomes of 503 children (<16 years) with acute leukaemia and transplanted with umbilical cord blo
15 to treat a wide array of diseases, including acute leukaemias and congenital blood disorders, but obt
16 We have analysed PTEN in a series of primary acute leukaemias and non-Hodgkin's lymphomas (NHLs) as w
17 are the most common genetic abnormalities in acute leukaemia, and congenital mutations in the related
18 CB grafts in transplantation for adults with acute leukaemia, and to establish whether current graft-
19 genic model of tumorigenesis by Lmo2, T-cell acute leukaemias arise after an asymptomatic phase in wh
20 le explanation for the clusters of childhood acute leukaemias around the nuclear processing plants of
21 LL oncogene give rise to a highly aggressive acute leukaemia associated with poor clinical outcome.
22 in the E26 avian retrovirus which elicits an acute leukaemia by transforming haemopoietic progenitors
23 cohort of 71 diagnosis-relapse cases and 270 acute leukaemia cases that did not relapse found that 18
24 ss-of-function screen in an MLL-AF4-positive acute leukaemia cell line, we identify ENL as an unrecog
26 markers useful in the classification of the acute leukaemias, especially the undifferentiated leukae
27 ingle agent oral OTX015 use in patients with acute leukaemia for further phase 2 studies is 80 mg on
28 mortality from haemorrhage in patients with acute leukaemia in the 1950s, the use of this therapy ha
29 ficient to cause embryonic stem cell-derived acute leukaemias in chimeric mice, and these tumours occ
31 tional oncogenic mutations result in a fatal acute leukaemia made of proliferating immature cells.
32 utropenia and infection-related mortality in acute leukaemia patients and those receiving high dose c
33 ectopic expression of LMO1 or LMO2 in T cell acute leukaemias resulting from chromosomal translocatio
34 yltransferase MOZ is also rearranged in some acute leukaemias, resulting in the expression of MOZ fus
36 rch for other molecular abnormalities in the acute leukaemias that might serve as therapeutic targets
37 the importance of both LMO2 and HOX genes in acute leukaemias, we further demonstrated that the regul
38 data support the use of UCB for adults with acute leukaemia when there is no HLA-matched unrelated a
39 y reported a fusion protein NUP98-IQCG in an acute leukaemia, which functions as an aberrant regulato
42 This is a retrospective analysis from the Acute Leukaemia Working Party of the European Group for
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