BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros
By C. Mullighan, C. Miller, I. Radtke, Letha A A Phillips, J. Dalton, Jing Ma, D. White, T. Hughes, M. L. Beau, Ching-Hon Pui and 3 more. Nature, 2008
1,112 citations recorded by the source corpus.
Subfields: Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/37ec8a7c6b935525f86f77ad3584ee64948b2a42
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In Public Health, Environmental and Occupational Health
Citations in the corpus
- JAK mutations in high-risk childhood acute lymphoblastic leukemia (2009, background): “Recent genome-wide analyses have identified common genetic alterations in childhood ALL that contribute to leukemogenesis (2, 3).”
- Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia (2012, background): “IZKF1 alteration is a hallmark of Philadelphia chromosome (Ph) ALL with BCRABL1 fusion (Mullighan et al., 2008; Iacobucci et al., 2009) and is also associated with poor outcome in both BCR-ABL1positive and BCR-ABL1-negative ALL (Den Boer et al.”
- Biology, risk stratification, and therapy of pediatric acute leukemias: an update. (2011, background): “Genetic Determinants of High-Risk B-Cell Precursor ALL In Philadelphia chromosome–positive ALL with constitutively active BCR-ABL1 tyrosine kinase, IKZF1 (encoding the lymphoid transcription factor IKAROS) is deleted in approximately 80% of the cases.(51) Interestingly, there is a high-risk subgroup”
- Rearrangement of CRLF2 in B-progenitor– and Down syndrome–associated acute lymphoblastic leukemia (2009, background): “65 56,XY,+X,+4,+6,+8,+10,+14,+17,+18,+21c,+21[2]/47,XY,+21c[16] 24 no No 3.”
- DNA sequencing of a cytogenetically normal acute myeloid leukemia genome (2008, background): “At relapse, the bone marrow had 78% myeloblasts, and contained a new clonal cytogenetic abnormality, t(10; 12) (p12; p13).”
- Targetable Kinase-Activating Lesions in Ph-like Acute Lymphoblastic Leukemia (2014, background): “Across the entire cohort, rearrangements activating kinase signaling were identified in 96 of 154 patients (62%), including 35 different rearrangements (16 of which were recurrent) in 13 kinase, cytokine, or cytokinereceptor genes: JAK2 (10 fusion partners), ABL1 (6), PDGFRB (4), ABL2 (3), CRLF2 (2)”