Rearrangement of CRLF2 in B-progenitor– and Down syndrome–associated acute lymphoblastic leukemia
By C. Mullighan, J. R. Collins-Underwood, Letha A A Phillips, M. Loudin, Wei Liu, Jinghui Zhang, Jing Ma, E. Coustan-Smith, R. Harvey, Cheryl L. Willman and 14 more. Nature Genetics, 2009
628 citations recorded by the source corpus.
Subfields: Hematology, Pediatrics, Perinatology and Child Health, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/f20f75986b823b398eefda1d13708aa17960ffad
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Citations in the corpus
- The genetic basis of early T-cell precursor acute lymphoblastic leukaemia (2012, background): “Rearrangement of CRLF2 is observed in B-progenitor AL”
- CREBBP mutations in relapsed acute lymphoblastic leukaemia (2011, background): “This cohort comprised AML cases with translocation (8;21) [RUNX1-RUNX1T1] (N 5 9), inversion/translocation (16;16) [CBFBSMMHC] (N 5 16), translocation (15;17) or related rearrangements involving RARA (N 5 7), M7 morphology (N 5 9), rearrangement of MLL (N 5 15), normal or miscellaneous karyotype (N ”
- Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing (2012, background): “P2RY8 is most notable for its involvement in a chromosomal translocation with CRLF2 in 7% of patients with B-progenitor acute lymphoblastic leukemia (ALL) and 53% of individuals with ALL and Down syndrome (21).”
- Biology, risk stratification, and therapy of pediatric acute leukemias: an update. (2011, background): “CRLF2 alteration was associated with activating mutations of JAK1 or JAK2; these two genetic lesions together resulted in constitutive Jak-Stat activation and the growth of cytokine-dependent mouse B-progenitor cell lines in the absence of exogenous cytokine, indicating that they are cooperative mut”
- Targetable Kinase-Activating Lesions in Ph-like Acute Lymphoblastic Leukemia (2014, background): “Patients with Ph-like ALL do not have the BCR–ABL1 fusion protein expressed from the t(9;22)(q34;q11.”
- Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia (2012, background): “Genome-wide analyses have identified genetic alterations targeting transcriptional regulators of lymphoid development (PAX5, EBF1, and IKZF1) in over 60% of B-ALL patients (Kuiper et al., 2007; Mullighan et al., 2007, 2009b).”
- A Comprehensive Review (2017, neutral): “P2RY8-CRLF2 fusion encodes full-length CRLF2, which results in high expression of this cytokine receptor.(16,17) CRLF2 rearrangements can also co-occur with iAMP21 or dic(9;20) as well as with high hyperdiploidy.”
- Childhood Acute Lymphoblastic Leukemia: Progress Through Collaboration. (2015, background): “Because up to 60% of patients with Down syndrome are Ph-like and are characterized by CRLF2 overexpression and JAK-STAT activation, they may potentially benefit from future therapy targeting kinase pathways.(49,50)”