JAK mutations in high-risk childhood acute lymphoblastic leukemia
By C. Mullighan, Jinghui Zhang, R. Harvey, J. R. Collins-Underwood, B. Schulman, Letha A A Phillips, S. Tasian, M. Loh, X. Su, Wei Liu and 11 more. Proceedings of the National Academy of Sciences of the United States of America, 2009
598 citations recorded by the source corpus.
Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/40e6840948881418119bb4124159aaa0a674dd29
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Citations in the corpus
- Outcomes for children and adolescents with cancer: challenges for the twenty-first century. (2010, background): “Proof of concept for the dramatic impact of effective targeted agents in the pediatric setting is seen for both all-trans retinoic acid for acute promyelocytic leukemia14 and for imatinib for Philadelphia chromosome–positive ALL.57,58 In each case, the targeted agent blocked the activity of a cancer”
- The origin and evolution of mutations in Acute Myeloid Leukemia (2012, unknown): “…spontaneous mutation in the Jak1 gene at position V657F (Wartman et al., 2011); this mutation that is identical to that found in some human patients with B lymphoblastic leukemia (Flex et al., 2008; Harvey et al., 2010; Mullighan et al., 2009) and a patient with M3 AML (Jeong et al., 2008).”
- 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).”