Pui, C.H. & Evans, W.E. Treatment of acute lymphoblastic leukemia. N. Engl. J. Med. 354, 166–178 (2006).
Pui, C.H., Mullighan, C.G., Evans, W.E. & Relling, M.V. Pediatric acute lymphoblastic leukemia: where are we going and how do we get there? Blood 120, 1165–1174 (2012).
Hunger, S.P. et al. Improved survival for children and adolescents with acute lymphoblastic leukemia between 1990 and 2005: a report from the Children's Oncology Group. J. Clin. Oncol. 30, 1663–1669 (2012).
Stanulla, M. et al. Integrating molecular information into treatment of childhood acute lymphoblastic leukemia—a perspective from the BFM Study Group. Blood Cells Mol. Dis. 39, 160–163 (2007).
Biondi, A. et al. Imatinib after induction for treatment of children and adolescents with Philadelphia-chromosome-positive acute lymphoblastic leukaemia (EsPhALL): a randomised, open-label, intergroup study. Lancet Oncol. 13, 936–945 (2012).
Den Boer, M.L. et al. A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study. Lancet Oncol. 10, 125–134 (2009).
Roberts, K.G. et al. Genetic alterations activating kinase and cytokine receptor signaling in high-risk acute lymphoblastic leukemia. Cancer Cell 22, 153–166 (2012).
Harvey, R.C. et al. Identification of novel cluster groups in pediatric high-risk B-precursor acute lymphoblastic leukemia with gene expression profiling: correlation with genome-wide DNA copy number alterations, clinical characteristics, and outcome. Blood 116, 4874–4884 (2010).
Mullighan, C.G. et al. Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. N. Engl. J. Med. 360, 470–480 (2009).
Harvey, R.C. et al. Rearrangement of CRLF2 is associated with mutation of JAK kinases, alteration of IKZF1, Hispanic/Latino ethnicity, and a poor outcome in pediatric B-progenitor acute lymphoblastic leukemia. Blood 115, 5312–5321 (2010).
Loh, M.L. et al. Tyrosine kinome sequencing of pediatric acute lymphoblastic leukemia: a report from the Children's Oncology Group TARGET Project. Blood 121, 485–488 (2013).
Papaemmanuil, E. et al. Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia. Nat. Genet. 41, 1006–1010 (2009).
Sherborne, A.L. et al. Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk. Nat. Genet. 42, 492–494 (2010).
Treviño, L.R. et al. Germline genomic variants associated with childhood acute lymphoblastic leukemia. Nat. Genet. 41, 1001–1005 (2009).
Xu, H. et al. Novel susceptibility variants at 10p12.31-12.2 for childhood acute lymphoblastic leukemia in ethnically diverse populations. J. Natl. Cancer Inst. 105, 733–742 (2013).
Xu, H. et al. ARID5B genetic polymorphisms contribute to racial disparities in the incidence and treatment outcome of childhood acute lymphoblastic leukemia. J. Clin. Oncol. 30, 751–757 (2012).
Paulsson, K. et al. Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc. Natl. Acad. Sci. USA 107, 21719–21724 (2010).
Jones, A.V. et al. JAK2 haplotype is a major risk factor for the development of myeloproliferative neoplasms. Nat. Genet. 41, 446–449 (2009).
Olcaydu, D. et al. A common JAK2 haplotype confers susceptibility to myeloproliferative neoplasms. Nat. Genet. 41, 450–454 (2009).
Kilpivaara, O. et al. A germline JAK2 SNP is associated with predisposition to the development of JAK2V617F-positive myeloproliferative neoplasms. Nat. Genet. 41, 455–459 (2009).
Yang, J.J. et al. Ancestry and pharmacogenomics of relapse in acute lymphoblastic leukemia. Nat. Genet. 43, 237–241 (2011).
Fujiwara, T. et al. Discovering hematopoietic mechanisms through genome-wide analysis of GATA factor chromatin occupancy. Mol. Cell 36, 667–681 (2009).
Wei, G. et al. Genome-wide analyses of transcription factor GATA3-mediated gene regulation in distinct T cell types. Immunity 35, 299–311 (2011).
Yagi, R., Zhu, J. & Paul, W.E. An updated view on transcription factor GATA3-mediated regulation of Th1 and Th2 cell differentiation. Int. Immunol. 23, 415–420 (2011).
Zhang, J. et al. The genetic basis of early T-cell precursor acute lymphoblastic leukaemia. Nature 481, 157–163 (2012).
Enciso-Mora, V. et al. A genome-wide association study of Hodgkin's lymphoma identifies new susceptibility loci at 2p16.1 (REL), 8q24.21 and 10p14 (GATA3). Nat. Genet. 42, 1126–1130 (2010).
Pasquet, M. et al. High frequency of GATA2 mutations in patients with mild chronic neutropenia evolving to MonoMac syndrome, myelodysplasia, and acute myeloid leukemia. Blood 121, 822–829 (2013).
Hahn, C.N. et al. Heritable GATA2 mutations associated with familial myelodysplastic syndrome and acute myeloid leukemia. Nat. Genet. 43, 1012–1017 (2011).
Davies, S.M. et al. Pharmacogenetics of minimal residual disease response in children with B-precursor acute lymphoblastic leukemia: a report from the Children's Oncology Group. Blood 111, 2984–2990 (2008).
Huang, R.S. et al. A genome-wide approach to identify genetic variants that contribute to etoposide-induced cytotoxicity. Proc. Natl. Acad. Sci. USA 104, 9758–9763 (2007).
Degner, J.F. et al. DNase I sensitivity QTLs are a major determinant of human expression variation. Nature 482, 390–394 (2012).
Borowitz, M.J. et al. Clinical significance of minimal residual disease in childhood acute lymphoblastic leukemia and its relationship to other prognostic factors: a Children's Oncology Group study. Blood 111, 5477–5485 (2008).
Shi, J. et al. Common variants on chromosome 6p22.1 are associated with schizophrenia. Nature 460, 753–757 (2009).
Purcell, S.M. et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 460, 748–752 (2009).
Troyer, J.L. et al. Genome-wide association study implicates PARD3B-based AIDS restriction. J. Infect. Dis. 203, 1491–1502 (2011).
Burchard, E.G. et al. Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects with asthma. Am. J. Respir. Crit. Care Med. 169, 386–392 (2004).
Korn, J.M. et al. Integrated genotype calling and association analysis of SNPs, common copy number polymorphisms and rare CNVs. Nat. Genet. 40, 1253–1260 (2008).
Pritchard, J.K., Stephens, M. & Donnelly, P. Inference of population structure using multilocus genotype data. Genetics 155, 945–959 (2000).
Mao, X. et al. A genomewide admixture mapping panel for Hispanic/Latino populations. Am. J. Hum. Genet. 80, 1171–1178 (2007).
Tibshirani, R., Hastie, T., Narasimhan, B. & Chu, G. Diagnosis of multiple cancer types by shrunken centroids of gene expression. Proc. Natl. Acad. Sci. USA 99, 6567–6572 (2002).
Liu, E.Y., Li, M., Wang, W. & Li, Y. MaCH-admix: genotype imputation for admixed populations. Genet. Epidemiol. 37, 25–37 (2013).
Pruim, R.J. et al. LocusZoom: regional visualization of genome-wide association scan results. Bioinformatics 26, 2336–2337 (2010).
Chen, I.M. et al. Outcome modeling with CRLF2, IKZF1, JAK, and minimal residual disease in pediatric acute lymphoblastic leukemia: a Children's Oncology Group study. Blood 119, 3512–3522 (2012).
Andersen, P.K. & Perme, M.P. Pseudo-observations in survival analysis. Stat. Methods Med. Res. 19, 71–99 (2010).
Duan, S. et al. Genetic architecture of transcript-level variation in humans. Am. J. Hum. Genet. 82, 1101–1113 (2008).
Spielman, R.S. et al. Common genetic variants account for differences in gene expression among ethnic groups. Nat. Genet. 39, 226–231 (2007).
Ernst, J. et al. Mapping and analysis of chromatin state dynamics in nine human cell types. Nature 473, 43–49 (2011).
Zhou, X. et al. The Human Epigenome Browser at Washington University. Nat. Methods 8, 989–990 (2011).