![]() ![]() The genomic landscape of pediatric and young adult T-lineage acute lymphoblastic leukemia. Landscape of driver mutations and their clinical impacts in pediatric B-cell precursor acute lymphoblastic leukemia. Transcriptional landscape of B cell precursor acute lymphoblastic leukemia based on an international study of 1,223 cases. PAX5-driven subtypes of B-progenitor acute lymphoblastic leukemia. PAX5 P80R mutation identifies a novel subtype of B-cell precursor acute lymphoblastic leukemia with favorable outcome. PAX5 biallelic genomic alterations define a novel subgroup of B-cell precursor acute lymphoblastic leukemia. New oncogenic subtypes in pediatric B-cell precursor acute lymphoblastic leukemia. A novel recurrent EP300-ZNF384 gene fusion in B-cell precursor acute lymphoblastic leukemia. Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia. Deregulation of DUX4 and ERG in acute lymphoblastic leukemia. Identification of ETV6-RUNX1-like and DUX4-rearranged subtypes in paediatric B-cell precursor acute lymphoblastic leukaemia. Philadelphia chromosome-like acute lymphoblastic leukemia. Why and how to treat Ph-like ALL? Best Pract. Deletion of IKZF1 and prognosis in acute lymphoblastic leukemia. A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study. The biology of B-progenitor acute lymphoblastic leukemia. Biologic and therapeutic implications of genomic alterations in acute lymphoblastic leukemia. Somatic mutation data can also be explored interactively using ProteinPaint 81 and GenomePaint 86 on St. All raw sequencing data are available under controlled access for protection of germline information and to ensure appropriate data usage, and approval can be obtained by application through the dbGaP portal (for TARGET datasets) or by contacting the PCGP steering committee for non-TARGET (EGA-deposited) datasets. The remaining (non-TARGET) data have been deposited in the European Genome Phenome Archive, accession nos. phs000218 (TARGET) and at NCI’s Genomic Data Commons ( ) under project TARGET. TARGET BAM and FASTQ sequence files are accessible through the database of genotypes and phenotypes (dbGaP ) under accession no. TARGET ALL data may be accessed through the TARGET website at. Genomic data are publicly available, and data accessions for RNA-seq, WES, WGS and SNP are listed for each case in Supplementary Table 1. Together, these results deepen understanding of the ALL genomic landscape and associated outcomes. Intriguingly, DUX4- and KMT2A-rearranged subtypes separate into CEBPA/FLT3- or NFATC4-expressing subgroups with potential clinical implications. We also demonstrate the prognostic significance of genetic alterations within subtypes. By contrast, ultraviolet-induced mutations precede chromosomal gains in B-ALL cases with intrachromosomal amplification of chromosome 21. In hyperdiploid B-ALL, chromosomal gains are acquired early and synchronously before ultraviolet-induced mutation. Most samples harbor at least one rare gene alteration, including 70 putative cancer driver genes associated with ubiquitination, SUMOylation, noncoding transcripts and other functions. Here, using whole-genome, exome and transcriptome sequencing of 2,754 childhood patients with ALL, we find that, despite a generally low mutation burden, ALL cases harbor a median of four putative somatic driver alterations per sample, with 376 putative driver genes identified varying in prevalence across ALL subtypes. Nature Genetics volume 54, pages 1376–1389 ( 2022) Cite this articleĪcute lymphoblastic leukemia (ALL) is the most common childhood cancer. The genomic landscape of pediatric acute lymphoblastic leukemia ![]()
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