Gary W. Swift

TL;DR: The interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblastomas reveals a link between MGMT promoter methylation and a hypermutator phenotype consequent to mismatch repair deficiency in treated gliobeasts, demonstrating that it can rapidly expand knowledge of the molecular basis of cancer.

TL;DR: DNMT3A mutations are highly recurrent in patients with de novo AML with an intermediate-risk cytogenetic profile and are independently associated with a poor outcome in Cox proportional-hazards analysis.

TL;DR: The data suggest that most of the mutations found in AML genomes are actually random events that occurred in HSPCs before they acquired the initiating mutation; the mutational history of that cell is "captured" as the clone expands.

TL;DR: Most of the genetic variation in iPSC clones is not caused by reprogramming per se, but is rather a consequence of cloning individual cells, which "captures" their mutational history.

TL;DR: A novel frameshift mutation in DNMT3A, one of the three genes in humans that encodes a DNA methyltransferase that catalyzes the addition of methyl groups to cytosine within CpG dinucleotides, is discovered.