Huei San Leong

TL;DR: A comprehensive analysis involving both simulations and experimental RNA-sequencing data demonstrates that this strategy leads to a universally more powerful analysis and fewer false discoveries when compared to conventional approaches.

TL;DR: This study reveals, for the first time to the authors' knowledge, where Smchd1 binds genome-wide, its hitherto unappreciated functional interaction with chromatin organizer CCCTC-binding factor in gene regulation, and which part of the protein is required for chromatin binding, which leads to a new model of Smd1 function, where it directly binds DNA to mediate 3D chromatin architecture.

TL;DR: It is shown in mouse that genetic inactivation of Smchd1 accelerates tumorigenesis in male mice, highlighting a hitherto uncharacterized role for SMCHD1 as a candidate tumor suppressor gene in hematopoietic cancers.

TL;DR: It is shown that, in contrast to PRC1, PRC2 is a tumor suppressor in Eµ-myc lymphomagenesis, because disease onset was accelerated by heterozygosity for Suz12 or by short hairpin RNA-mediated knockdown of Suz 12 or Ezh2, and this finding provides new insight regarding the functional contribution of mutations inPRC2 in a range of leukemias.

TL;DR: The methodology for malignant transformation of mouse embryonic fibroblasts for transplantation into immunodeficient nude mice, as used in Leong et al. (2013), is described.