Ding Yan Wang
University of Toronto
4 Papers
111 Citations
Ding Yan Wang is an academic researcher from University of Toronto. The author has contributed to research in topics: Gene & Loss of heterozygosity. The author has an hindex of 3, co-authored 4 publications.
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Papers
Mutation, SNP, and isoform analysis of fibroblast growth factor receptor 3 (FGFR3) in 150 newly diagnosed multiple myeloma patients.
Obiageli N. Onwuazor,Xiao-Yan Wen,Ding Yan Wang,Lihua Zhuang,Esther Masih-Khan,Jaimie Claudio,Bart Barlogie,John D. Shaughnessy,A. Keith Stewart +8 more
TL;DR: The t(4;14) translocation in multiple myeloma (MM) is identified in 15% of patient samples and dysregulates both FGFR3 and multiple myELoma SET domain (MMSET).
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Identification of a novel lipase gene mutated in lpd mice with hypertriglyceridemia and associated with dyslipidemia in humans
Xiao-Yan Wen,Robert A. Hegele,Jian Wang,Ding Yan Wang,Joseph Y. Cheung,Michael D. Wilson,Maryam Yahyapour,Yahong Bai,Lihua Zhuang,Jennifer Skaug,T. Kue Young,Philip W. Connelly,Ben F. Koop,Lap-Chee Tsui,Lap-Chee Tsui,A. Keith Stewart +15 more
TL;DR: Using shotgun sequencing and bioinformatics, a novel lipase gene lpdl (lpd lipase) is identified within the lpd locus, and the genetic disruption of exon 10 of l pdl in the lPD mutant locus is demonstrated, which may identify novel molecular mechanisms for plasma and/or tissue TG metabolism.
A Deficiency in the Region Homologous to Human 17q21.33–q23.2 Causes Heart Defects in Mice
Y. Eugene Yu,Masae Morishima,Annie Pao,Ding Yan Wang,Xiao-Yan Wen,Antonio Baldini,Allan Bradley +6 more
TL;DR: Phenotypic analyses of the mutant mouse lines showed that the Dp(11)18/Dp( 11)18 genotype was responsible for embryonic or adolescent lethality, whereas the Df(11]18/+ genotypes were responsible for heart defects, and a new dosage-sensitive genomic region was identified that may be critical for normal heart development in both mice and humans.
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Chromosome Condensation 1-Like (Chc1L) Is a Novel Tumor Suppressor Involved in Development of Histiocyte-Rich Neoplasms.
David Spillane,Ding Yan Wang,Susan Newbigging,Youdong Wang,Chang-Xin Shi,Hae-Ra Cho,Hiroki Shimizu,Anthony O. Gramolini,Mingyao Liu,Xiao-Yan Wen +9 more
TL;DR: This study suggests that Chc1L is involved in suppression of these two histiocyte-rich neoplasms in mice and supports clinical data suggesting that CHC1L loss of function is an important step in the pathogenesis of cancers containing 13q14 deletion.