J
Jason H. Bielas
Researcher at Fred Hutchinson Cancer Research Center
Publications - 62
Citations - 8448
Jason H. Bielas is an academic researcher from Fred Hutchinson Cancer Research Center. The author has contributed to research in topics: Mitochondrial DNA & Mutation. The author has an hindex of 27, co-authored 59 publications receiving 6198 citations. Previous affiliations of Jason H. Bielas include University of Washington Medical Center & University of Washington.
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Journal ArticleDOI
Massively parallel digital transcriptional profiling of single cells
Grace X.Y. Zheng,Jessica M. Terry,Phillip Belgrader,Paul Ryvkin,Zachary Bent,Ryan Wilson,Solongo B. Ziraldo,Tobias Daniel Wheeler,Geoffrey P. McDermott,Junjie Zhu,Mark T. Gregory,Joe Shuga,Luz Montesclaros,Jason G. Underwood,Donald A. Masquelier,Stefanie Y. Nishimura,Michael Schnall-Levin,Paul Wyatt,Christopher Hindson,Rajiv Bharadwaj,Alexander Wong,Kevin D. Ness,Lan Beppu,H. Joachim Deeg,Christopher McFarland,Keith R. Loeb,Keith R. Loeb,William J. Valente,William J. Valente,Nolan G. Ericson,Emily A. Stevens,Jerald P. Radich,Tarjei S. Mikkelsen,Benjamin J. Hindson,Jason H. Bielas +34 more
TL;DR: A droplet-based system that enables 3′ mRNA counting of tens of thousands of single cells per sample is described and sequence variation in the transcriptome data is used to determine host and donor chimerism at single-cell resolution from bone marrow mononuclear cells isolated from transplant patients.
Journal ArticleDOI
Mitochondrial point mutations do not limit the natural lifespan of mice
Marc Vermulst,Jason H. Bielas,Gregory C. Kujoth,Warren C. Ladiges,Peter S. Rabinovitch,Tomas A. Prolla,Lawrence A. Loeb +6 more
TL;DR: The results strongly indicate that mitochondrial mutations do not limit the lifespan of wild-type mice and that the mutation frequency in mouse mitochondria is more than ten times lower than previously reported.
Journal ArticleDOI
Human cancers express a mutator phenotype
TL;DR: Measurements of random single-nucleotide substitutions in normal and neoplastic human tissues indicate that accelerated mutagenesis prevails late into tumor progression, and suggest that elevation of random mutation frequency in tumors might serve as a novel prognostic indicator.
Journal ArticleDOI
DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice.
Marc Vermulst,Jonathan Wanagat,Gregory C. Kujoth,Jason H. Bielas,Peter S. Rabinovitch,Tomas A. Prolla,Lawrence A. Loeb +6 more
TL;DR: It is demonstrated that the rate at which mtDNA mutations reach phenotypic expression differs markedly among tissues, which may be an important factor in determining the tolerance of a tissue to random mitochondrial mutagenesis.
Journal ArticleDOI
Heterogeneity of tumor-induced gene expression changes in the human metabolic network
Jie Hu,Jason W. Locasale,Jason H. Bielas,Jason H. Bielas,Jacintha O'Sullivan,Kieran Sheahan,Lewis C. Cantley,Lewis C. Cantley,Matthew G. Vander Heiden,Matthew G. Vander Heiden,Dennis Vitkup +10 more
TL;DR: Overall, the metabolic gene expression program in tumors is similar to that in the corresponding normal tissues, and many hundreds of metabolic isoenzymes show significant and tumor-specific expression changes, which are potential targets for anticancer therapy.