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Shi, Jiantao

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Shi

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Jiantao

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Shi, Jiantao

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2015 - 20173

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Author's Publications: search.filters.isAuthorOfPublication.20c87e65-1b18-4498-abf7-13353caa797e

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Now showing 1 - 3 of 3
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    edgeRun: an R package for sensitive, functionally relevant differential expression discovery using an unconditional exact test
    (Oxford University Press, 2015) Dimont, Emmanuel; Shi, Jiantao; Kirchner, Rory; Hide, Winston
    Summary: Next-generation sequencing platforms for measuring digital expression such as RNA-Seq are displacing traditional microarray-based methods in biological experiments. The detection of differentially expressed genes between groups of biological conditions has led to the development of numerous bioinformatics tools, but so far, few exploit the expanded dynamic range afforded by the new technologies. We present edgeRun, an R package that implements an unconditional exact test that is a more powerful version of the exact test in edgeR. This increase in power is especially pronounced for experiments with as few as two replicates per condition, for genes with low total expression and with large biological coefficient of variation. In comparison with a panel of other tools, edgeRun consistently captures functionally similar differentially expressed genes. Availability and implementation: The package is freely available under the MIT license from CRAN (http://cran.r-project.org/web/packages/edgeRun). Contact: edimont@mail.harvard.edu Supplementary information: Supplementary data are available at Bioinformatics online.
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    The Mutational Landscape of Circulating Tumor Cells in Multiple Myeloma
    (2017) Mishima, Yuji; Paiva, Bruno; Shi, Jiantao; Park, Jihye; Manier, Salomon; Takagi, Satoshi; Massoud, Mira; Perilla-Glen, Adriana; Aljawai, Yosra; Huynh, Daisy; Roccaro, Aldo M.; Sacco, Antonio; Capelletti, Marzia; Detappe, Alexandre; Alignani, Diego; Anderson, Kenneth; Munshi, Nikhil; Prosper, Felipe; Lohr, Jens; Ha, Gavin; Freeman, Sam; Van Allen, Eliezer; Adalsteinsson, Viktor A.; Michor, Franziska; San Miguel, Jesus F.; Ghobrial, Irene
    Summary The development of sensitive and non-invasive “liquid biopsies” presents new opportunities for longitudinal monitoring of tumor dissemination and clonal evolution. The number of circulating tumor cells (CTCs) is prognostic in multiple myeloma (MM), but there is little information on their genetic features. Here, we have analyzed the genomic landscape of CTCs from 29 MM patients, including eight cases with matched/paired bone marrow (BM) tumor cells. Our results show that 100% of clonal mutations in patient BM were detected in CTCs and that 99% of clonal mutations in CTCs were present in BM MM. These include typical driver mutations in MM such as in KRAS, NRAS, or BRAF. These data suggest that BM and CTC samples have similar clonal structures, as discordances between the two were restricted to subclonal mutations. Accordingly, our results pave the way for potentially less invasive mutation screening of MM patients through characterization of CTCs.
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    Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer
    (2017) Smith, Zachary; Shi, Jiantao; Gu, Hongcang; Donaghey, Julie; Clement, Kendell; Cacciarelli, Davide; Gnirke, Andreas; Michor, Franziska; Meissner, Alexander
    In mammals, the canonical somatic DNA methylation landscape is established upon specification of the embryo proper and subsequently disrupted within many cancer types1-4. However, the underlying mechanisms that direct this genome-scale transformation remain elusive, with no clear model for its systematic acquisition or potential developmental utility5,6. Here we analyzed global remethylation from the mouse preimplantation embryo into the early epiblast and extraembryonic ectoderm. We show that these two states acquire highly divergent genomic distributions with substantial disruption of bimodal, CpG density-dependent methylation in the placental progenitor7,8. The extraembryonic epigenome includes specific de novo methylation at hundreds of embryonically-protected CpG island promoters particularly those that are associated with key developmental regulators and orthologously methylated across most human cancer types9. Our data suggest that the evolutionary innovation of extraembryonic tissues may have required cooption of DNA methylation-based suppression as an alternative to the embryonically utilized Polycomb group proteins, which coordinate germlayer formation in response to extraembryonic cues10. Moreover, we establish that this decision is made deterministically downstream of promiscuously utilized, and frequently oncogenic, signaling pathways via a novel combination of epigenetic cofactors. Methylation of developmental gene promoters during tumorigenesis may therefore reflect the misappropriation of an innate trajectory and the spontaneous reacquisition of a latent, developmentally-encoded epigenetic landscape.