Readman Chiu
BC Cancer Agency
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Publication
Featured researches published by Readman Chiu.
Nature | 2011
Ryan D. Morin; Maria Mendez-Lago; Andrew J. Mungall; Rodrigo Goya; Karen Mungall; Richard Corbett; Nathalie A. Johnson; Tesa Severson; Readman Chiu; Matthew A. Field; Shaun D. Jackman; Martin Krzywinski; David W. Scott; Diane L. Trinh; Jessica Tamura-Wells; Sa Li; Marlo Firme; Sanja Rogic; Malachi Griffith; Susanna Chan; Oleksandr Yakovenko; Irmtraud M. Meyer; Eric Zhao; Duane E. Smailus; Michelle Moksa; Lisa M. Rimsza; Angela Brooks-Wilson; John J. Spinelli; Susana Ben-Neriah; Barbara Meissner
Follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) are the two most common non-Hodgkin lymphomas (NHLs). Here we sequenced tumour and matched normal DNA from 13 DLBCL cases and one FL case to identify genes with mutations in B-cell NHL. We analysed RNA-seq data from these and another 113 NHLs to identify genes with candidate mutations, and then re-sequenced tumour and matched normal DNA from these cases to confirm 109 genes with multiple somatic mutations. Genes with roles in histone modification were frequent targets of somatic mutation. For example, 32% of DLBCL and 89% of FL cases had somatic mutations in MLL2, which encodes a histone methyltransferase, and 11.4% and 13.4% of DLBCL and FL cases, respectively, had mutations in MEF2B, a calcium-regulated gene that cooperates with CREBBP and EP300 in acetylating histones. Our analysis suggests a previously unappreciated disruption of chromatin biology in lymphomagenesis.
Nature Methods | 2010
Gordon Robertson; Jacqueline E. Schein; Readman Chiu; Richard Corbett; Matthew A. Field; Shaun D. Jackman; Karen Mungall; Sam Lee; Hisanaga Mark Okada; Jenny Q. Qian; Malachi Griffith; Anthony Raymond; Nina Thiessen; Timothee Cezard; Yaron S N Butterfield; Richard Newsome; Simon K. Chan; Rong She; Richard Varhol; Baljit Kamoh; Anna-Liisa Prabhu; Angela Tam; Yongjun Zhao; Richard A. Moore; Martin Hirst; Marco A. Marra; Steven J.M. Jones; Pamela A. Hoodless; Inanc Birol
We describe Trans-ABySS, a de novo short-read transcriptome assembly and analysis pipeline that addresses variation in local read densities by assembling read substrings with varying stringencies and then merging the resulting contigs before analysis. Analyzing 7.4 gigabases of 50-base-pair paired-end Illumina reads from an adult mouse liver poly(A) RNA library, we identified known, new and alternative structures in expressed transcripts, and achieved high sensitivity and specificity relative to reference-based assembly methods.
Nature Genetics | 2013
Trevor J. Pugh; Olena Morozova; Edward F. Attiyeh; Shahab Asgharzadeh; Jun S. Wei; Daniel Auclair; Scott L. Carter; Kristian Cibulskis; Megan Hanna; Adam Kiezun; Jaegil Kim; Michael S. Lawrence; Lee Lichenstein; Aaron McKenna; Chandra Sekhar Pedamallu; Alex H. Ramos; Erica Shefler; Andrey Sivachenko; Carrie Sougnez; Chip Stewart; Adrian Ally; Inanc Birol; Readman Chiu; Richard Corbett; Martin Hirst; Shaun D. Jackman; Baljit Kamoh; Alireza Hadj Khodabakshi; Martin Krzywinski; Allan Lo
Neuroblastoma is a malignancy of the developing sympathetic nervous system that often presents with widespread metastatic disease, resulting in survival rates of less than 50%. To determine the spectrum of somatic mutation in high-risk neuroblastoma, we studied 240 affected individuals (cases) using a combination of whole-exome, genome and transcriptome sequencing as part of the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) initiative. Here we report a low median exonic mutation frequency of 0.60 per Mb (0.48 nonsilent) and notably few recurrently mutated genes in these tumors. Genes with significant somatic mutation frequencies included ALK (9.2% of cases), PTPN11 (2.9%), ATRX (2.5%, and an additional 7.1% had focal deletions), MYCN (1.7%, causing a recurrent p.Pro44Leu alteration) and NRAS (0.83%). Rare, potentially pathogenic germline variants were significantly enriched in ALK, CHEK2, PINK1 and BARD1. The relative paucity of recurrent somatic mutations in neuroblastoma challenges current therapeutic strategies that rely on frequently altered oncogenic drivers.
Proceedings of the National Academy of Sciences of the United States of America | 2011
Sébastien Duplessis; Christina A. Cuomo; Yao-Cheng Lin; Andrea Aerts; Emilie Tisserant; Claire Veneault-Fourrey; David L. Joly; Stéphane Hacquard; Joelle Amselem; Brandi L. Cantarel; Readman Chiu; Pedro M. Coutinho; Nicolas Feau; Matthew A. Field; Pascal Frey; Eric Gelhaye; Jonathan M. Goldberg; Manfred Grabherr; Chinnappa D. Kodira; Annegret Kohler; Ursula Kües; Erika Lindquist; Susan Lucas; Rohit Mago; Evan Mauceli; Emmanuelle Morin; Claude Murat; Jasmyn Pangilinan; Robert F. Park; Matthew Pearson
Rust fungi are some of the most devastating pathogens of crop plants. They are obligate biotrophs, which extract nutrients only from living plant tissues and cannot grow apart from their hosts. Their lifestyle has slowed the dissection of molecular mechanisms underlying host invasion and avoidance or suppression of plant innate immunity. We sequenced the 101-Mb genome of Melampsora larici-populina, the causal agent of poplar leaf rust, and the 89-Mb genome of Puccinia graminis f. sp. tritici, the causal agent of wheat and barley stem rust. We then compared the 16,399 predicted proteins of M. larici-populina with the 17,773 predicted proteins of P. graminis f. sp tritici. Genomic features related to their obligate biotrophic lifestyle include expanded lineage-specific gene families, a large repertoire of effector-like small secreted proteins, impaired nitrogen and sulfur assimilation pathways, and expanded families of amino acid and oligopeptide membrane transporters. The dramatic up-regulation of transcripts coding for small secreted proteins, secreted hydrolytic enzymes, and transporters in planta suggests that they play a role in host infection and nutrient acquisition. Some of these genomic hallmarks are mirrored in the genomes of other microbial eukaryotes that have independently evolved to infect plants, indicating convergent adaptation to a biotrophic existence inside plant cells.
Proceedings of the National Academy of Sciences of the United States of America | 2011
Sébastien Duplessis; Christina A. Cuomo; Yao-Cheng Lin; Andrea Aerts; Emilie Tisserant; Claire Veneault-Fourrey; David L. Joly; Stéphane Hacquard; Joelle Amselem; Brandi L. Cantarel; Readman Chiu; Pedro Couthinho; Nicolas Feau; Matthew A. Field; Pascal Frey; Eric Gelhaye; Jonathan M. Goldberg; Manfred Grabherr; Chinnappa D. Kodira; Annegret Kohler; Ursula Kües; Erika Lindquist; Susan Lucas; Rohit Mago; Evan Mauceli; Emmanuelle Morin; Claude Murat; Jasmyn Pangilinan; Robert F. Park; Matthew Pearson
Rust fungi are some of the most devastating pathogens of crop plants. They are obligate biotrophs, which extract nutrients only from living plant tissues and cannot grow apart from their hosts. Their lifestyle has slowed the dissection of molecular mechanisms underlying host invasion and avoidance or suppression of plant innate immunity. We sequenced the 101-Mb genome of Melampsora larici-populina, the causal agent of poplar leaf rust, and the 89-Mb genome of Puccinia graminis f. sp. tritici, the causal agent of wheat and barley stem rust. We then compared the 16,399 predicted proteins of M. larici-populina with the 17,773 predicted proteins of P. graminis f. sp tritici. Genomic features related to their obligate biotrophic lifestyle include expanded lineage-specific gene families, a large repertoire of effector-like small secreted proteins, impaired nitrogen and sulfur assimilation pathways, and expanded families of amino acid and oligopeptide membrane transporters. The dramatic up-regulation of transcripts coding for small secreted proteins, secreted hydrolytic enzymes, and transporters in planta suggests that they play a role in host infection and nutrient acquisition. Some of these genomic hallmarks are mirrored in the genomes of other microbial eukaryotes that have independently evolved to infect plants, indicating convergent adaptation to a biotrophic existence inside plant cells.
Nature | 2002
Simon G. Gregory; Mandeep Sekhon; Jacqueline E. Schein; Shaying Zhao; Kazutoyo Osoegawa; Carol Scott; Richard S. Evans; Paul W. Burridge; Tony Cox; Christopher A. Fox; Richard D. Hutton; Ian R. Mullenger; Kimbly J. Phillips; James Smith; Jim Stalker; Glen Threadgold; Ewan Birney; Kristine M. Wylie; Asif T. Chinwalla; John W. Wallis; LaDeana W. Hillier; Jason Carter; Tony Gaige; Sara Jaeger; Colin Kremitzki; Dan Layman; Jason Maas; Rebecca McGrane; Kelly Mead; Rebecca Walker
A physical map of a genome is an essential guide for navigation, allowing the location of any gene or other landmark in the chromosomal DNA. We have constructed a physical map of the mouse genome that contains 296 contigs of overlapping bacterial clones and 16,992 unique markers. The mouse contigs were aligned to the human genome sequence on the basis of 51,486 homology matches, thus enabling use of the conserved synteny (correspondence between chromosome blocks) of the two genomes to accelerate construction of the mouse map. The map provides a framework for assembly of whole-genome shotgun sequence data, and a tile path of clones for generation of the reference sequence. Definition of the human–mouse alignment at this level of resolution enables identification of a mouse clone that corresponds to almost any position in the human genome. The human sequence may be used to facilitate construction of other mammalian genome maps using the same strategy.
The Journal of Pathology | 2012
Stephen Yip; Yaron S N Butterfield; Olena Morozova; Michael D. Blough; Jianghong An; Inanc Birol; Charles Chesnelong; Readman Chiu; Eric Chuah; Richard Corbett; Rod Docking; Marlo Firme; Martin Hirst; Shaun D. Jackman; Aly Karsan; Haiyan Li; David N. Louis; Alexandra Maslova; Richard A. Moore; Annie Moradian; Karen Mungall; Marco Perizzolo; Jenny Q. Qian; Gloria Roldán; Eric E. Smith; Jessica Tamura-Wells; Nina Thiessen; Richard Varhol; Samuel Weiss; Wei Wu
Oligodendroglioma is characterized by unique clinical, pathological, and genetic features. Recurrent losses of chromosomes 1p and 19q are strongly associated with this brain cancer but knowledge of the identity and function of the genes affected by these alterations is limited. We performed exome sequencing on a discovery set of 16 oligodendrogliomas with 1p/19q co‐deletion to identify new molecular features at base‐pair resolution. As anticipated, there was a high rate of IDH mutations: all cases had mutations in either IDH1 (14/16) or IDH2 (2/16). In addition, we discovered somatic mutations and insertions/deletions in the CIC gene on chromosome 19q13.2 in 13/16 tumours. These discovery set mutations were validated by deep sequencing of 13 additional tumours, which revealed seven others with CIC mutations, thus bringing the overall mutation rate in oligodendrogliomas in this study to 20/29 (69%). In contrast, deep sequencing of astrocytomas and oligoastrocytomas without 1p/19q loss revealed that CIC alterations were otherwise rare (1/60; 2%). Of the 21 non‐synonymous somatic mutations in 20 CIC‐mutant oligodendrogliomas, nine were in exon 5 within an annotated DNA‐interacting domain and three were in exon 20 within an annotated protein‐interacting domain. The remaining nine were found in other exons and frequently included truncations. CIC mutations were highly associated with oligodendroglioma histology, 1p/19q co‐deletion, and IDH1/2 mutation (p < 0.001). Although we observed no differences in the clinical outcomes of CIC mutant versus wild‐type tumours, in a background of 1p/19q co‐deletion, hemizygous CIC mutations are likely important. We hypothesize that the mutant CIC on the single retained 19q allele is linked to the pathogenesis of oligodendrogliomas with IDH mutation. Our detailed study of genetic aberrations in oligodendroglioma suggests a functional interaction between CIC mutation, IDH1/2 mutation, and 1p/19q co‐deletion. Copyright
Blood | 2013
Ryan D. Morin; Karen Mungall; Erin Pleasance; Andrew J. Mungall; Rodrigo Goya; Ryan D. Huff; David W. Scott; Jiarui Ding; Andrew Roth; Readman Chiu; Richard Corbett; Fong Chun Chan; Maria Mendez-Lago; Diane L. Trinh; Madison Bolger-Munro; Greg Taylor; Alireza Hadj Khodabakhshi; Susana Ben-Neriah; Julia R. Pon; Barbara Meissner; Bruce Woolcock; Noushin Farnoud; Sanja Rogic; Emilia L. Lim; Nathalie A. Johnson; Sohrab P. Shah; Steven J.M. Jones; Christian Steidl; Robert A. Holt; Inanc Birol
Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.
Plant Journal | 2015
René L. Warren; Christopher I. Keeling; Macaire Man Saint Yuen; Anthony Raymond; Greg Taylor; Benjamin P. Vandervalk; Hamid Mohamadi; Daniel Paulino; Readman Chiu; Shaun D. Jackman; Gordon Robertson; Chen Yang; Brian Boyle; Margarete Hoffmann; Detlef Weigel; David R. Nelson; Carol Ritland; Nathalie Isabel; Barry Jaquish; Alvin Yanchuk; Jean Bousquet; Steven J.M. Jones; John MacKay; Inanc Birol; Joerg Bohlmann
White spruce (Picea glauca), a gymnosperm tree, has been established as one of the models for conifer genomics. We describe the draft genome assemblies of two white spruce genotypes, PG29 and WS77111, innovative tools for the assembly of very large genomes, and the conifer genomics resources developed in this process. The two white spruce genotypes originate from distant geographic regions of western (PG29) and eastern (WS77111) North America, and represent elite trees in two Canadian tree-breeding programs. We present an update (V3 and V4) for a previously reported PG29 V2 draft genome assembly and introduce a second white spruce genome assembly for genotype WS77111. Assemblies of the PG29 and WS77111 genomes confirm the reconstructed white spruce genome size in the 20 Gbp range, and show broad synteny. Using the PG29 V3 assembly and additional white spruce genomics and transcriptomics resources, we performed MAKER-P annotation and meticulous expert annotation of very large gene families of conifer defense metabolism, the terpene synthases and cytochrome P450s. We also comprehensively annotated the white spruce mevalonate, methylerythritol phosphate and phenylpropanoid pathways. These analyses highlighted the large extent of gene and pseudogene duplications in a conifer genome, in particular for genes of secondary (i.e. specialized) metabolism, and the potential for gain and loss of function for defense and adaptation.
Genome Biology | 2007
Warren M Snelling; Readman Chiu; Jacqueline E. Schein; Matthew Hobbs; Colette A. Abbey; David L. Adelson; Jan Aerts; Gary L Bennett; Ian Bosdet; Mekki Boussaha; Rudiger Brauning; Alexandre R Caetano; Marcos M Costa; A. M. Crawford; Brian P. Dalrymple; A. Eggen; Annelie Everts-van der Wind; Sandrine Floriot; Mathieu Gautier; C. A. Gill; Ronnie D Green; Robert A. Holt; Oliver Jann; Steven J.M. Jones; S. M. Kappes; J. W. Keele; Pieter J. de Jong; Denis M. Larkin; Harris A. Lewin; J. C. McEwan
BackgroundCattle are important agriculturally and relevant as a model organism. Previously described genetic and radiation hybrid (RH) maps of the bovine genome have been used to identify genomic regions and genes affecting specific traits. Application of these maps to identify influential genetic polymorphisms will be enhanced by integration with each other and with bacterial artificial chromosome (BAC) libraries. The BAC libraries and clone maps are essential for the hybrid clone-by-clone/whole-genome shotgun sequencing approach taken by the bovine genome sequencing project.ResultsA bovine BAC map was constructed with HindIII restriction digest fragments of 290,797 BAC clones from animals of three different breeds. Comparative mapping of 422,522 BAC end sequences assisted with BAC map ordering and assembly. Genotypes and pedigree from two genetic maps and marker scores from three whole-genome RH panels were consolidated on a 17,254-marker composite map. Sequence similarity allowed integrating the BAC and composite maps with the bovine draft assembly (Btau3.1), establishing a comprehensive resource describing the bovine genome. Agreement between the marker and BAC maps and the draft assembly is high, although discrepancies exist. The composite and BAC maps are more similar than either is to the draft assembly.ConclusionFurther refinement of the maps and greater integration into the genome assembly process may contribute to a high quality assembly. The maps provide resources to associate phenotypic variation with underlying genomic variation, and are crucial resources for understanding the biology underpinning this important ruminant species so closely associated with humans.