Updated on 2021/10/25

写真a

 
HAYASHI Shuto
 
Organization
Graduate School of Medicine Center for Neurological Diseases and Cance Designated associate professor
Title
Designated associate professor

Degree 1

  1. 博士(情報理工学) ( 2019.3   東京大学 ) 

Research Interests 2

  1. Bayesian Statistics

  2. Bioinformatics

Research Areas 3

  1. Informatics / Statistical science

  2. Informatics / Life, health and medical informatics

  3. Life Science / System genome science

Research History 2

  1. Nagoya University   Graduate School of Medicine Division of Systems Biology   Designated associate professor

    2021.4

  2. The University of Tokyo   Graduate School of Medicine Department of Preventive Medicine   Assistant Professor

    2019.4 - 2021.3

Education 3

  1. The University of Tokyo   The Graduate School of Information Science and Technology   Department of Computer Science Doctoral Course

    2016.4 - 2019.3

  2. The University of Tokyo   The Graduate School of Information Science and Technology   Department of Computer Science Master Course

    2014.4 - 2016.3

  3. The University of Tokyo   Faculty of Science   Department of Information Science

    2010.4 - 2014.3

Professional Memberships 1

  1. The Japanese Society for Hygiene

    2020.5

 

Papers 14

  1. Immunogenomic pan-cancer landscape reveals immune escape mechanisms and immunoediting histories Reviewed International journal

    Shinichi Mizuno, Rui Yamaguchi, Takanori Hasegawa, Shuto Hayashi, Masashi Fujita, Fan Zhang, Youngil Koh, Su Yeon Lee, Sung Soo Yoon, Eigo Shimizu, Mitsuhiro Komura, Akihiro Fujimoto, Momoko Nagai, Mamoru Kato, Han Liang, Satoru Miyano, Zemin Zhang, Hidewaki Nakagawa, Seiya Imoto

    Scientific Reports   Vol. 11 ( 1 ) page: 15713 - 15713   2021.12

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PORTFOLIO  

    Immune reactions in the tumor microenvironment are an important hallmark of cancer, and emerging immune therapies have been proven effective against several types of cancers. To investigate cancer genome-immune interactions and the role of immunoediting or immune escape mechanisms in cancer development, we analyzed 2834 whole genome and RNA sequencing datasets across 31 distinct tumor types with respect to key immunogenomic aspects and provided comprehensive immunogenomic profiles of pan-cancers. We found that selective copy number changes in immune-related genes may contribute to immune escape. Furthermore, we developed an index of the immunoediting history of each tumor sample based on the information of mutations in exonic regions and pseudogenes and evaluated the immunoediting history of each tumor. Our immuno-genomic analyses of pan-cancers have the potential to identify a subset of tumors with immunogenicity and diverse backgrounds or intrinsic pathways associated with their immune status and immunoediting history.

    DOI: 10.1038/s41598-021-95287-x

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  2. Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples Reviewed

    Matthew H. Bailey, William U. Meyerson, Lewis Jonathan Dursi, Liang Bo Wang, Guanlan Dong, Wen Wei Liang, Amila Weerasinghe, Shantao Li, Sean Kelso, Rehan Akbani, Pavana Anur, Matthew H. Bailey, Alex Buchanan, Kami Chiotti, Kyle Covington, Allison Creason, Li Ding, Kyle Ellrott, Yu Fan, Steven Foltz, Gad Getz, Walker Hale, David Haussler, Julian M. Hess, Carolyn M. Hutter, Cyriac Kandoth, Katayoon Kasaian, Melpomeni Kasapi, Dave Larson, Ignaty Leshchiner, John Letaw, Singer Ma, Michael D. McLellan, Yifei Men, Gordon B. Mills, Beifang Niu, Myron Peto, Amie Radenbaugh, Sheila M. Reynolds, Gordon Saksena, Heidi Sofia, Chip Stewart, Adam J. Struck, Joshua M. Stuart, Wenyi Wang, John N. Weinstein, David A. Wheeler, Christopher K. Wong, Liu Xi, Kai Ye, Matthew H. Bailey, Beifang Niu, Matthias Bieg, Paul C. Boutros, Ivo Buchhalter, Adam P. Butler, Ken Chen, Zechen Chong, Li Ding, Oliver Drechsel, Lewis Jonathan Dursi, Roland Eils, Kyle Ellrott, Shadrielle M.G. Espiritu, Yu Fan, Robert S. Fulton, Shengjie Gao, Josep L.l. Gelpi, Mark B. Gerstein, Gad Getz, Santiago Gonzalez, Ivo G. Gut, Faraz Hach, Michael C. Heinold, Julian M. Hess, Jonathan Hinton, Taobo Hu, Vincent Huang, Yi Huang, Barbara Hutter, David R. Jones, Jongsun Jung, Natalie Jäger, Hyung Lae Kim, Kortine Kleinheinz, Sushant Kumar, Yogesh Kumar, Christopher M. Lalansingh, Ignaty Leshchiner, Ivica Letunic, Dimitri Livitz, Eric Z. Ma, Yosef E. Maruvka, R. Jay Mashl, Michael D. McLellan, Andrew Menzies, Ana Milovanovic, Morten Muhlig Nielsen, Stephan Ossowski, Nagarajan Paramasivam

    Nature Communications   Vol. 11 ( 1 )   2020.12

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    The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts.

    DOI: 10.1038/s41467-020-18151-y

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  3. Sex differences in oncogenic mutational processes Reviewed

    Constance H. Li, Stephenie D. Prokopec, Ren X. Sun, Fouad Yousif, Nathaniel Schmitz, Fatima Al-Shahrour, Gurnit Atwal, Peter J. Bailey, Andrew V. Biankin, Paul C. Boutros, Peter J. Campbell, David K. Chang, Susanna L. Cooke, Vikram Deshpande, Bishoy M. Faltas, William C. Faquin, Levi Garraway, Gad Getz, Sean M. Grimmond, Syed Haider, Katherine A. Hoadley, Wei Jiao, Vera B. Kaiser, Rosa Karlić, Mamoru Kato, Kirsten Kübler, Alexander J. Lazar, Constance H. Li, David N. Louis, Adam Margolin, Sancha Martin, Hardeep K. Nahal-Bose, G. Petur Nielsen, Serena Nik-Zainal, Larsson Omberg, Christine P’ng, Marc D. Perry, Paz Polak, Esther Rheinbay, Mark A. Rubin, Colin A. Semple, Dennis C. Sgroi, Tatsuhiro Shibata, Reiner Siebert, Jaclyn Smith, Lincoln D. Stein, Miranda D. Stobbe, Ren X. Sun, Kevin Thai, Derek W. Wright, Chin Lee Wu, Ke Yuan, Junjun Zhang, Lauri A. Aaltonen, Federico Abascal, Adam Abeshouse, Hiroyuki Aburatani, David J. Adams, Nishant Agrawal, Keun Soo Ahn, Sung Min Ahn, Hiroshi Aikata, Rehan Akbani, Kadir C. Akdemir, Hikmat Al-Ahmadie, Sultan T. Al-Sedairy, Fatima Al-Shahrour, Malik Alawi, Monique Albert, Kenneth Aldape, Ludmil B. Alexandrov, Adrian Ally, Kathryn Alsop, Eva G. Alvarez, Fernanda Amary, Samirkumar B. Amin, Brice Aminou, Ole Ammerpohl, Matthew J. Anderson, Yeng Ang, Davide Antonello, Pavana Anur, Samuel Aparicio, Elizabeth L. Appelbaum, Yasuhito Arai, Axel Aretz, Koji Arihiro, Shun ichi Ariizumi, Joshua Armenia, Laurent Arnould, Sylvia Asa, Yassen Assenov, Gurnit Atwal, Sietse Aukema, J. Todd Auman, Miriam R. Aure, Philip Awadalla, Marta Aymerich, Gary D. Bader, Adrian Baez-Ortega

    Nature Communications   Vol. 11 ( 1 )   2020.12

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    Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.

    DOI: 10.1038/s41467-020-17359-2

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  4. Neoantimon: A multifunctional R package for identification of tumor-specific neoantigens Reviewed International journal

    Takanori Hasegawa, Shuto Hayashi, Eigo Shimizu, Shinichi Mizuno, Atsushi Niida, Rui Yamaguchi, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    Bioinformatics   Vol. 36 ( 18 ) page: 4813 - 4816   2020.9

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:OXFORD UNIV PRESS  

    It is known that some mutant peptides, such as those resulting from missense mutations and frameshift insertions, can bind to the major histocompatibility complex and be presented to antitumor T cells on the surface of a tumor cell. These peptides are termed neoantigen, and it is important to understand this process for cancer immunotherapy. Here, we introduce an R package termed Neoantimon that can predict a list of potential neoantigens from a variety of mutations, which include not only somatic point mutations but insertions, deletions and structural variants. Beyond the existing applications, Neoantimon is capable of attaching and reflecting several additional information, e.g. wild-type binding capability, allele specific RNA expression levels, single nucleotide polymorphism information and combinations of mutations to filter out infeasible peptides as neoantigen.

    DOI: 10.1093/bioinformatics/btaa616

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    Other Link: https://dblp.uni-trier.de/db/journals/bioinformatics/bioinformatics36.html#HasegawaHSMNYMN20

  5. Classification of primary liver cancer with immunosuppression mechanisms and correlation with genomic alterations Reviewed International journal

    Masashi Fujita, Rui Yamaguchi, Takanori Hasegawa, Shu Shimada, Koji Arihiro, Shuto Hayashi, Kazuhiro Maejima, Kaoru Nakano, Akihiro Fujimoto, Atsushi Ono, Hiroshi Aikata, Masaki Ueno, Shinya Hayami, Hiroko Tanaka, Satoru Miyano, Hiroki Yamaue, Kazuaki Chayama, Kazuhiro Kakimi, Shinji Tanaka, Seiya Imoto, Hidewaki Nakagawa

    EBioMedicine   Vol. 53   page: 102659 - 102659   2020.3

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ELSEVIER  

    Background: The tumor microenvironment can be classified into immunologically active “inflamed” tumors and inactive “non-inflamed” tumors based on the infiltration of cytotoxic immune cells. Previous studies on liver cancer have reported a superior prognosis for inflamed tumors compared to non-inflamed tumors. However, liver cancer is highly heterogeneous immunologically and genetically, and a finer classification of the liver cancer microenvironment may improve our understanding of its immunological diversity and response to immune therapy. Methods: We characterized the immune gene signatures of 234 primary liver cancers, mainly virus-related, from a Japanese population using RNA-Seq of tumors and matched non-tumorous hepatitis livers. We then compared them with the somatic alterations detected using the whole-genome sequencing. Findings: Liver cancers expressed lower levels of immune marker genes than non-tumorous hepatitis livers, indicating immunosuppression in the tumor microenvironment. Several immunosuppression mechanisms functioned actively and mutually exclusively, resulting in four immune subclasses of liver cancer: tumor-associated macrophage (TAM), CTNNB1, cytolytic activity (CYT), and regulatory T cell (Treg). The CYT and Treg subclasses represented inflamed tumors, while the TAM and CTNNB1 subclasses represented non-inflamed tumors. The TAM subclass, which comprised 31% of liver cancers, showed a poor survival, expressed elevated levels of extracellular matrix genes, and was associated with somatic mutations of chromatin regulator ARID2. The results of cell line experiments suggested a functional link between ARID2 and chemokine production by liver cancer cells. Interpretation: Primary liver cancer was classified into four subclasses based on mutually exclusive mechanisms for immunosuppression. This classification indicate the importance of immunosuppression mechanisms, such as TAM and Treg, as therapeutic targets for liver cancer. Funding: The Japan Agency for Medical Research and Development (AMED).

    DOI: 10.1016/j.ebiom.2020.102659

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  6. Pan-cancer analysis of whole genomes Reviewed

    Peter J. Campbell, Gad Getz, Jan O. Korbel, Joshua M. Stuart, Jennifer L. Jennings, Lincoln D. Stein, Marc D. Perry, Hardeep K. Nahal-Bose, B. F.Francis Ouellette, Constance H. Li, Esther Rheinbay, G. Petur Nielsen, Dennis C. Sgroi, Chin Lee Wu, William C. Faquin, Vikram Deshpande, Paul C. Boutros, Alexander J. Lazar, Katherine A. Hoadley, David N. Louis, L. Jonathan Dursi, Christina K. Yung, Matthew H. Bailey, Gordon Saksena, Keiran M. Raine, Ivo Buchhalter, Kortine Kleinheinz, Matthias Schlesner, Junjun Zhang, Wenyi Wang, David A. Wheeler, Li Ding, Jared T. Simpson, Brian D. O’Connor, Sergei Yakneen, Kyle Ellrott, Naoki Miyoshi, Adam P. Butler, Romina Royo, Solomon I. Shorser, Miguel Vazquez, Tobias Rausch, Grace Tiao, Sebastian M. Waszak, Bernardo Rodriguez-Martin, Suyash Shringarpure, Dai Ying Wu, German M. Demidov, Olivier Delaneau, Shuto Hayashi, Seiya Imoto, Nina Habermann, Ayellet V. Segre, Erik Garrison, Andy Cafferkey, Eva G. Alvarez, José María Heredia-Genestar, Francesc Muyas, Oliver Drechsel, Alicia L. Bruzos, Javier Temes, Jorge Zamora, Adrian Baez-Ortega, Hyung Lae Kim, R. Jay Mashl, Kai Ye, Anthony DiBiase, Kuan lin Huang, Ivica Letunic, Michael D. McLellan, Steven J. Newhouse, Tal Shmaya, Sushant Kumar, David C. Wedge, Mark H. Wright, Venkata D. Yellapantula, Mark Gerstein, Ekta Khurana, Tomas Marques-Bonet, Arcadi Navarro, Carlos D. Bustamante, Reiner Siebert, Hidewaki Nakagawa, Douglas F. Easton, Stephan Ossowski, Jose M.C. Tubio, Francisco M. De La Vega, Xavier Estivill, Denis Yuen, George L. Mihaiescu, Larsson Omberg, Vincent Ferretti, Radhakrishnan Sabarinathan, Oriol Pich, Abel Gonzalez-Perez, Amaro Taylor-Weiner, Matthew W. Fittall, Jonas Demeulemeester, Maxime Tarabichi, Nicola D. Roberts

    Nature   Vol. 578 ( 7793 ) page: 82 - 93   2020.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE RESEARCH  

    Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1–3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10–18.

    DOI: 10.1038/s41586-020-1969-6

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  7. A Bayesian model integration for mutation calling through data partitioning Reviewed International journal

    Takuya Moriyama, Seiya Imoto, Shuto Hayashi, Yuichi Shiraishi, Satoru Miyano, Rui Yamaguchi

    Bioinformatics   Vol. 35 ( 21 ) page: 4247 - 4254   2019.11

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:OXFORD UNIV PRESS  

    Motivation: Detection of somatic mutations from tumor and matched normal sequencing data has become among the most important analysis methods in cancer research. Some existing mutation callers have focused on additional information, e.g. heterozygous single-nucleotide polymorphisms (SNPs) nearby mutation candidates or overlapping paired-end read information. However, existing methods cannot take multiple information sources into account simultaneously. Existing Bayesian hierarchical model-based methods construct two generative models, the tumor model and error model, and limited information sources have been modeled. Results: We proposed a Bayesian model integration framework named as partitioning-based model integration. In this framework, through introducing partitions for paired-end reads based on given information sources, we integrate existing generativemodels and utilizemultiple information sources. Based on that, we constructed a novel Bayesian hierarchical model-based method named as OHVarfinDer. In both the tumor model and error model, we introduced partitions for a set of paired-end reads that cover a mutation candidate position, and applied a different generative model for each category of paired-end reads. We demonstrated that our method can utilize both heterozygous SNP information and overlapping paired-end read information effectively in simulation datasets and real datasets. Availability and implementation: https://github.com/takumorizo/OHVarfinDer.

    DOI: 10.1093/bioinformatics/btz233

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    Other Link: https://dblp.uni-trier.de/db/journals/bioinformatics/bioinformatics35.html#MoriyamaIHSMY19

  8. Alphlard-nt: Bayesian method for human leukocyte antigen genotyping and mutation calling through simultaneous analysis of normal and tumor whole-genome sequence data Reviewed International journal

    Shuto Hayashi, Takuya Moriyama, Rui Yamaguchi, Shinichi Mizuno, Mitsuhiro Komura, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    Journal of Computational Biology   Vol. 26 ( 9 ) page: 923 - 937   2019.9

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    Authorship:Lead author   Language:English   Publishing type:Research paper (international conference proceedings)   Publisher:MARY ANN LIEBERT, INC  

    Human leukocyte antigen (HLA) genes provide useful information on the relationship between cancer and the immune system. Despite the ease of obtaining these data through next-generation sequencing methods, interpretation of these relationships remains challenging owing to the complexity of HLA genes. To resolve this issue, we developed a Bayesian method, ALPHLARD-NT, to identify HLA germline and somatic mutations as well as HLA genotypes from whole-exome sequencing (WES) and whole-genome sequencing (WGS) data. ALPHLARD-NT showed 99.2% accuracy for WGS-based HLA genotyping and detected five HLA somatic mutations in 25 colon cancer cases. In addition, ALPHLARD-NT identified 88 HLA somatic mutations, including recurrent mutations and a novel HLA-B type, from WES data of 343 colon adenocarcinoma cases. These results demonstrate the potential of ALPHLARD-NT for conducting an accurate analysis of HLA genes even from low-coverage data sets. This method can become an essential tool for comprehensive analyses of HLA genes from WES and WGS data, helping to advance understanding of immune regulation in cancer as well as providing guidance for novel immunotherapy strategies.

    DOI: 10.1089/cmb.2018.0224

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    Other Link: https://dblp.uni-trier.de/db/journals/jcb/jcb26.html#HayashiMYMKMNI19

  9. Quantifying immune-based counterselection of somatic mutations Reviewed International journal

    Fan Yang, Dae Kyum Kim, Hidewaki Nakagawa, Shuto Hayashi, Seiya Imoto, Lincoln Stein, Frederick P. Roth

    PLoS Genetics   Vol. 15 ( 7 ) page: e1008227   2019.7

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:PUBLIC LIBRARY SCIENCE  

    Somatic mutations in protein-coding regions can generate ‘neoantigens’ causing developing cancers to be eliminated by the immune system. Quantitative estimates of the strength of this counterselection phenomenon have been lacking. We quantified the extent to which somatic mutations are depleted in peptides that are predicted to be displayed by major histocompatibility complex (MHC) class I proteins. The extent of this depletion depended on expression level of the neoantigenic gene, and on whether the patient had one or two MHC-encoding alleles that can display the peptide, suggesting MHC-encoding alleles are incompletely dominant. This study provides an initial quantitative understanding of counter-selection of identifiable subclasses of neoantigenic somatic variation.

    DOI: 10.1371/journal.pgen.1008227

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  10. A temporal shift of the evolutionary principle shaping intratumor heterogeneity in colorectal cancer Reviewed International journal

    Tomoko Saito, Atsushi Niida, Ryutaro Uchi, Hidenari Hirata, Hisateru Komatsu, Shotaro Sakimura, Shuto Hayashi, Sho Nambara, Yosuke Kuroda, Shuhei Ito, Hidetoshi Eguchi, Takaaki Masuda, Keishi Sugimachi, Taro Tobo, Haruto Nishida, Tsutomu Daa, Kenichi Chiba, Yuichi Shiraishi, Tetsuichi Yoshizato, Masaaki Kodama, Tadayoshi Okimoto, Kazuhiro Mizukami, Ryo Ogawa, Kazuhisa Okamoto, Mitsutaka Shuto, Kensuke Fukuda, Yusuke Matsui, Teppei Shimamura, Takanori Hasegawa, Yuichiro Doki, Satoshi Nagayama, Kazutaka Yamada, Mamoru Kato, Tatsuhiro Shibata, Masaki Mori, Hiroyuki Aburatani, Kazunari Murakami, Yutaka Suzuki, Seishi Ogawa, Satoru Miyano, Koshi Mimori

    Nature Communications   Vol. 9 ( 1 ) page: 2884 - 2884   2018.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    Advanced colorectal cancer harbors extensive intratumor heterogeneity shaped by neutral evolution; however, intratumor heterogeneity in colorectal precancerous lesions has been poorly studied. We perform multiregion whole-exome sequencing on ten early colorectal tumors, which contained adenoma and carcinoma in situ. By comparing with sequencing data from advanced colorectal tumors, we show that the early tumors accumulate a higher proportion of subclonal driver mutations than the advanced tumors, which is highlighted by subclonal mutations in KRAS and APC. We also demonstrate that variant allele frequencies of subclonal mutations tend to be higher in early tumors, suggesting that the subclonal mutations are subject to selective sweep in early tumorigenesis while neutral evolution is dominant in advanced ones. This study establishes that the evolutionary principle underlying intratumor heterogeneity shifts from Darwinian to neutral evolution during colorectal tumor progression.

    DOI: 10.1038/s41467-018-05226-0

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  11. Genomic insights into immune suppression in liver cancer Reviewed

    Masashi Fujita, Seiya Imoto, Rui Yamaguchi, Takanori Hasegawa, Shuto Hayashi, Kazuhiro Kakimi, Satoru Miyano, Hiroki Yamaue, Kazuaki Chayama, Hidewaki Nakagawa

    CANCER SCIENCE   Vol. 109   page: 640 - 640   2018.12

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    Language:English   Publisher:WILEY  

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  12. ALPHLARD: A Bayesian method for analyzing HLA genes from whole genome sequence data Reviewed International journal

    Shuto Hayashi, Rui Yamaguchi, Shinichi Mizuno, Mitsuhiro Komura, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    BMC Genomics   Vol. 19 ( 1 ) page: 790 - 790   2018.11

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:BMC  

    Background: Although human leukocyte antigen (HLA) genotyping based on amplicon, whole exome sequence (WES), and RNA sequence data has been achieved in recent years, accurate genotyping from whole genome sequence (WGS) data remains a challenge due to the low depth. Furthermore, there is no method to identify the sequences of unknown HLA types not registered in HLA databases. Results: We developed a Bayesian model, called ALPHLARD, that collects reads potentially generated from HLA genes and accurately determines a pair of HLA types for each of HLA-A, -B, -C, -DPA1, -DPB1, -DQA1, -DQB1, and -DRB1 genes at 3rd field resolution. Furthermore, ALPHLARD can detect rare germline variants not stored in HLA databases and call somatic mutations from paired normal and tumor sequence data. We illustrate the capability of ALPHLARD using 253 WES data and 25 WGS data from Illumina platforms. By comparing the results of HLA genotyping from SBT and amplicon sequencing methods, ALPHLARD achieved 98.8% for WES data and 98.5% for WGS data at 2nd field resolution. We also detected three somatic point mutations and one case of loss of heterozygosity in the HLA genes from the WGS data. Conclusions: ALPHLARD showed good performance for HLA genotyping even from low-coverage data. It also has a potential to detect rare germline variants and somatic mutations in HLA genes. It would help to fill in the current gaps in HLA reference databases and unveil the immunological significance of somatic mutations identified in HLA genes.

    DOI: 10.1186/s12864-018-5169-9

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  13. Immuno-genomic subtype of liver cancer correlates with mechanisms of immune suppression and prognosis Reviewed

    Masashi Fujita, Seiya Imoto, Rui Yamaguchi, Takanori Hasegawa, Shuto Hayashi, Satoru Miyano, Hiroki Yamaue, Kazuaki Chayama, Hidewaki Nakagawa

    HUMAN GENOMICS   Vol. 12   2018.3

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    Language:English   Publisher:BIOMED CENTRAL LTD  

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  14. An in silico automated pipeline to identify tumor specic neoantigens from whole genome and exome sequencing data Reviewed

    Takanori Hasegawa, Shuto Hayashi, Eigo Shimizu, Shinichi Mizuno, Rui Yamaguchi, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    Proceeding of 12th International Symposium on Bioinformatics Research and Applications     2016

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MISC 5

  1. ヒト胃癌環境における主要な抗体クローンとして同定された抗硫酸化グリコサミノグリカン抗体の解析

    古谷 弦太, 加藤 洋人, 林 周斗, 河村 大輔, 石川 俊平

    日本衛生学雑誌   Vol. 75 ( Suppl. ) page: S202 - S202   2020.3

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    Language:Japanese   Publisher:(一社)日本衛生学会  

  2. 凍結臨床試料を用いたシングルセルRNA-seq法の確立

    橋本 至, 加藤 洋人, 林 周斗, 河村 大輔, 大島 貴, 利野 靖, 益田 宗孝, 石川 俊平

    日本衛生学雑誌   Vol. 75 ( Suppl. ) page: S187 - S187   2020.3

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    Language:Japanese   Publisher:(一社)日本衛生学会  

  3. 肝臓がんにおける免疫抑制機構のゲノム解析(Genomic insights into immune suppression in liver cancer)

    藤田 征志, 井元 清哉, 山口 類, 長谷川 嵩矩, 林 周斗, 垣見 和宏, 宮野 悟, 山上 裕機, 茶山 一彰, 中川 英刀

    日本癌学会総会記事   Vol. 77回   page: 906 - 906   2018.9

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  4. 肝臓がんおよび大腸がんのゲノム・トランスクリプトーム解析による腫瘍免疫微小環境の特性評価

    藤田 征志, 井元 清哉, 山口 類, 長谷川 嵩矩, 林 周斗, 宮野 悟, 松原 長秀, 冨田 尚裕, 山上 裕機, 茶山 一彰, 中川 英刀

    日本がん免疫学会総会プログラム・抄録集   Vol. 22回   page: 152 - 152   2018.7

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    Language:Japanese   Publisher:日本がん免疫学会  

  5. ヒトにおけるCancer Immunosurveillance-PanCancer全ゲノム解析によるアプローチ

    水野 晋一, 林 周斗, 長谷川 嵩矩, 清水 英悟, 上村 光弘, 山口 類, 宮野 悟, 中川 英刀, 井元 清哉

    日本がん免疫学会総会プログラム・抄録集   Vol. 20回   page: 168 - 168   2016.6

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    Language:Japanese   Publisher:日本がん免疫学会  

Presentations 6

  1. ヒトB細胞レパトアにおける網羅的構造多様性解析

    林 周斗, 橋本 至, 加藤 洋人, 河村 大輔, 石川 俊平

    第91回 日本衛生学会学術総会  2021.3.8 

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    Event date: 2021.3

    Presentation type:Oral presentation (general)  

  2. 分子動力学を用いた抗体構造ランドスケープ解析

    林 周斗

    第5回 理論免疫学ワークショップ  2021.2.13 

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    Event date: 2021.2

    Language:Japanese  

  3. ヒト抗体における網羅的構造多様性解析

    林 周斗

    第9回 生命医薬情報学連合大会  2020.9.3 

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    Event date: 2020.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

  4. Whole genome sequence-based analysis of HLA genes with Bayesian statistical model

    Shuto Hayashi, Rui Yamaguchi, Shinichi Mizuno, Mitsuhiro Komura, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    17th International Workshop on Bioinformatics and Systems Biology  2017.7.26 

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    Event date: 2017.7

    Language:English   Presentation type:Oral presentation (general)  

  5. Statistical method for comprehensive analysis of HLA class I and II genes.

    Shuto Hayashi, Rui Yamaguchi, Shinichi Mizuno, Mitsuhiro Komura, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    16th International Workshop on Bioinformatics and Systems Biology  2016.8.9 

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    Event date: 2016.8

    Language:English   Presentation type:Oral presentation (general)  

  6. Bayesian Method for HLA Genotyping from Whole Genome Sequencing Data

    Shuto Hayashi, Rui Yamaguchi, Shinichi Mizuno, Mitsuhiro Komura, Satoru Miyano, Hidewaki Nakagawa, Seiya Imoto

    15th International Workshop on Bioinformatics and Systems Biology  2015.7.21 

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    Event date: 2015.7

    Language:English   Presentation type:Oral presentation (general)  

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