Housheng Hansen HE, PhD

Associate Professor, Department of Medical
Biophysics, University of Toronto, Canada
Senior Scientist, Princess Margaret Cancer Centre,
University Health Network, Canada

Dr. He received his B.S. degree in physics from Beijing Normal University in the year of 2003, and then transitioned to the genomics and noncoding RNA fields for his Ph.D training in the Institute of Biophysics, Chinese Academy of Sciences. He received his postdoctoral training in cancer genomics and epigenomics at Dana-Farber Cancer Institute. After completing his postdoctoral training in 2011, Dr. He worked as an instructor at Harvard Medical School and was recruited as a scientist at the Princess Margaret Cancer Centre in 2013.

The He laboratory applies a variety of genomic, epigenomic experimental and computational approaches to elucidate the functional role of epigenetic regulation in cancer development, progression and drug response/resistance, with a special focus on the interplay between epigenetic regulator and noncoding RNA under stress conditions such as hypoxia. Dr. He’s work in the fields of noncoding RNA and epigenetics has resulted in ~50 peer-reviewed publications in high-impact journals including Nature, Cell, Nature Genetics, Nature Methods, Cancer Cell and Genome Research.

Presentation Title
Genetic variation, noncoding RNA and Chromatin regulation
Summary
The prostate cancer (PCa) risk-associated single nucleotide polymorphism (SNP) rs11672691 is positively associated with aggressive disease at diagnosis. Here, we replicated the finding in a cohort of 127 intermediate risk PCa patients, showing that the risk variant is associated with increased risk of relapse after therapy. rs11672691 is located in the promoter region of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long). We find that the risk variant is associated with decreased levels of PCAT19-short, but increased levels of PCAT19-long. Mechanistically, risk variants of rs11672691 and its linkage disequilibrium SNP rs887391 decrease binding of NKX3.1 and YY1 to the promoter of PCAT19-short, converting this region to an enhancer that loops to the PCAT19-long promoter. PCAT19-long interacts with HNRNPAB to activate a subset of cell cycle genes that are associated with PCa progression, thereby promoting cell proliferation, migration, tumor growth and metastasis in vitro and in vivo. Taken together, these findings reveal a novel risk SNP mediated promoter-enhancer switching mechanism underlying both initiation and progression of aggressive PCa.

Tetsuro HIROSE,PhD

Institute for Genetic Medicine
Hokkaido University, Japan

TBD

Presentation Title
TBD
Summary
TBD

Chandrasekhar KANDURI, PhD

Professor in RNA Biology
Department of Medical Biochemistry and Cell Biology
University of Gothenburg, Sweden

Dr. Chandra Kanduri received his PhD from Banaras Hindu University, India, in 1997. For postdoctoral training, he moved to Prof Rolf Ohlsson’s lab at Uppsala University, Sweden, where he explored the functional role of chromatin insulator protein CTCF in genomic imprinting using H19 and IGF2 imprinted cluster as a model system. He later continued his work on long noncoding RNA Kcnq1ot1 and genomic imprinting as an independent investigator. His work, as an early career scientist, contributed significantly towards understanding the functional interaction between RNA and chromatin. His further work on RNA-chromatin connection, revealed RNA molecules enriched in the active and inactive chromatin regions, and also possible mechanisms by which chromatin enriched lncRNAs targeted across the genome.

He became full professor of RNA biology at Uppsala university in 2010. In 2012, he moved his research activities to University of Gothenburg. His current research primarily focused on developing novel long noncoding RNAs (lncRNA) based strategies for the treatment of drug resistant and difficult to treat cancers through exploiting cell cycle based functional screens.

Presentation Title

Functional and mechanistic roles of long noncoding RNAs (lncRNAs) in cancer development and progression

Summary

Despite rapid improvements in unveiling the importance of long noncoding RNAs (lncRNA) in all aspects of cancer biology, there is still a lot of void in how lncRNAs mechanistically influence various biological processes associated with cancer development. Towards this, by using RNA-seq data from cell cycle-based high-throughput functional screens and different neuroblastoma (NB) prognostic sub-groups, we have identified several cancer-relevant, therapeutically applicable lncRNAs. Functional investigations of these lncRNAs revealed their nexus with oncogenic and tumor-suppressor pathways. I will discuss how these cancer relevant lncRNAs can be used as potential therapeutic targets in different cancer types.

Ailong KE, PhD

Professor, Department of Molecular Biology and Genetics, Cornell University, US

TBD
Presentation Title

Spacer acquisition mechanism in type II-A CRISPR system.

Summary

Molecular memory is created when a short foreign DNA-derived prespacer is integrated
into the CRISPR array as a new spacer. Whereas the RNA-guided CRISPR interference
mechanism varies widely among CRISPR-Cas systems, the spacer integration
mechanism is essentially identical. The conserved Cas1 and Cas2 proteins form an
integrase complex consisting of two distal Cas1 dimers bridged by a Cas2 dimer. The
prespacer is bound by Cas1-Cas2 as a dual-forked DNA, and the terminal 3′-OH of each
3′ overhang serves as an attacking nucleophile during integration. The prespacer is
preferentially integrated into the leader-proximal region of the CRISPR array, guided by
the leader sequence and a pair of inverted repeats inside the CRISPR repeat. Spacer
integration in the well-studied Escherichia coli type I-E CRISPR system also relies on the
bacterial integration host factor. In type II-A CRISPR, however, Cas1-Cas2 alone
integrates spacers efficiently in vitro; other Cas proteins (such as Cas9 and Csn2) have
accessory roles in the biogenesis phase of prespacers. I will present our structural and
biochemical efforts in revealing the spacer acquisition mechanism in the Enterococcus
faecalis type II-A CRISPR system.

Ekkehard LEBERER, PhD

Professor, Senior Director, Sanofi, Germany
Founding Director, COMPACT Consortium

Dr. Leberer received his Ph.D. in Biology at the University of Konstanz, Germany (1986). He conducted post-doctoral training in molecular biology at the Banting and Best Institute of the University of Toronto, Canada, and then became a Professor of Biochemistry at the University of Konstanz, Germany (1992). He is currently responsible for R&D Alliance Management at Sanofi, and is the Scientific Managing Director of the Innovative Medicine Initiative COMPACT Consortium on the delivery of biopharmaceuticals across biological barriers and cellular membranes (www.compact-research.org).

Since joining Hoechst Marion Roussel in 1998, Dr. Leberer carried out various managing roles in this company, Sanofi’s predecessor companies and Sanofi itself, including responsibilities in functional genomics, biological sciences and external innovation for oligonucleotide-based therapeutics. He has also served as Head of Biotechnology Germany and a member of the Scientific Review Committee of Aventis Pharma Germany.

Prior to joining pharmaceutical industry, Dr. Leberer served as Senior Research Officer in genetics and genomics at the Biotechnology Research Institute, National Research Council of Canada, Montreal. His research has focused on the molecular mechanisms of signal transduction and the role of signalling molecules in human diseases. He is the principal discoverer of the p21 activated protein kinase (PAK) family of cell signalling proteins and of novel virulence-inducing genes in pathogenic fungi. He is co-author of more than 60 publications in prestigious peer-reviewed journals including Nature and Science.

Presentation Title

Delivering Therapeutic Oligonucleotides across Biobarriers: Opportunities and Challenges in Drug Development

Summary
TBD

Dong-ki LEE, PhD

Professor of Chemistry, Sungkyunkwan University, Korea
Founder and CEO, OliX Pharmaceuticals, Korea

Prof. Dong-ki Lee received B. S. in Chemistry from Korea Advanced Institute of Science and Technology (KAIST) in 1993, and Ph. D. in Biochemistry from Cornell University in 1999. After post-doctoral training in Pohang University of Science and Technology (POSTECH), Toolgen Inc., and KAIST, he joined POSTECH as an assistant professor in 2004. In 2008, He moved to Sungkyunkwan University and is a full professor of Chemistry since 2012. In 2008, Prof. Lee was selected as the principal investigator of the Global Research Laboratory program, funded by Korean government, to develop novel RNAi medicine. He is currently serving as the Asian editor of “Nucleic Acid Therapeutics” and a editorial board member of “Molecular Therapy: Nucleic Acids”. His work on novel siRNA structures, nucleic acid aptamers, and eukaryotic gene regulation has been published as over 80 papers including prestigious journals such as Nature, Cell, PNAS, and Molecular Therapy. In 2010, he founded OliX Pharmaceuticals, a RNAi therapeutics company focusing on topically administrable diseases, and serves as Chief Executive Officer. OliX successfully went public in July 2018, with 370M USD valuation.

Presentation Title

Asymmetric siRNA Targeting Fibrotic and Ocular Disorders

Summary

OLX10010, an anti-fibrotic cell-penetrating asymmetric siRNA (cp-asiRNA) targeting connective tissue growth factor (CTGF), effectively reduces target gene expression as well as expression of fibrotic markers in animal model study. Preclinical as well as clinical study update of OLX10010 in anti-skin scar will be presented. In addition to skin scar, OLX10010 has a potential to be developed as therapeutics targeting various fibrotic disorders. We will present preclinical study data of OLX10010 in other fibrotic diseases in lung and eye, such as idiopathic pulmonary fibrosis (IPF) and subretinal fibrosis.

Wei LI, PhD

Professor of Bioinformatics, Dan L. Duncan Cancer Center
Department of Molecular and Cellular Biology
Baylor College of Medicine, US
A

Dr. Wei Li is a Professor of Bioinformatics in the Dan L. Duncan Cancer Center at Baylor College of Medicine. He received his PhD in Bioinformatics from the Chinese Academy of Sciences (2003), and was an Associate Director of Bioinformatics at Beijing Genomics Institute (BGI; 2002-2004). After his postdoctoral training with Dr. Xiaole Shirley Liu in the Department of Biostatistics and Computational Biology at Harvard (2004-2007), he was recruited to Baylor as an Assistant Professor in 2007 and was promoted to tenured Full Professor in 2016. His research is focused on the design and application of bioinformatics algorithms to elucidate global epigenetic mechanisms in normal development and diseases, such as cancer. He has a solid track record in developing widely used open-source bioinformatics software, such as MACS (~5,000 citations) for ChIP-seq. Since establishing his own bioinformatics lab, he has (as of April 2018) (1) Published ~120 peer-reviewed papers through solid methodology development and extensive collaborative research, including 19 senior-author papers in Nature and Cell series. (2) Been well-funded with total external funding >$1.0 million per year, including 4 PI grants from NIH and Texas CPRIT. (3) Mentored the first 6 postdoc trainees to start their tenure-track faculty positions in the US. Dr. Li received many prestigious awards, including the New Investigator Award from Department of Defense (2010), and the Michael E. DeBakey Excellence in Research Award (2016).
Presentation Title
3ʹ-UTR Shortening Represses Tumor Suppressor Genes in trans by Disrupting ceRNA Crosstalk
Summary
Alternative polyadenylation (APA) is emerging as a pervasive mechanism in the regulation of more than 70% of human genes. The role of APA in human cancer is largely overlooked due to the lack of genome-wide APA profiling on large clinical cohorts. To overcome this limitation, we recently developed DaPars algorithm (Nature Communications 2014) for the de novo identification of APA from standard RNA-seq. Through DaPars analyses of thousands of TCGA tumor RNA-seq data, we revealed ~1,300 highly recurrent 3’UTR shortening genes, nominated CFIm25 (Nature 2014) as a master regulator of 3`-UTR shortening that links APA to glioblastoma tumor suppression, and suggested a surprising enrichment of 3’UTR shortening among transcripts that are predicted to act as competing-endogenous RNAs (ceRNAs) for tumor suppressor genes (Nature Genetics 2018).

Zhen LI, PhD

Zhen Li, PhD
Senior Vice President, Chemistry and Non-Clinical Development
Arrowhead Pharmaceuticals, USA

Dr. Zhen Li is Senior Vice President, Chemistry and Non-Clinical Development at Arrowhead Pharmaceuticals. She leads discovery chemistry, biology and non-clinical development at Arrowhead. She has led the discovery and development of Arrowhead TRiMTM platform for RNAi based therapeutics for hepatic and non-hepatic targets, and she is the key inventor of the platform. Prior to joining Arrowhead in 2014, she held leadership positions at Merck, Schering-Plough and Novartis, and led teams in drug discovery and process development in small molecule pharmaceuticals as well as RNAi therapeutics covering a range of disease areas. She has a demonstrated track record in leading multiple drug development programs from early to late stage. Dr. Zhen Li received her Bachelor of Science degree from Peking University and her Ph.D. from Harvard University.

Presentation Title

TRiMTM Platform Based RNAi Therapeutics in Treating HBV and Cardiometabolic Diseases

Summary

One of the more important recent advances in biology, RNA interference is a natural cellular process where short oligonucleotides can be used to silence gene expression and regulate the production of proteins. Arrowhead’s RNAi-based therapeutics leverage this natural pathway to shut down specific genes that cause disease.
The presentation will focus on Arrowhead’s clinical candidate ARO-HBV for the treatment of Hepatitis B Virus infection. HBV infection presents a huge unmet medical need, as it affects over 250 million people worldwide and currently there is no cure for this devastating disease. In the presentation, some of our earliest clinical data on ARO-HBV will be presented, and the journey in discovering this powerful drug candidate will be discussed. The presentation will also discuss Arrowhead’s preclinical candidates ARO-ANG3 and ARO-APOC3 for the treatment of cardiometabolic disease such as hypertriglyceridemia. Gene knockdown, reduction of protein levels, and reduction of triglycerides in disease models for Arrowhead’s preclinical candidates ARO-ANG3 and ARO-APOC3 will be presented.

Muthiah MANOHARAN, PhD

Senior Vice President, Drug Discovery, Alnylam Pharmaceuticals, USA
Board Director, Oligonucleotide Therapeutics Society

Dr. Muthiah Manoharan serves as Senior Vice President of Innovation Chemistry at Alnylam Pharmaceuticals, Cambridge, Massachusetts, USA. Dr. Manoharan joined Alnylam in 2003. He built the chemistry group at Alnylam and pioneered the discovery of GalNAc conjugated siRNAs for RNA interference (RNAi) based human therapeutics. He was the former Executive Director of Medicinal Chemistry at Isis Pharmaceuticals, Inc., a leading biotechnology company focused on antisense oligonucleotide-based therapeutics where he had a12-year tenure. With a distinguished career as a world-leading nucleic acid and bioconjugate chemist, Dr. Manoharan is an author of nearly 200 publications and over 300 abstracts, as well as the inventor of over 200 issued U.S. patents. Prior to Isis Pharmaceuticals, He earned his Ph.D. in chemistry at the University of North Carolina-Chapel Hill and conducted post-doctoral work at Yale University and the University of Maryland. He was the recipient of the M. L. Wolfrom award of the ACS Carbohydrate Chemistry Division in 2007.

Presentation Title
TBD
Summary
TBD

Craig MELLO, PhD

Professor, University of Massachusetts
Howard Hughes Medical Institute, USA
Nobel Prize in Physiology or Medicine (2006)

Dr. Mello’s lab uses the nematode C. elegans as a model system to study embryogenesis and gene silencing. His collaborative work with Dr. Andrew Fire led to the discovery of RNA interference (RNAi), for which they shared the 2006 Nobel Prize in Physiology or Medicine. Together they showed that when C. elegans is exposed to double-stranded ribonucleic acid (dsRNA), a molecule that mimics a signature of viral infection, the worm mounts a sequence-specific silencing reaction that interferes with the expression of cognate cellular RNAs. Using readily produced short synthetic dsRNAs, researchers can now silence any gene inorganisms as diverse as rice and humans. RNAi allows researchers to rapidly “knock out” the expression of specific genes and, thus, to define thebiological functions of those genes. RNAi also provides a potential therapeutic avenue to silence genes that cause or contribute to diseases.

Dr. Mello received his BS degree in Biochemistry from Brown University in 1982, and PhD from Harvard University in 1990. From 1990 to 1994, he conducted postdoctoral research at the Fred Hutchinson Cancer Research Center in Seattle, WA. Now Dr. Mello is an Investigator of the Howard Hughes Medical Institute, the Blais University Chair in Molecular Medicine and Co-director of the RNA Therapeutics Institute at the University of Massachusetts Medical School.

Besides the Nobel Prize, Dr. Mello’s work was recognized with numerous awards and honors, including the National Academy of Sciences Molecular Biology Award (2003), the Wiley Prize in Biomedical Sciences from Rockefeller University (2003), Brandeis University’s Lewis S. Rosnstiel Award for Distinguished Work in Medical Research (2005), the Gairdner Foundation International Award (2005), the Massry Prize (2005), the Paul Ehrlich and Ludwig Darmstaedter Award (2006), the Dr. Paul Janssen Award for Biomedical Research (2006), the Hope Funds Award of Excellence in Basic Research (2008). He is a member of the National Academy of Sciences, the American Academy of Arts and Sciences, and the American Philosophical Society.

Presentation Title

RNA mediated inheritance

Summary
TBD

Joseph (Jody) PUGLISI, PhD

Professor, Department of Structural Biology
Stanford University School of Medicine, USA
Member of the US National Academy of Sciences

TBD
Presentation Title

How mRNA controls the dynamics of translation

Summary
TBD

Elisabetta Viani PUGLISI, PhD

Senior Research Scientist Department of Structural Biology,
Stanford University School of Medicine, USA

TBD
Presentation Title

Architecture of the HIV-1 reverse transcriptase initiation complex

Summary
TBD

Laura SEPP-LORENZINO, PhD

Vice President, Head of Nucleic Acid Therapies,
Vertex Pharmaceuticals, USA

Dr. Sepp-Lorenzino joined Vertex Pharmaceuticals in 2017 where she leads Nucleic Acid Therapies, including strategic collaborations with Crispr Therapeutics and Moderna. As part of this effort, CTX001, an investigational CRISPR/Cas9 clinical candidate is being developed for the treatment of beta-thalassemia and sickle cell disease. Before joining Vertex, Dr. Sepp-Lorenzino was VP and Entrepreneur-in-Residence at Alnylam Pharmaceuticals where she was responsible for the Hepatic Infectious Disease therapeutic area, which she successfully partnered with Vir Biotechnology, and Merck & Co., where she was Executive Director and Department Head, RNA Therapeutics Discovery Biology. In this role, she was responsible for identification and optimization of siRNAs and delivery vehicles, advancement of pre-clinical candidates, and development of an siRNA-conjugate platform to expand the repertoire of tissues accessible to in vivo siRNA delivery. Prior to RNAi, Laura worked in oncology drug discovery and development, having led the Cancer Research Department at Merck West Point, and having been an Assistant Lab Member at Memorial Sloan-Kettering Cancer Center. Laura received her Professional Degree in Biochemistry from the University of Buenos Aires, and her M.S. and Ph.D. in Biochemistry from New York University.
Presentation Title
TBD
Summary
TBD

Mikiko C. SIOMI, PhD

Professor, Department of Biological Sciences,
Graduate School of Science, The University of Tokyo, Japan

Mikiko C. Siomi earned her Ph.D. in Agricultural Chemistry from Kyoto University, Japan in 1994, and then did post-doctoral studies with Prof. Gideon Dreyfuss, HHMI/University of Pennsylvania School of Medicine. Later, Dr. Siomi earned another Ph.D. in Medical Science from the University of Tokushima, Japan in 2003. Dr. Siomi started a joint laboratory with Prof. Haruhiko Siomi in the University of Tokushima, Japan in 1999 for elucidating the function of FMRP and the mechanism of RNAi using the Drosophila system. The laboratory discovered that Ago2 protein, the key player of RNAi, interacts with FMRP, an RNA-binding protein that is encoded by the fmr1 gene, the responsible gene for causing Fragile X Mental Retardation. Later, Dr. Siomi focused on elucidating how RNAi mechanistically occurs and the molecular mechanisms of piRNA biogenesis in the germlines. Dr. Siomi started her own laboratory at the University of Tokyo in 2012 (http://www-siomilab.biochem.s.u-tokyo.ac.jp/index.html). Dr. Siomi co-authored numerous research articles, reviews and book chapters, and currently serves as the president of the RNA Society of Japan and the vise-president of the Molecular Biology Society of Japan.
Presentation Title

piRNA biogenesis and functions

Summary
TBD

Andreas STRASSER, PhD

Division Head, Molecular Genetics of Cancer,
The Walter and Eliza Hall Institute of Medical Research, Australia

TBD
Presentation Title
TBD
Summary
TBD

Bruce SULLENGER, PhD

Professor, Duke University Medical Center, USA

Dr. Sullenger is the Director of the Translational Research Institute (DTRI) and the Joseph and Dorothy Beard Professor of Surgery and the Vice Chair of Research in the Department of Surgery at Duke University Medical Center (Durham, NC). Dr. Sullenger also serves as the Scientific Director of the NHLBI supported Translational Research Center for Thrombotic and Hemostatic Disorders (TRC-THD) that he cofounded at Duke. He has authored over 120 papers published in basic science and translational research journals.

Dr. Sullenger’s research program focuses upon the discovery and development of therapeutic RNAs. His group has been a leader in the development of nucleic acid aptamers for inhibiting the activities of therapeutically important proteins including coagulation factors and platelet proteins. He is on the Board of Directors of the American Society of Gene and Cell Therapy and the Oligonucleotide Therapeutics Society and is Editor-in-Chief for the Society’s journal Nucleic Acid Therapeutics. Dr. Sullenger founded Regado Biosciences Inc, a company focused upon the development and commercialization of the aptamer-antidote technology his laboratory invented. The lead compound, an aptamer targeting factor IXa and its matched antidote, is in phase 3 clinical studies.

Dr. Sullenger earned his Bachelor of Science Degree from Indiana University (Bloomington, IN) and his Ph.D. from Cornell University Graduate School of Medical Sciences (New York, NY) working at the Memorial Sloan-Kettering Cancer Center. He performed postdoctoral studies at the University of Colorado (Boulder, CO) in the Department of Biochemistry in Dr. Thomas Cech’s laboratory.

Presentation Title
Translating RNA Aptamers into the Clinic and Back to the Lab
Summary
Clinical evaluation of our factor IXa RNA aptamer in two thousand patients undergoing angioplasty has demonstrated that aptamers can rapidly and potently inhibit their target proteins in patients and that antidote molecules can rapidly and precisely control such activity in the minute time frame. These observations suggest that aptamers represent useful molecules to tightly control biochemical processes in humans in real time. To begin to explore this potential further, we have started to evaluate the utility of antidote-mediated control of aptamers for a variety of other therapeutic and diagnostic applications. We will describe our recent progress developing a rapidly controllable factor Xa anticoagulant aptamer to effectively yet reversibly control blood coagulation during cardiopulmonary bypass surgery and a rapidly reversible VWF aptamer for improving the treatment of thrombotic stroke. Collectively these clinical and preclinical studies lead us to believe that rapidly controllable aptamers represent valuable therapeutic and diagnostic agents that will provide physicians the ability to monitor and precisely control blood coagulation, as well as other biological pathways, in real time in response to individual patients’ needs.

Andrew YOO, PhD

Associate Professor, Department of Developmental Biology,
Washington University School of Medicine, USA

Dr. Yoo’s lab studies the function of microRNAs as effectors of neurogenesis and develops cellular reprogramming approaches to generate human neurons by directly converting non-neural somatic cells. By interrogating how microRNAs affect the chromatin state, Dr. Yoo’s lab dissects epigenetic factors controlled by microRNAs to promote the neuronal identity and devises reprogramming paradigms to generate distinct neuronal subtypes to model late-onset neurodegenerative disorders in patient-derived neurons. Dr. Yoo received his B.Sc. degree in Neurophysiology from McGill University in Montreal in 1995 and M.Sc. degree from the University of British Columbia in 1997. He then moved to New York to complete his Ph.D. degree at Columbia University in Dr. Iva Greenwlad’s lab in 2005. From 2006 to 2011, Dr. Yoo conducted postdoctoral work at Stanford University to study the role of microRNAs and chromatin remodeling complexes during neural development in Dr. Gerald Crabtree’s lab. In 2011, Dr. Yoo started his independent lab at Washington University School of Medicine in St. Louis where he is currently an associate professor of Developmental Biology. Dr. Yoo has received awards in recognition of his work including the Presidential Early Career Award for Scientists and Engineers (PECASE) from the White House, NIH Director’s New Innovator Award, and Mallinckrodt Scholar Award.
Presentation Title

MicroRNAs as cell fate controllers and cellular reprogramming factors

Summary
TBD

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