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Necdin Regulates Hematopoietic Stem Cell Quiescence and Sensitivity to Genotoxic Stress.

Blood 2009年第22期114卷 379-379页

作者： Takashi Asai Yan Liu Silvana Di Giandomenico Anthony Deblasio Silvia Menendez Jack Antipin Boris Reva Rachel Wevrick Stephen D. Nimer Molecular Pharmacology and Cheminstry Program Sloan-Kettering Institute Memorial Sloan-Kettering Cancer Center New York NY USA Computational Biology Program Sloan-Kettering Institute Memorial Sloan-Kettering Cancer Center New York NY USA Department of Medical Genetics University of Alberta Edmonton AL Canada

Abstract 379 Necdin, a member of MAGE (melanoma antigen) family proteins, is a growth suppressing protein that was first identified in post mitotic neurons. The gene encoding necdin is one of several deleted in individuals with Prader-Willi syndrome, a neurobehavioural disorder associated with an increased risk of myeloid leukemia. It is reported that necdin interacts with p53 and represses p53-mediated apoptosis in neurons, but its role in hematopoiesis is largely unknown. Recently, we defined a critical role of p53 in regulating hematopoietic stem cell quiescence, and identified necdin as a target gene of p53, that is highly expressed in LT-HSCs (Liu Y et al., Cell Stem Cell, 2009). To define the role of necdin in hematopoiesis, we have analyzed the hematopoietic compartment of necdin-null mice. As necdin-null mice die perinatally, we first investigated fetal hematopoiesis and found no alteration in the frequency of fetal liver HSCs, defined as Lin - Sca1 + Mac1 + CD48 - CD150 + within the fetal liver cells. Although necdin-null fetal liver HSCs increase serial replating capability in methylcellulose and maintain stemness in long-term stromal based cultures better than wild type HSCs, necdin-null fetal liver HSCs repopulate lethally irradiated recipient mice similar to wild type HSCs, in primary, secondary, and tertiary serial bone marrow transplantation assays. In addition, necdin-null HSCs show almost comparable repopulating ability as wild type HSCs, after secondary competitive bone marrow transplantation assays. These imply that necdin is dispensable for HSC self renewal. On the other hand, BM-derived necdin-null HSCs show decreased quiescence 4 months after transplantation, and increased proliferation as indicated by in vivo BrdU incorporation assays. Furthermore, recipient mice repopulated with necdin-null HSCs show enhanced sensitivity both to weekly 5-FU administration and to total body irradiation, as manifested by increased mortality. This suggests that

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SYNTHESIS: cancer research meets evolutionary biology

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Evolutionary Applications 2009年第1期2卷

作者： John W. Pepper C. Scott Findlay Rees Kassen Sabrina L. Spencer Carlo C. Maley Department of Ecology and Evolutionary Biology University of Arizona Tucson AZ USA The Santa Fe Institute Santa Fe NM USA Department of Biology University of Ottawa Ottawa ON Canada Institute of Environment University of Ottawa Ottawa ON Canada Program in Cancer Therapeutics Ottawa Hospital Cancer Centre Ottawa ON Canada Centre for Advanced Research in Environmental Genomics University of Ottawa Ottawa ON Canada Computational and Systems Biology Massachusetts Institute of Technology Cambridge MA USA Molecular and Cellular Oncogenesis Program The Wistar Institute Philadelphia PA USA

There is increasing evidence that Darwin’s theory of evolution by natural selection provides insights into the etiology and treatment of cancer. On a microscopic scale, neoplastic cells meet the conditions for evolution by Darwinian selection: cell reproduction with heritable variability that affects cell survival and replication. This suggests that, like other areas of biological and biomedical research, Darwinian theory can provide a general framework for understanding many aspects of cancer, including problems of great clinical importance. With the availability of raw molecular data increasing rapidly, this theory may provide guidance in translating data into understanding and progress. Several conceptual and analytical tools from evolutionary biology can be applied to cancer biology. Two clinical problems may benefit most from the application of Darwinian theory: neoplastic progression and acquired therapeutic resistance. The Darwinian theory of cancer has especially profound implications for drug development, both in terms of explaining past difficulties, and pointing the way toward new approaches. Because cancer involves complex evolutionary processes, research should incorporate both tractable (simplified) experimental systems, and also longitudinal observational studies of the evolutionary dynamics of cancer in laboratory animals and in human patients. cancer biology will require new tools to control the evolution of neoplastic cells.

关键词： acquired drug resistance cancer progression drug development natural selection neoplasms somatic evolution stem cells transdisciplinary research

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Developmental systems biology flourishing on new technologies

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Journal of genetics and Genomics 2008年第10期35卷 577-584页

作者： Jing-Dong J. Han Yi Liu Huiling Xue Kai Xia Hong Yu Shanshan Zhu Zhang Chen Wei Zhang Zheng Huang Chunyu Jin Bo Xian Jing Li Lei Hou Yixing Han Chaoqun Niu Timothy C. Alcon Chinese Academy of Sciences Key Laboratory of Molecular Developmental Biology Center for Molecular Systems Biology Institute of Genetics and Developmental Biology Chinese Academy of Sciences Beijing 100101 China Key Laboratory of Machine Perception （Ministry of Education） Peking University Beijing 100871 China Bioinformatics and Computational Biology Graduate Program Iowa State University Ames IA 50011-1040 USA

Organism development is a systems level process. It has benefited greatly from the recent technological advances in the field of systems biology. DNA microarray, phenome, interactome and transcriptome mapping, the new generation of deep sequencing technologies, and faster and better computational and modeling approaches have opened new frontiers for both systems biologists and developmental biologists to reexamine the old developmental biology questions, such as pattern formation, and to tackle new problems, such as stem cell reprogramming. As showcased in the International Developmental systems biology Symposium organized by Chinese Academy of Sciences, developmental systems biology is flourishing in many perspectives, from the evolution of developmental systems, to the underlying genetic and molecular pathways and networks, to the genomic, epigenomic and noncoding levels, to the computational analysis and modeling. We believe that the field will continue to reap rewards into the future with these new approaches.

关键词： developmental systems biology new technologies symposium

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Second Annual Huntington Disease Clinical Research Symposium: Organized by the Huntington Study Group

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Neurotherapeutics 2009年第1期6卷 202-202页

作者： Charles Sabine K. Trembath A. Churchyard Z. Horton L. Tippett V. Hogg R. Roxburgh D. Velakoulis V. Collins M. Delatycki E. Aylward P. Nopoulos H. Johnson A. Juhl V. Magnotta R. Pierson D. Langbehn C. Ross J. Paulsen PREDICT-HD Investigators of the Huntington Study Group Lewis Maltby K. L. Poston C. Tang A. Feigin Y. Ma M. Guttman J. S. Paulsen V. Dhawan D. Eidelberg The Huntington Study Group Russell Katz L. Veatch Goodman J. Giuliano D. Lovecky K. Quaid L. Dure A. Goh O. Yastrubetskaya E. Chiu K. Evans K. Anderson B. Borowsky K. Duff A. Ho T. Sills A. Vaccarino D. Van Kammen FuRST-pHD and PREDICT-HD Investigators and Coordinators of the Huntington Study Group R. C. Block E. R. Dorsey C. A. Beck I. Shoulson Huntington Study Group TREND-HD Investigators E. Pirogovsky B. Bartlett A. Callazo J. Goldstein G. Peavy M. Jacobson J. Corey-Bloom P. Gilbert S. Lessig G. M. Peavy K. E. Weaver T. L. Richards O. Liang E. H. Aylward L. J. Beglinger W. H. Adams H. Paulson J. G. Fiedorowicz D. R. Langbehn A. Leserman K. E. Conley S. Jubrias C. Amara E. Shankland D. J. Marcinek J. F. O’Rourke C. Wang J. C. Stout K. Rowe A. D. Kloos D. A. Kegelmeyer S. K. Kostyk P. Chua P. Desmond S. Christensen C. Steward F. Judd J. Lloyd B. Tress M. Pugliese P. Phan J. Sanchez-Ramos E. Oster J. Bausch A. Shinaman E. Kayson D. Oakes Huntington Study Group PHAROS Investigators Huntington Study Group COHORT Investigators L. Oelke L. Butterfield C. Cimino M. McCall L. Ling B. Stell J. Annis J. Cha P. Como NBC News Correspondent Telbury Gloucestershire UK rid.416107.***Bruce Lefroy Centre for Genetic Health Research Murdoch Childrens Research Institute Royal Children’s Hospital Parkville Australia Huntington Service Calvary Healthcare Bethlehem Caulfield Australia rid.9654.e***Department of Psychology The University of Auckland Auckland New Zealand rid.414055.***Department of Neurology Auckland City Hospital Auckland New Zealand rid.416153.***Neuropsychiatry Unit Royal Melbourne Hospital Parkville Australia rid.416153.***Melbourne Neuropsychiatry Centre Royal Melbourne Hospital Parkville Victoria Australia rid.1008.***Department of Psychiatry University of Melbourne Parkville Victoria Australia rid.416107.***Genetic Health Services Victoria Royal Children’s Hospital Parkville Australia rid.34477.***7University of Washington Seattle WA USA rid.412623.***University of Washington Medical Center Seattle WA USA rid.214572.***University of Iowa Iowa City IA USA rid.214572.***Department of Neurology University of Iowa Iowa City IA USA rid.21107.***1Johns Hopkins University Baltimore MD USA National Workrights Institute Princeton NJ USA rid.250903.d***Center for Neurosciences The Feinstein Institute for Medical Research North Shore-Long Island Jewish Health System Manhasset NY USA Department of Neurology North Shore University Hospital and New York University School of Medicine New York NY USA rid.17063.33Department of Neurology University of Toronto Toronto Ontario Canada The Center for Movement Disorders Markham Ontario Canada rid.412750.***University of Rochester Medical Center Rochester NY USA rid.417587.***Division of Neurology Products Food and Drug Administration Rockville MD USA HD Drug Works Seattle WA USA rid.453209.***CHDI Foundation Princeton NJ USA Huntington’s Disease Society of America New York NY USA rid.257413.***Indiana University School of Medicine Indianapolis IN USA rid.257413.***Department of Medical and Molecular Genetics Indiana Unive

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Workshop on imaging science development for cancer prevention and preemption

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cancer Biomarkers 2007年第1期3卷 1-33页

作者： Kelloff, Gary J. Sullivan, Daniel C. Baker, Houston Clarke, Lawrence P. Nordstrom, Robert Tatum, James L. Dorfman, Gary S. Jacobs, Paula Berg, Christine D. Pomper, Martin G. Birrer, Michael J. Tempero, Margaret Higley, Howard R. Petty, Brenda Gumbs Sigman, Caroline C. Maley, Carlo Sharma, Prateek Wax, Adam Ginsberg, Gregory G. Dannenberg, Andrew J. Hawk, Ernest T. Messing, Edward M. Grossman, H. Barton Harisinghani, Mukesh Bigio, Irving J. Griebel, Donna Henson, Donald E. Fabian, Carol J. Ferrara, Katherine Fantini, Sergio Schnall, Mitchell D. Zujewski, Jo Anne Hayes, Wendy Klein, Eric A. DeMarzo, Angelo Ocak, Iclal Ketterling, Jeffrey A. Tempany, Clare Shtern, Faina Parnes, Howard L. Gomez, Jorge Srivastava, Sudhir Szabo, Eva Lam, Stephen Seibel, Eric J. Massion, Pierre McLennan, Geoffrey Cleary, Kevin Suh, Robert Burt, Randall W. Pfeiffer, Ruth M. Hoffman, John M. Roy, Hemant K. Wang, Thomas Limburg, Paul J. El-Deiry, Wafik S. Papadimitrakopoulou, Vali Hittelman, Walter N. MacAulay, Calum Veltri, Robert W. Solomonzz, Diane Jeronimo, Jose Richards-Kortum, Rebecca Johnson, Karen A. Viner, Jaye L. Stratton, Steven P. Rajadhyaksha, Milind Dhawan, Atam NIH/NCI/DCTD Cancer Imaging Program Bethesda MD United States NIH/NCI/DCTD Cancer Imaging Program NCI-Frederick Frederick MD United States NIH/NCI/DCP Early Detection Research Group Bethesda MD United States The Johns Hopkins University School of Medicine Departments of Radiology Pharmacology and Oncology Division of Neuroradiology Baltimore MD United States NIH/NCI/CCR Cell and Cancer Biology Branch Bethesda MD United States University of California San Francisco Department of Medicine Division of Medical Oncology San Francisco CA United States CCS Associates Inc. Mountain View CA United States Wistar Institute Molecular and Cellular Oncogenesis Program Philadelphia PA United States University of Kansas School of Medicine VA Hospital Kansas City MO United States Duke University Department of Biomedical Engineering Medical Physics Program Durham NC United States University of Pennsylvania School of Medicine Department of Gastroenterology Philadelphia PA United States New York Presbyterian Hospital Weill Medical College of Cornell University New York NY United States NIH/NCI/OD Office of Centers for Training and Resources Bethesda MD United States University of Rochester Medical Center Department of Urology Rochester NY United States University of Texas MD Anderson Cancer Center Department of Urology Houston TX United States Massachusetts General Hospital Abdominal Imaging/Interventional Radiology Boston MA United States Boston University Biomedical Engineering Electrical and Computer Engineering and Physics Boston MA United States NIH/NCI/DCP Gastrointestinal and Other Cancers Research Group Bethesda MD United States The George Washington University Cancer Institute Office of Cancer Prevention and Control Washington DC United States University of Kansas Cancer Center Clinical Oncology Kansas City KS United States University of California Davis Department of Biomedical Engineering Davis CA United States Tufts University De

The concept of intraepithelial neoplasm (IEN) as a near-obligate precursor of cancers has generated opportunities to examine drug or device intervention strategies that may reverse or retard the sometimes lengthy process of carcinogenesis. Chemopreventive agents with high therapeutic indices, well-monitored for efficacy and safety, are greatly needed, as is development of less invasive or minimally disruptive visualization and assessment methods to safely screen nominally healthy but at-risk patients, often for extended periods of time and at repeated intervals. Imaging devices, alone or in combination with anticancer drugs, may also provide novel interventions to treat or prevent precancer.

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Identifying and characterizing a five-gene cluster of ATP-binding cassette transporters mapping to human chromosome 17q24: a new subgroup within the ABCA subfamily

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GeneScreen 2002年第3期1卷 157-164页

作者： Isabelle Arnould Lynn M. Schriml Catherine Prades Marcia Lachtermacher-Triunfol Thomas Schneider Christelle Maintoux Cendrine Lemoine Delphine Debono Catherine Devaud Laurent Naudin Stéphanie Bauché Mélanie Annat Tarmo Annilo Rando Allikmets Bert Gold Patrice Denèfle Marie Rosier Michael Dean Evry Genomics Center Aventis Pharma Evry France These authors contributed equally to the study. Human Genetics Section Laboratory of Genomic Diversity Present address: National Center for Biotechnology Information NLM NIH Bethesda MD U.S.A. Intramural Research and Support Program SAIC-Frederick Frederick MD 21702 U.S.A. Laboratory of Experimental and Computational Biology National Cancer Institute-Frederick Cancer Research and Development Center Departments of Ophthalmology and Pathology Columbia University New York NY

Abstract Introduction The ATP-binding cassette (ABC) gene superfamily encodes a series of transporter proteins that move a wide variety of substances across extra- and intracellular membranes. Forty-eight known human ABC genes can be divided into seven phylogenetically distinct subfamilies. The ABCA gene subfamily is found exclusively in multicellular eukaryotes. Results We report here on a unique tandem array of five ABCA genes on chromosome 17q24 defining a phylogenetically distinct group. This is the largest cluster of mammalian ABC genes described to date. They are arranged head-to-tail and have similar intron/exon organization in both mouse and human. Northern analysis reveals a heterogeneous pattern of expression in human tissues, with ABCA5 and ABCA10 expressed in skeletal muscle, ABCA6 in the liver, ABCA9 in the heart, and ABCA8 in ovaries. This suggests that these proteins have distinct functions.

关键词： ABC gene cluster chromosome 17 ATP-binding cassette transporter ABCA subfamily

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Single-Cell Technologies for Studying the Evolution and Function of Mitochondrial DNA Heteroplasmy in cancer

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cancer biology 1000年第1期9卷 161-180页

作者： Sonia Boscenco Erin M. Cumming Minsoo Kim Caleb Lareau Ed Reznik 1Computational Oncology Service Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA email: reznike@*** 2Computational and Systems Biology Program Sloan Kettering Institute New York NY USA email: lareauc@***

The mitochondrial genome, which encodes genes essential for respiration and cellular homeostasis, is the target of abundant and highly diverse somatic alterations in cancers. Somatic alterations to mitochondrial DNA (mtDNA) nearly always arise heteroplasmically, producing heterogeneous ensembles of mtDNA within single cells. Here, we review new insights derived from exponential increases in genomic sequencing data that have uncovered the nature of, selective pressure for, and functional consequences of cancer-associated mtDNA alterations. As many discoveries have been limited by their ability to determine cell-to-cell variation in mtDNA genotype, we describe a new generation of single-cell sequencing approaches that resolve otherwise indeterminate models of mtDNA heteroplasmy. In tandem with novel approaches for mtDNA editing and modeling of mutations, these advances foreshadow the quantitative dissection of dosage-dependent mtDNA phenotypes that underlie both tumor evolution and heterogeneous response to therapies.

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computational Methods for Single-Cell RNA Sequencing

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Biomedical Data Science 1000年第1期3卷 339-364页

作者： Brian Hie Joshua Peters Sarah K. Nyquist Alex K. Shalek Bonnie Berger Bryan D. Bryson 1Computer Science and Artificial Intelligence Laboratory (CSAIL) Massachusetts Institute of Technology Cambridge Massachusetts 02139 USA email: bab@mit.edu 3Ragon Institute of MGH MIT and Harvard Cambridge Massachusetts 02139 USA 2Department of Biological Engineering Massachusetts Institute of Technology Cambridge Massachusetts 02139 USA email: bryand@mit.edu 4Program in Computational and Systems Biology Massachusetts Institute of Technology Cambridge Massachusetts 02139 USA 5Department of Chemistry Institute for Medical Engineering & Science (IMES) and Koch Institute for Integrative Cancer Research Massachusetts Institute of Technology Cambridge Massachusetts 02139 USA 6Department of Mathematics Massachusetts Institute of Technology Cambridge Massachusetts 02139 USA

Single-cell RNA sequencing (scRNA-seq) has provided a high-dimensional catalog of millions of cells across species and diseases. These data have spurred the development of hundreds of computational tools to derive novel biological insights. Here, we outline the components of scRNA-seq analytical pipelines and the computational methods that underlie these steps. We describe available methods, highlight well-executed benchmarking studies, and identify opportunities for additional benchmarking studies and computational methods. As the biochemical approaches for single-cell omics advance, we propose coupled development of robust analytical pipelines suited for the challenges that new data present and principled selection of analytical methods that are suited for the biological questions to be addressed.

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