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  • 1
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    AID stabilizes stem-cell phenotype by removing epigenetic memory of pluripotency genes (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-06-28
    Description: The activation-induced cytidine deaminase (AID; also known as AICDA) enzyme is required for somatic hypermutation and class switch recombination at the immunoglobulin locus. In germinal-centre B cells, AID is highly expressed, and has an inherent mutator activity that helps generate antibody diversity. However, AID may also regulate gene expression epigenetically by directly deaminating 5-methylcytosine in concert with base-excision repair to exchange cytosine. This pathway promotes gene demethylation, thereby removing epigenetic memory. For example, AID promotes active demethylation of the genome in primordial germ cells. However, different studies have suggested either a requirement or a lack of function for AID in promoting pluripotency in somatic nuclei after fusion with embryonic stem cells. Here we tested directly whether AID regulates epigenetic memory by comparing the relative ability of cells lacking AID to reprogram from a differentiated murine cell type to an induced pluripotent stem cell. We show that Aid-null cells are transiently hyper-responsive to the reprogramming process. Although they initiate expression of pluripotency genes, they fail to stabilize in the pluripotent state. The genome of Aid-null cells remains hypermethylated in reprogramming cells, and hypermethylated genes associated with pluripotency fail to be stably upregulated, including many MYC target genes. Recent studies identified a late step of reprogramming associated with methylation status, and implicated a secondary set of pluripotency network components. AID regulates this late step, removing epigenetic memory to stabilize the pluripotent state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762466/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762466/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Ritu -- DiMenna, Lauren -- Schrode, Nadine -- Liu, Ting-Chun -- Franck, Philipp -- Munoz-Descalzo, Silvia -- Hadjantonakis, Anna-Katerina -- Zarrin, Ali A -- Chaudhuri, Jayanta -- Elemento, Olivier -- Evans, Todd -- AI072194/AI/NIAID NIH HHS/ -- HL056182/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 HD052115/HD/NICHD NIH HHS/ -- R37 HL056182/HL/NHLBI NIH HHS/ -- T32 AI007621/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Aug 1;500(7460):89-92. doi: 10.1038/nature12299. Epub 2013 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Weill Cornell Medical College, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Dedifferentiation/genetics ; Cellular Reprogramming/genetics ; Cytidine Deaminase/genetics/*metabolism ; Epigenesis, Genetic/*genetics ; Female ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; HEK293 Cells ; Humans ; Male ; Mice ; Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Reprogramming human endothelial cells to haematopoietic cells requires vascular induction (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-18
    Description: Generating engraftable human haematopoietic cells from autologous tissues is a potential route to new therapies for blood diseases. However, directed differentiation of pluripotent stem cells yields haematopoietic cells that engraft poorly. Here, we have devised a method to phenocopy the vascular-niche microenvironment of haemogenic cells, thereby enabling reprogramming of human endothelial cells into engraftable haematopoietic cells without transition through a pluripotent intermediate. Highly purified non-haemogenic human umbilical vein endothelial cells or adult dermal microvascular endothelial cells were transduced with the transcription factors FOSB, GFI1, RUNX1 and SPI1 (hereafter referred to as FGRS), and then propagated on serum-free instructive vascular niche monolayers to induce outgrowth of haematopoietic colonies containing cells with functional and immunophenotypic features of multipotent progenitor cells (MPPs). These endothelial cells that have been reprogrammed into human MPPs (rEC-hMPPs) acquire colony-forming-cell potential and durably engraft into immune-deficient mice after primary and secondary transplantation, producing long-term rEC-hMPP-derived myeloid (granulocytic/monocytic, erythroid, megakaryocytic) and lymphoid (natural killer and B cell) progenies. Conditional expression of FGRS transgenes, combined with vascular induction, activates endogenous FGRS genes, endowing rEC-hMPPs with a transcriptional and functional profile similar to that of self-renewing MPPs. Our approach underscores the role of inductive cues from the vascular niche in coordinating and sustaining haematopoietic specification and may prove useful for engineering autologous haematopoietic grafts to treat inherited and acquired blood disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159670/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159670/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandler, Vladislav M -- Lis, Raphael -- Liu, Ying -- Kedem, Alon -- James, Daylon -- Elemento, Olivier -- Butler, Jason M -- Scandura, Joseph M -- Rafii, Shahin -- CA159175/CA/NCI NIH HHS/ -- CA163167/CA/NCI NIH HHS/ -- HL055748/HL/NHLBI NIH HHS/ -- HL119872/HL/NHLBI NIH HHS/ -- R01 DK095039/DK/NIDDK NIH HHS/ -- R01 HL097797/HL/NHLBI NIH HHS/ -- R01 HL115128/HL/NHLBI NIH HHS/ -- R01 HL119872/HL/NHLBI NIH HHS/ -- R01DK095039/DK/NIDDK NIH HHS/ -- R01HL097797/HL/NHLBI NIH HHS/ -- R01HL119872/HL/NHLBI NIH HHS/ -- U01 HL099997/HL/NHLBI NIH HHS/ -- U01-HL099997/HL/NHLBI NIH HHS/ -- U54 CA163167/CA/NCI NIH HHS/ -- U54CA163167/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jul 17;511(7509):312-8. doi: 10.1038/nature13547. Epub 2014 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ansary Stem Cell Institute, Department of Genetic Medicine, and Howard Hughes Medical Institute, Weill Cornell Medical College, New York, New York 10065, USA. ; 1] Ansary Stem Cell Institute, Department of Genetic Medicine, and Howard Hughes Medical Institute, Weill Cornell Medical College, New York, New York 10065, USA [2] Ronald O. Perelman and Claudia Cohen Center for Reproductive Medicine, Weill Cornell Medical College, New York, New York 10065, USA. ; HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Weill Cornell Medical College, New York, New York 10065, USA. ; Department of Medicine, Hematology-Oncology, Weill Cornell Medical College and the New York Presbyterian Hospital, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25030167" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/cytology/metabolism/transplantation ; Animals ; Aorta ; Cell Lineage ; *Cellular Microenvironment ; *Cellular Reprogramming ; Endothelial Cells/*cytology/metabolism ; Female ; Gene Expression Regulation ; Gonads ; Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/metabolism ; Humans ; Lymphocytes/cytology ; Mesonephros ; Mice ; Multipotent Stem Cells/*cytology/metabolism/transplantation ; Myeloid Cells/cytology ; Pluripotent Stem Cells ; Time Factors ; Transcription Factors/genetics/metabolism ; Transgenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    NFIB is a governor of epithelial-melanocyte stem cell behaviour in a shared niche (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-02-08
    Description: Adult stem cells reside in specialized niches where they receive environmental cues to maintain tissue homeostasis. In mammals, the stem cell niche within hair follicles is home to epithelial hair follicle stem cells and melanocyte stem cells, which sustain cyclical bouts of hair regeneration and pigmentation. To generate pigmented hairs, synchrony is achieved such that upon initiation of a new hair cycle, stem cells of each type activate lineage commitment. Dissecting the inter-stem-cell crosstalk governing this intricate coordination has been difficult, because mutations affecting one lineage often affect the other. Here we identify transcription factor NFIB as an unanticipated coordinator of stem cell behaviour. Hair follicle stem-cell-specific conditional targeting of Nfib in mice uncouples stem cell synchrony. Remarkably, this happens not by perturbing hair cycle and follicle architecture, but rather by promoting melanocyte stem cell proliferation and differentiation. The early production of melanin is restricted to melanocyte stem cells at the niche base. Melanocyte stem cells more distant from the dermal papilla are unscathed, thereby preventing hair greying typical of melanocyte stem cell differentiation mutants. Furthermore, we pinpoint KIT-ligand as a dermal papilla signal promoting melanocyte stem cell differentiation. Additionally, through chromatin-immunoprecipitation with high-throughput-sequencing and transcriptional profiling, we identify endothelin 2 (Edn2) as an NFIB target aberrantly activated in NFIB-deficient hair follicle stem cells. Ectopically induced Edn2 recapitulates NFIB-deficient phenotypes in wild-type mice. Conversely, endothelin receptor antagonists and/or KIT blocking antibodies prevent precocious melanocyte stem cell differentiation in the NFIB-deficient niche. Our findings reveal how melanocyte and hair follicle stem cell behaviours maintain reliance upon cooperative factors within the niche, and how this can be uncoupled in injury, stress and disease states.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3635831/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3635831/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Chiung-Ying -- Pasolli, H Amalia -- Giannopoulou, Eugenia G -- Guasch, Geraldine -- Gronostajski, Richard M -- Elemento, Olivier -- Fuchs, Elaine -- R01 AR031737/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- R01-AR31737/AR/NIAMS NIH HHS/ -- R01-HL080624/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 7;495(7439):98-102. doi: 10.1038/nature11847. Epub 2013 Feb 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23389444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation ; Cell Proliferation ; Chromatin Immunoprecipitation ; Endothelin-2/genetics/metabolism ; Epithelial Cells/cytology/metabolism ; Hair/cytology/growth & development ; Hair Color ; Hair Follicle/*cytology/metabolism ; Melanocytes/*cytology/metabolism ; Mice ; NFI Transcription Factors/deficiency/genetics/*metabolism ; Sequence Analysis ; Stem Cell Factor/metabolism ; *Stem Cell Niche ; Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    A stable transcription factor complex nucleated by oligomeric AML1-ETO controls leukaemogenesis (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-03
    Description: Transcription factors are frequently altered in leukaemia through chromosomal translocation, mutation or aberrant expression. AML1-ETO, a fusion protein generated by the t(8;21) translocation in acute myeloid leukaemia, is a transcription factor implicated in both gene repression and activation. AML1-ETO oligomerization, mediated by the NHR2 domain, is critical for leukaemogenesis, making it important to identify co-regulatory factors that 'read' the NHR2 oligomerization and contribute to leukaemogenesis. Here we show that, in human leukaemic cells, AML1-ETO resides in and functions through a stable AML1-ETO-containing transcription factor complex (AETFC) that contains several haematopoietic transcription (co)factors. These AETFC components stabilize the complex through multivalent interactions, provide multiple DNA-binding domains for diverse target genes, co-localize genome wide, cooperatively regulate gene expression, and contribute to leukaemogenesis. Within the AETFC complex, AML1-ETO oligomerization is required for a specific interaction between the oligomerized NHR2 domain and a novel NHR2-binding (N2B) motif in E proteins. Crystallographic analysis of the NHR2-N2B complex reveals a unique interaction pattern in which an N2B peptide makes direct contact with side chains of two NHR2 domains as a dimer, providing a novel model of how dimeric/oligomeric transcription factors create a new protein-binding interface through dimerization/oligomerization. Intriguingly, disruption of this interaction by point mutations abrogates AML1-ETO-induced haematopoietic stem/progenitor cell self-renewal and leukaemogenesis. These results reveal new mechanisms of action of AML1-ETO, and provide a potential therapeutic target in t(8;21)-positive acute myeloid leukaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732535/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Xiao-Jian -- Wang, Zhanxin -- Wang, Lan -- Jiang, Yanwen -- Kost, Nils -- Soong, T David -- Chen, Wei-Yi -- Tang, Zhanyun -- Nakadai, Tomoyoshi -- Elemento, Olivier -- Fischle, Wolfgang -- Melnick, Ari -- Patel, Dinshaw J -- Nimer, Stephen D -- Roeder, Robert G -- CA113872/CA/NCI NIH HHS/ -- CA129325/CA/NCI NIH HHS/ -- CA163086/CA/NCI NIH HHS/ -- CA166835/CA/NCI NIH HHS/ -- R01 CA163086/CA/NCI NIH HHS/ -- R01 CA166835/CA/NCI NIH HHS/ -- UL1 RR024143/RR/NCRR NIH HHS/ -- UL1RR024143/RR/NCRR NIH HHS/ -- England -- Nature. 2013 Aug 1;500(7460):93-7. doi: 10.1038/nature12287. Epub 2013 Jun 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812588" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Binding Sites ; Cell Division ; Cell Line, Tumor ; *Cell Transformation, Neoplastic/genetics ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; Hematopoietic Stem Cells/cytology/metabolism/pathology ; Humans ; Leukemia, Myeloid, Acute/genetics/*metabolism/*pathology ; Mice ; Models, Molecular ; Molecular Sequence Data ; Multiprotein Complexes/chemistry/*metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Point Mutation ; Protein Binding ; Protein Multimerization ; Protein Stability ; Protein Structure, Tertiary ; Transcription Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: More than half of human colorectal cancers (CRCs) carry either KRAS or BRAF mutations and are often refractory to approved targeted therapies. We found that cultured human CRC cells harboring KRAS or BRAF mutations are selectively killed when exposed to high levels of vitamin C. This effect is due to increased uptake of the oxidized form of vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter. Increased DHA uptake causes oxidative stress as intracellular DHA is reduced to vitamin C, depleting glutathione. Thus, reactive oxygen species accumulate and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Inhibition of GAPDH in highly glycolytic KRAS or BRAF mutant cells leads to an energetic crisis and cell death not seen in KRAS and BRAF wild-type cells. High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice. These results provide a mechanistic rationale for exploring the therapeutic use of vitamin C for CRCs with KRAS or BRAF mutations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778961/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yun, Jihye -- Mullarky, Edouard -- Lu, Changyuan -- Bosch, Kaitlyn N -- Kavalier, Adam -- Rivera, Keith -- Roper, Jatin -- Chio, Iok In Christine -- Giannopoulou, Eugenia G -- Rago, Carlo -- Muley, Ashlesha -- Asara, John M -- Paik, Jihye -- Elemento, Olivier -- Chen, Zhengming -- Pappin, Darryl J -- Dow, Lukas E -- Papadopoulos, Nickolas -- Gross, Steven S -- Cantley, Lewis C -- KL2 TR000458/TR/NCATS NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- P01 CA117969-09/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-07/CA/NCI NIH HHS/ -- S10 RR022615/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Dec 11;350(6266):1391-6. doi: 10.1126/science.aaa5004. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. ; Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. Biological and Biomedical Sciences Graduate Program, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA. ; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. ; Molecular Oncology Research Institute and Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA. ; Department of Physiology and Biophysics, Weill Cornell Medical College, New York, NY 10065, USA. ; Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA. ; Division of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Biostatistics and Epidemiology, Weill Cornell Medical College, New York, NY 10065, USA. ; Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA. lcantley@med.cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26541605" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/genetics ; Animals ; Ascorbic Acid/administration & dosage/pharmacology/*therapeutic use ; Cell Line, Tumor ; Colorectal Neoplasms/*drug therapy/*genetics ; Dehydroascorbic Acid/metabolism ; Female ; Glucose Transporter Type 1/metabolism ; Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism ; Glycolysis/drug effects ; Humans ; Mice ; Mice, Mutant Strains ; Mice, Nude ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins B-raf/*genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Reactive Oxygen Species/metabolism ; Xenograft Model Antitumor Assays ; ras Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Genetic regulation of vesiculogenesis and immunomodulation in Mycobacterium tuberculosis (2013)
    National Academy of Sciences
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    Publication Date: 2013-11-18
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 7
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    Identification of functionally active, low frequency copy number variants at 15q21.3 and 12q21.31 associated with prostate cancer risk (2012)
    National Academy of Sciences
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    Publication Date: 2012-04-10
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
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    Oncogene-mediated alterations in chromatin conformation (2012)
    National Academy of Sciences
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    Publication Date: 2012-05-21
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 9
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    Histone variant H3.3 is an essential maternal factor for oocyte reprogramming (2014)
    National Academy of Sciences
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    Publication Date: 2014-05-05
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
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    A primer on precision medicine informatics (2016)
    Oxford University Press
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    Publication Date: 2016-01-21
    Description: In this review, we describe key components of a computational infrastructure for a precision medicine program that is based on clinical-grade genomic sequencing. Specific aspects covered in this review include software components and hardware infrastructure, reporting, integration into Electronic Health Records for routine clinical use and regulatory aspects. We emphasize informatics components related to reproducibility and reliability in genomic testing, regulatory compliance, traceability and documentation of processes, integration into clinical workflows, privacy requirements, prioritization and interpretation of results to report based on clinical needs, rapidly evolving knowledge base of genomic alterations and clinical treatments and return of results in a timely and predictable fashion. We also seek to differentiate between the use of precision medicine in germline and cancer.
    Print ISSN: 1467-5463
    Electronic ISSN: 1477-4054
    Topics: Biology , Computer Science
    Published by Oxford University Press
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