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  • 1
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    New York, N.Y. : New York Academy of Sciences
    Call number: 04-ZELL:155/2
    Keywords: Cytoplasmic filaments / Congresses
    Notes: Papers presented at the International Conference on Intermediate Filaments, held by the New York Academy of Sciences, New York, N.Y., May 21-23, 1984.
    Pages: 832 p. : ill.
    ISBN: 0897663055
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    04-ZELL:155/2 departmental collection or stack – please contact the library
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  • 2
    Keywords: CANCER ; EXPRESSION ; COMBINATION ; LUNG ; MODEL ; MODELS ; TOXICITY ; CLASSIFICATION ; liver ; GENE ; GENE-EXPRESSION ; microarray ; validation ; QUALITY ; BREAST ; breast cancer ; BREAST-CANCER ; PERFORMANCE ; gene expression ; MICROARRAY DATA ; HUMANS ; microarrays ; PREDICTION ; PROJECT ; FOLLICULAR LYMPHOMA ; MULTIPLE-MYELOMA ; rodent ; neuroblastoma ; development ; methods ; GENE-EXPRESSION DATA ; DNA MICROARRAYS ; rodents ; RECOMMENDATIONS ; EXPRESSION DATA ; CONTROL MAQC PROJECT ; PUBLISHED MICROARRAY ; RISK-STRATIFICATION
    Abstract: Gene expression data from microarrays are being applied to predict preclinical and clinical endpoints, but the reliability of these predictions has not been established. In the MAQC-II project, 36 independent teams analyzed six microarray data sets to generate predictive models for classifying a sample with respect to one of 13 endpoints indicative of lung or liver toxicity in rodents, or of breast cancer, multiple myeloma or neuroblastoma in humans. In total, 〉30,000 models were built using many combinations of analytical methods. The teams generated predictive models without knowing the biological meaning of some of the endpoints and, to mimic clinical reality, tested the models on data that had not been used for training. We found that model performance depended largely on the endpoint and team proficiency and that different approaches generated models of similar performance. The conclusions and recommendations from MAQC-II should be useful for regulatory agencies, study committees and independent investigators that evaluate methods for global gene expression analysis
    Type of Publication: Journal article published
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  • 3
    Publication Date: 2018-11-21
    Description: Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood with an unmet clinical need for decades. A single oncogenic fusion gene is associated with treatment resistance and a 40 to 45% decrease in overall survival. We previously showed that expression of this PAX3:FOXO1 fusion oncogene in alveolar RMS (aRMS) mediates tolerance to chemotherapy and radiotherapy and that the class I–specific histone deacetylase (HDAC) inhibitor entinostat reduces PAX3:FOXO1 protein abundance. Here, we established the antitumor efficacy of entinostat with chemotherapy in various preclinical cell and mouse models and found that HDAC3 inhibition was the primary mechanism of entinostat-induced suppression of PAX3:FOXO1 abundance. HDAC3 inhibition by entinostat decreased the activity of the chromatin remodeling enzyme SMARCA4, which, in turn, derepressed the microRNA miR-27a. This reexpression of miR-27a led to PAX3:FOXO1 mRNA destabilization and chemotherapy sensitization in aRMS cells in culture and in vivo. Furthermore, a phase 1 clinical trial (ADVL1513) has shown that entinostat is tolerable in children with relapsed or refractory solid tumors and is planned for phase 1B cohort expansion or phase 2 clinical trials. Together, these results implicate an HDAC3–SMARCA4–miR-27a–PAX3:FOXO1 circuit as a driver of chemoresistant aRMS and suggest that targeting this pathway with entinostat may be therapeutically effective in patients.
    Print ISSN: 1945-0877
    Topics: Medicine
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  • 4
    Publication Date: 2018-07-17
    Description: Comprehensive multi-center assessment of small RNA-seq methods for quantitative miRNA profiling Comprehensive multi-center assessment of small RNA-seq methods for quantitative miRNA profiling, Published online: 16 July 2018; doi:10.1038/nbt.4183 Systematic evaluation of library preparation methods for small RNA-seq identifies reproducible and accurate methods.
    Print ISSN: 1087-0156
    Electronic ISSN: 1546-1696
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
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  • 5
    Publication Date: 2018-08-25
    Description: Association between thyroglobulin polymorphisms and autoimmune thyroid disease: a systematic review and meta-analysis of case–control studies Association between thyroglobulin polymorphisms and autoimmune thyroid disease: a systematic review and meta-analysis of case–control studies, Published online: 24 August 2018; doi:10.1038/s41435-018-0042-z Association between thyroglobulin polymorphisms and autoimmune thyroid disease: a systematic review and meta-analysis of case–control studies
    Print ISSN: 1466-4879
    Electronic ISSN: 1476-5470
    Topics: Biology , Medicine
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  • 6
    Publication Date: 2011-06-10
    Description: Cyclin D1 is a component of the core cell cycle machinery. Abnormally high levels of cyclin D1 are detected in many human cancer types. To elucidate the molecular functions of cyclin D1 in human cancers, we performed a proteomic screen for cyclin D1 protein partners in several types of human tumours. Analyses of cyclin D1 interactors revealed a network of DNA repair proteins, including RAD51, a recombinase that drives the homologous recombination process. We found that cyclin D1 directly binds RAD51, and that cyclin D1-RAD51 interaction is induced by radiation. Like RAD51, cyclin D1 is recruited to DNA damage sites in a BRCA2-dependent fashion. Reduction of cyclin D1 levels in human cancer cells impaired recruitment of RAD51 to damaged DNA, impeded the homologous recombination-mediated DNA repair, and increased sensitivity of cells to radiation in vitro and in vivo. This effect was seen in cancer cells lacking the retinoblastoma protein, which do not require D-cyclins for proliferation. These findings reveal an unexpected function of a core cell cycle protein in DNA repair and suggest that targeting cyclin D1 may be beneficial also in retinoblastoma-negative cancers which are currently thought to be unaffected by cyclin D1 inhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134411/" 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/PMC3134411/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jirawatnotai, Siwanon -- Hu, Yiduo -- Michowski, Wojciech -- Elias, Joshua E -- Becks, Lisa -- Bienvenu, Frederic -- Zagozdzon, Agnieszka -- Goswami, Tapasree -- Wang, Yaoyu E -- Clark, Alan B -- Kunkel, Thomas A -- van Harn, Tanja -- Xia, Bing -- Correll, Mick -- Quackenbush, John -- Livingston, David M -- Gygi, Steven P -- Sicinski, Piotr -- P01 CA080111/CA/NCI NIH HHS/ -- P01 CA080111-12/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P01 CA109901-07/CA/NCI NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 CA083688/CA/NCI NIH HHS/ -- R01 CA083688-10/CA/NCI NIH HHS/ -- R01 CA138804/CA/NCI NIH HHS/ -- R01 CA138804-02/CA/NCI NIH HHS/ -- Z01 ES065089-11/Intramural NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):230-4. doi: 10.1038/nature10155.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654808" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Comet Assay ; Cyclin D1/deficiency/*metabolism ; DNA Damage/radiation effects ; *DNA Repair/radiation effects ; HeLa Cells ; Humans ; Mice ; Neoplasms/genetics/*metabolism/pathology ; Protein Binding/radiation effects ; *Protein Interaction Mapping ; Rad51 Recombinase/*metabolism ; Radiation, Ionizing ; Recombination, Genetic/genetics ; Retinoblastoma Protein/deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2018-10-16
    Description: Purpose: Kaposi sarcoma (KS) is a vascular tumor initiated by infection of endothelial cells (ECs) with KS–associated herpesvirus (KSHV). KS is dependent on sustained proinflammatory signals provided by intralesional leukocytes and continued infection of new ECs. However, the sources of these cytokines and infectious virus within lesions are not fully understood. Here, mast cells (MCs) are identified as proinflammatory cells within KS lesions that are permissive for, and activated by, infection with KSHV. Experimental Design: Three validated MC lines were used to assess permissivity of MCs to infection with KSHV and to evaluate MCs activation following infection. Biopsies from 31 AIDS-KS cases and 11 AIDS controls were evaluated by IHC for the presence of MCs in KS lesions and assessment of MC activation state and infection with KSHV. Plasma samples from 26 AIDS-KS, 13 classic KS, and 13 healthy adults were evaluated for levels of MC granule contents tryptase and histamine. Results: In culture, MCs supported latent and lytic KSHV infection, and infection-induced MC degranulation. Within KS lesions, MCs were closely associated with spindle cells. Furthermore, MC activation was extensive within patients with KS, reflected by elevated circulating levels of tryptase and a histamine metabolite. One patient with clinical signs of extensive MC activation was treated with antagonists of MC proinflammatory mediators, which resulted in a rapid and durable regression of AIDS-KS lesions. Conclusions: Using complimentary in vitro and in vivo studies we identify MCs as a potential long-lived reservoir for KSHV and a source of proinflammatory mediators within the KS lesional microenvironment. In addition, we identify MC antagonists as a promising novel therapeutic approach for KS. Clin Cancer Res; 24(20); 5085–97. ©2018 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 8
    Publication Date: 2013-06-07
    Description: Previous investigations of the core gene regulatory circuitry that controls the pluripotency of embryonic stem (ES) cells have largely focused on the roles of transcription, chromatin and non-coding RNA regulators. Alternative splicing represents a widely acting mode of gene regulation, yet its role in regulating ES-cell pluripotency and differentiation is poorly understood. Here we identify the muscleblind-like RNA binding proteins, MBNL1 and MBNL2, as conserved and direct negative regulators of a large program of cassette exon alternative splicing events that are differentially regulated between ES cells and other cell types. Knockdown of MBNL proteins in differentiated cells causes switching to an ES-cell-like alternative splicing pattern for approximately half of these events, whereas overexpression of MBNL proteins in ES cells promotes differentiated-cell-like alternative splicing patterns. Among the MBNL-regulated events is an ES-cell-specific alternative splicing switch in the forkhead family transcription factor FOXP1 that controls pluripotency. Consistent with a central and negative regulatory role for MBNL proteins in pluripotency, their knockdown significantly enhances the expression of key pluripotency genes and the formation of induced pluripotent stem cells during somatic cell reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933998/" 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/PMC3933998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Hong -- Irimia, Manuel -- Ross, P Joel -- Sung, Hoon-Ki -- Alipanahi, Babak -- David, Laurent -- Golipour, Azadeh -- Gabut, Mathieu -- Michael, Iacovos P -- Nachman, Emil N -- Wang, Eric -- Trcka, Dan -- Thompson, Tadeo -- O'Hanlon, Dave -- Slobodeniuc, Valentina -- Barbosa-Morais, Nuno L -- Burge, Christopher B -- Moffat, Jason -- Frey, Brendan J -- Nagy, Andras -- Ellis, James -- Wrana, Jeffrey L -- Blencowe, Benjamin J -- R01 HG002439/HG/NHGRI NIH HHS/ -- R33 MH087908/MH/NIMH NIH HHS/ -- R33MH087908/MH/NIMH NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Jun 13;498(7453):241-5. doi: 10.1038/nature12270. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research and Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739326" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing/genetics ; Amino Acid Motifs ; Animals ; Cell Differentiation/genetics ; Cell Line ; *Cellular Reprogramming ; DNA-Binding Proteins/chemistry/deficiency/genetics/*metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Fibroblasts/cytology/metabolism ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; HeLa Cells ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Kinetics ; Mice ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Repressor Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2011-11-19
    Description: The utility of ferroelectric materials stems from the ability to nucleate and move polarized domains using an electric field. To understand the mechanisms of polarization switching, structural characterization at the nanoscale is required. We used aberration-corrected transmission electron microscopy to follow the kinetics and dynamics of ferroelectric switching at millisecond temporal and subangstrom spatial resolution in an epitaxial bilayer of an antiferromagnetic ferroelectric (BiFeO(3)) on a ferromagnetic electrode (La(0.7)Sr(0.3)MnO(3)). We observed localized nucleation events at the electrode interface, domain wall pinning on point defects, and the formation of ferroelectric domains localized to the ferroelectric and ferromagnetic interface. These results show how defects and interfaces impede full ferroelectric switching of a thin film.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher T -- Gao, Peng -- Jokisaari, Jacob R -- Heikes, Colin -- Adamo, Carolina -- Melville, Alexander -- Baek, Seung-Hyub -- Folkman, Chad M -- Winchester, Benjamin -- Gu, Yijia -- Liu, Yuanming -- Zhang, Kui -- Wang, Enge -- Li, Jiangyu -- Chen, Long-Qing -- Eom, Chang-Beom -- Schlom, Darrell G -- Pan, Xiaoqing -- New York, N.Y. -- Science. 2011 Nov 18;334(6058):968-71. doi: 10.1126/science.1206980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22096196" target="_blank"〉PubMed〈/a〉
    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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  • 10
    Publication Date: 2013-11-23
    Description: The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression, and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here, we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy. In antibiotics-treated or germ-free mice, tumor-infiltrating myeloid-derived cells responded poorly to therapy, resulting in lower cytokine production and tumor necrosis after CpG-oligonucleotide treatment and deficient production of reactive oxygen species and cytotoxicity after chemotherapy. Thus, optimal responses to cancer therapy require an intact commensal microbiota that mediates its effects by modulating myeloid-derived cell functions in the tumor microenvironment. These findings underscore the importance of the microbiota in the outcome of disease treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iida, Noriho -- Dzutsev, Amiran -- Stewart, C Andrew -- Smith, Loretta -- Bouladoux, Nicolas -- Weingarten, Rebecca A -- Molina, Daniel A -- Salcedo, Rosalba -- Back, Timothy -- Cramer, Sarah -- Dai, Ren-Ming -- Kiu, Hiu -- Cardone, Marco -- Naik, Shruti -- Patri, Anil K -- Wang, Ena -- Marincola, Francesco M -- Frank, Karen M -- Belkaid, Yasmine -- Trinchieri, Giorgio -- Goldszmid, Romina S -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):967-70. doi: 10.1126/science.1240527.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/administration & dosage ; Antigen Presentation/genetics ; Antineoplastic Agents/therapeutic use ; Bacteria/drug effects ; Bacterial Physiological Phenomena/drug effects ; Down-Regulation ; Gene Expression Regulation ; Germ-Free Life ; Immunotherapy ; Inflammation/genetics ; Intestines/*microbiology ; Melanoma, Experimental ; Mice ; Mice, Inbred C57BL ; Microbiota/drug effects/*physiology ; Neoplasm Transplantation ; Neoplasms/*immunology/microbiology/*therapy ; Oligodeoxyribonucleotides/therapeutic use ; Organoplatinum Compounds/therapeutic use ; Phagocytosis/genetics ; Reactive Oxygen Species/metabolism ; Symbiosis ; Tumor Microenvironment/*immunology ; Tumor Necrosis Factor-alpha/metabolism
    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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