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  • 1
    Publication Date: 2018-11-10
    Description: Lithium (Li) metal anodes have attracted considerable interest due to their ultrahigh theoretical gravimetric capacity and very low redox potential. However, the issues of nonuniform lithium deposits (dendritic Li) during cycling are hindering the practical applications of Li metal batteries. Herein, we propose a concept of ion redistributors to eliminate dendrites by redistributing Li ions with Al-doped Li 6.75 La 3 Zr 1.75 Ta 0.25 O 12 (LLZTO) coated polypropylene (PP) separators. The LLZTO with three-dimensional ion channels can act as a redistributor to regulate the movement of Li ions, delivering a uniform Li ion distribution for dendrite-free Li deposition. The standard deviation of ion concentration beneath the LLZTO composite separator is 13 times less than that beneath the routine PP separator. A Coulombic efficiency larger than 98% over 450 cycles is achieved in a Li | Cu cell with the LLZTO-coated separator. This approach enables a high specific capacity of 140 mAh g –1 for LiFePO 4 | Li pouch cells and prolonged cycle life span of 800 hours for Li | Li pouch cells, respectively. This strategy is facile and efficient in regulating Li-ion deposition by separator modifications and is a universal method to protect alkali metal anodes in rechargeable batteries.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 2
    Publication Date: 2018-05-25
    Description: Primary liver tumors and liver metastasis currently represent the leading cause of cancer-related death. Commensal bacteria are important regulators of antitumor immunity, and although the liver is exposed to gut bacteria, their role in antitumor surveillance of liver tumors is poorly understood. We found that altering commensal gut bacteria in mice induced a liver-selective antitumor effect, with an increase of hepatic CXCR6 + natural killer T (NKT) cells and heightened interferon- production upon antigen stimulation. In vivo functional studies showed that NKT cells mediated liver-selective tumor inhibition. NKT cell accumulation was regulated by CXCL16 expression of liver sinusoidal endothelial cells, which was controlled by gut microbiome-mediated primary-to-secondary bile acid conversion. Our study suggests a link between gut bacteria–controlled bile acid metabolism and liver antitumor immunosurveillance.
    Keywords: Immunology, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2018-01-03
    Description: Endothelial cells (ECs) in the tumor microenvironment have been reported to play a more active role in solid tumor growth and metastatic dissemination than simply providing the physical structure to form conduits for blood flow; however, the involvement of ECs in the process of triple-negative breast cancer (TNBC) metastasis has not been addressed. Here, we demonstrate that ECs—when mixed with TNBC cells—could increase TNBC cell metastatic potency. After treatment with TGF-β to induce endothelial–mesenchymal transition (EMT), TNBC cells could produce plasminogen activator inhibitor-1 (PAI-1) and stimulate the expression and secretion of the chemokine, CCL5, from ECs, which then acts in a paracrine fashion on TNBC cells to enhance their migration, invasion, and metastasis. CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback loop. Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 signaling via the chemokine receptor, CCR5. Of importance, key features of this pathway are manifested in patients with TNBC and in The Cancer Genome Atlas database. Taken together, our results suggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and illustrate the potential of developing new PAI-1– and CCL5-targeting therapy for patients with TNBC.—Zhang, W., Xu, J., Fang, H., Tang, L., Chen, W., Sun, Q., Zhang, Q., Yang, F., Sun, Z., Cao, L., Wang, Y., Guan, X. Endothelial cells promote triple-negative breast cancer cell metastasis via PAI-1 and CCL5 signaling.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
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  • 4
    Keywords: APOPTOSIS ; neoplasms ; POLYMORPHISMS ; SUSCEPTIBILITY ; leukemia ; FOLLICULAR LYMPHOMA ; TNF ; RHEUMATOID-ARTHRITIS ; GENOME-WIDE ASSOCIATION ; germline variation
    Abstract: Many common genetic variants have been associated with non-Hodgkin lymphoma (NHL), but individual study results are often conflicting. To confirm the role of putative risk alleles in B-cell NHL etiology, we performed a validation genotyping study of 67 candidate single nucleotide polymorphisms within InterLymph, a large international consortium of NHL case-control studies. A meta-analysis was performed on data from 5633 B-cell NHL cases and 7034 controls from 8 InterLymph studies. rs3789068 in the proapoptotic BCL2L11 gene was associated with an increased risk for B-cell NHL (odds ratio = 1.21, P random = 2.21 x 10(-11)), with similar risk estimates for common B-cell subtypes. PRRC2A rs3132453 in the HLA complex class III region conferred a reduced risk of B-cell NHL (odds ratio = 0.68, P random = 1.07 x 10(-9)) and was likewise evident for common B-cell subtypes. These results are consistent with the known biology of NHL and provide insights into shared pathogenic components, including apoptosis and immune regulation, for the major B-cell lymphoma subtypes.
    Type of Publication: Journal article published
    PubMed ID: 23047821
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  • 5
    Abstract: Reduced cardiac vagal control reflected in low heart rate variability (HRV) is associated with greater risks for cardiac morbidity and mortality. In two-stage meta-analyses of genome-wide association studies for three HRV traits in up to 53,174 individuals of European ancestry, we detect 17 genome-wide significant SNPs in eight loci. HRV SNPs tag non-synonymous SNPs (in NDUFA11 and KIAA1755), expression quantitative trait loci (eQTLs) (influencing GNG11, RGS6 and NEO1), or are located in genes preferentially expressed in the sinoatrial node (GNG11, RGS6 and HCN4). Genetic risk scores account for 0.9 to 2.6% of the HRV variance. Significant genetic correlation is found for HRV with heart rate (-0.74〈rg〈-0.55) and blood pressure (-0.35〈rg〈-0.20). These findings provide clinically relevant biological insight into heritable variation in vagal heart rhythm regulation, with a key role for genetic variants (GNG11, RGS6) that influence G-protein heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization.
    Type of Publication: Journal article published
    PubMed ID: 28613276
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  • 6
    ISSN: 1432-0800
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Type of Medium: Electronic Resource
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  • 7
    Publication Date: 2018-07-24
    Description: The intestinal immune system is crucial for protection from pathogenic infection and maintenance of mucosal homeostasis. We studied the intestinal immune microenvironment in a Salmonella enterica serovar Typhimurium intestinal infection mouse model. Intestinal lamina propria macrophages are the main effector cells in innate resistance to intracellular microbial pathogens. We found that S . Typhimurium infection augmented Tim-3 expression on intestinal lamina propria CD4 + T cells and enhanced galectin-9 expression on F4/80 + CD11b + macrophages. Moreover, CD4 + T cells promoted the activation and bactericidal activity of intestinal F4/80 + CD11b + macrophages via the Tim-3/galectin-9 interaction during S . Typhimurium infection. Blocking the Tim-3/galectin-9 interaction with α-lactose significantly attenuated the bactericidal activity of intracellular S . Typhimurium by macrophages. Furthermore, the Tim-3/galectin-9 interaction promoted the formation and activation of inflammasomes, which led to caspase-1 cleavage and interleukin 1β (IL-1β) secretion. The secretion of active IL-1β further improved bactericidal activity of macrophages and galectin-9 expression on macrophages. These results demonstrated the critical role of the cross talk between CD4 + T cells and macrophages, particularly the Tim-3/galectin-9 interaction, in antimicrobial immunity and the control of intestinal pathogenic infections.
    Print ISSN: 0019-9567
    Electronic ISSN: 1098-5522
    Topics: Medicine
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  • 8
    Publication Date: 2014-09-05
    Description: Agriculture faces great challenges to ensure global food security by increasing yields while reducing environmental costs. Here we address this challenge by conducting a total of 153 site-year field experiments covering the main agro-ecological areas for rice, wheat and maize production in China. A set of integrated soil-crop system management practices based on a modern understanding of crop ecophysiology and soil biogeochemistry increases average yields for rice, wheat and maize from 7.2 million grams per hectare (Mg ha(-1)), 7.2 Mg ha(-1) and 10.5 Mg ha(-1) to 8.5 Mg ha(-1), 8.9 Mg ha(-1) and 14.2 Mg ha(-1), respectively, without any increase in nitrogen fertilizer. Model simulation and life-cycle assessment show that reactive nitrogen losses and greenhouse gas emissions are reduced substantially by integrated soil-crop system management. If farmers in China could achieve average grain yields equivalent to 80% of this treatment by 2030, over the same planting area as in 2012, total production of rice, wheat and maize in China would be more than enough to meet the demand for direct human consumption and a substantially increased demand for animal feed, while decreasing the environmental costs of intensive agriculture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xinping -- Cui, Zhenling -- Fan, Mingsheng -- Vitousek, Peter -- Zhao, Ming -- Ma, Wenqi -- Wang, Zhenlin -- Zhang, Weijian -- Yan, Xiaoyuan -- Yang, Jianchang -- Deng, Xiping -- Gao, Qiang -- Zhang, Qiang -- Guo, Shiwei -- Ren, Jun -- Li, Shiqing -- Ye, Youliang -- Wang, Zhaohui -- Huang, Jianliang -- Tang, Qiyuan -- Sun, Yixiang -- Peng, Xianlong -- Zhang, Jiwang -- He, Mingrong -- Zhu, Yunji -- Xue, Jiquan -- Wang, Guiliang -- Wu, Liang -- An, Ning -- Wu, Liangquan -- Ma, Lin -- Zhang, Weifeng -- Zhang, Fusuo -- England -- Nature. 2014 Oct 23;514(7523):486-9. doi: 10.1038/nature13609. Epub 2014 Sep 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] College of Resources &Environmental Sciences, China Agricultural University, Beijing 100193, China [2]. ; College of Resources &Environmental Sciences, China Agricultural University, Beijing 100193, China. ; Department of Biology, Stanford University, Stanford, California 94305, USA. ; Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing 100081, China. ; College of Resources &Environmental Sciences, Agricultural University of Hebei, Baoding 071001, China. ; College of Agronomy, Shandong Agricultural University, Tai'an 271000, China. ; Institute of Soil Science, Chinese Academy of Sciences, Nanjing 210008, China. ; Key Laboratory of Crop Genetics and Physiology of Jiangsu Province, Yangzhou University, Yangzhou 225009, China. ; State Key Laboratory of Soil Erosion and Dryland Farming on the Loess Plateau, Northwest Agriculture and Forestry University, Yangling 712100, China. ; College of Resources &Environmental Sciences, Jilin Agricultural University, Changchun 130118, China. ; Institute of Agricultural Environment and Resource, Shanxi Academy of Agricultural Sciences, Taiyuan 030031, China. ; College of Resources &Environmental Sciences, Nanjing Agricultural University, Nanjing 210095, China. ; Research Center of Agricultural Environment &Resources, Jilin Academy of Agricultural Sciences, Changchun 130033, China. ; College of Resources &Environmental Sciences, Henan Agricultural University, Zhengzhou 450000, China. ; Northwest Agriculture and Forestry University, Yangling 712100, China. ; College of Plant Science &Technology, Huazhong Agricultural University, Wuhan 430070, China. ; Crop Physiology, Ecology &Production Center, Hunan Agricultural University, Changsha 410128, China. ; Soil &Fertilizer Research Institute, Anhui Academy of Agricultural Sciences, Hefei 230031, China. ; College of Resources &Environmental Sciences, Northeast Agricultural University, Harbin 150030, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25186728" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*methods ; Animal Feed ; China ; Edible Grain/*growth & development/*supply & distribution ; *Environment ; Fertilizers/utilization ; Greenhouse Effect/statistics & numerical data ; Nitrogen/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: 2015-08-21
    Description: Nearly three-quarters of the growth in global carbon emissions from the burning of fossil fuels and cement production between 2010 and 2012 occurred in China. Yet estimates of Chinese emissions remain subject to large uncertainty; inventories of China's total fossil fuel carbon emissions in 2008 differ by 0.3 gigatonnes of carbon, or 15 per cent. The primary sources of this uncertainty are conflicting estimates of energy consumption and emission factors, the latter being uncertain because of very few actual measurements representative of the mix of Chinese fuels. Here we re-evaluate China's carbon emissions using updated and harmonized energy consumption and clinker production data and two new and comprehensive sets of measured emission factors for Chinese coal. We find that total energy consumption in China was 10 per cent higher in 2000-2012 than the value reported by China's national statistics, that emission factors for Chinese coal are on average 40 per cent lower than the default values recommended by the Intergovernmental Panel on Climate Change, and that emissions from China's cement production are 45 per cent less than recent estimates. Altogether, our revised estimate of China's CO2 emissions from fossil fuel combustion and cement production is 2.49 gigatonnes of carbon (2 standard deviations = +/-7.3 per cent) in 2013, which is 14 per cent lower than the emissions reported by other prominent inventories. Over the full period 2000 to 2013, our revised estimates are 2.9 gigatonnes of carbon less than previous estimates of China's cumulative carbon emissions. Our findings suggest that overestimation of China's emissions in 2000-2013 may be larger than China's estimated total forest sink in 1990-2007 (2.66 gigatonnes of carbon) or China's land carbon sink in 2000-2009 (2.6 gigatonnes of carbon).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhu -- Guan, Dabo -- Wei, Wei -- Davis, Steven J -- Ciais, Philippe -- Bai, Jin -- Peng, Shushi -- Zhang, Qiang -- Hubacek, Klaus -- Marland, Gregg -- Andres, Robert J -- Crawford-Brown, Douglas -- Lin, Jintai -- Zhao, Hongyan -- Hong, Chaopeng -- Boden, Thomas A -- Feng, Kuishuang -- Peters, Glen P -- Xi, Fengming -- Liu, Junguo -- Li, Yuan -- Zhao, Yu -- Zeng, Ning -- He, Kebin -- England -- Nature. 2015 Aug 20;524(7565):335-8. doi: 10.1038/nature14677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts 02138, USA. ; Institute of Applied Ecology, Chinese Academy of Sciences, Shenyang 110016, China. ; Resnick Sustainability Institute, California Institute of Technology, Pasadena, California 91125, USA. ; Ministry of Education Key Laboratory for Earth System Modeling, Center for Earth System Science, Tsinghua University, Beijing 100084, China. ; School of International Development, University of East Anglia, Norwich NR4 7TJ, UK. ; CAS Key Laboratory of Low-carbon Conversion Science and Engineering, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai 201203, China. ; Department of Earth System Science, University of California, Irvine, California 92697, USA. ; Laboratoire des Sciences du Climat et de l'Environnement, CEA-CNRS-UVSQ, CE Orme des Merisiers, 91191 Gif sur Yvette Cedex, France. ; State Key Laboratory of Coal Conversion, Institute of Coal Chemistry, Chinese Academy of Science, Taiyuan 030001, China. ; CNRS and UJF Grenoble 1, Laboratoire de Glaciologie et Geophysique de l'Environnement (LGGE, UMR5183), 38041 Grenoble, France. ; Department of Geographical Sciences, University of Maryland, College Park, Maryland 20742, USA. ; Research Institute for Environment, Energy, and Economics, Appalachian State University, Boone, North Carolina 28608, USA. ; Carbon Dioxide Information Analysis Center, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, USA. ; Cambridge Centre for Climate Change Mitigation Research, Department of Land Economy, University of Cambridge, 19 Silver Street, Cambridge CB3 9EP, UK. ; Laboratory for Climate and Ocean-Atmosphere Studies, Department of Atmospheric and Oceanic Sciences, School of Physics, Peking University, Beijing 100871, China. ; State Key Joint Laboratory of Environment Simulation and Pollution Control, School of Environment, Tsinghua University, Beijing 100084, China. ; Center for International Climate and Environmental Research-Oslo (CICERO), N-0318 Oslo, Norway. ; CAS Key Laboratory of Pollution Ecology and Environmental Engineering, Chinese Academy of Sciences, Shenyang 110016, China. ; School of Nature Conservation, Beijing Forestry University, Beijing 10083, China. ; Ecosystems Services &Management Program, International Institute for Applied Systems Analysis, Schlossplatz 1, A-2361 Laxenburg, Austria. ; School of Environmental Science and Engineering, South University of Science and Technology of China, Shenzhen 518055, China. ; State Key Laboratory of Pollution Control &Resource Reuse and School of the Environment, Nanjing University, Nanjing 210023, China. ; Department of Atmospheric and Oceanic Science and Earth System Science Interdisciplinary Center, University of Maryland, College Park, Maryland 20742-2425, USA. ; Institute of Atmospheric Physics, Chinese Academy of Sciences, Beijing, 100029, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26289204" target="_blank"〉PubMed〈/a〉
    Keywords: Carbon/*analysis ; Carbon Dioxide/analysis ; Carbon Sequestration ; China ; Climate Change ; Coal/utilization ; Construction Materials/*supply & distribution ; Fossil Fuels/*utilization ; Trees/metabolism ; Uncertainty
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2015-10-20
    Description: The development of life-threatening cancer metastases at distant organs requires disseminated tumour cells' adaptation to, and co-evolution with, the drastically different microenvironments of metastatic sites. Cancer cells of common origin manifest distinct gene expression patterns after metastasizing to different organs. Clearly, the dynamic interaction between metastatic tumour cells and extrinsic signals at individual metastatic organ sites critically effects the subsequent metastatic outgrowth. Yet, it is unclear when and how disseminated tumour cells acquire the essential traits from the microenvironment of metastatic organs that prime their subsequent outgrowth. Here we show that both human and mouse tumour cells with normal expression of PTEN, an important tumour suppressor, lose PTEN expression after dissemination to the brain, but not to other organs. The PTEN level in PTEN-loss brain metastatic tumour cells is restored after leaving the brain microenvironment. This brain microenvironment-dependent, reversible PTEN messenger RNA and protein downregulation is epigenetically regulated by microRNAs from brain astrocytes. Mechanistically, astrocyte-derived exosomes mediate an intercellular transfer of PTEN-targeting microRNAs to metastatic tumour cells, while astrocyte-specific depletion of PTEN-targeting microRNAs or blockade of astrocyte exosome secretion rescues the PTEN loss and suppresses brain metastasis in vivo. Furthermore, this adaptive PTEN loss in brain metastatic tumour cells leads to an increased secretion of the chemokine CCL2, which recruits IBA1-expressing myeloid cells that reciprocally enhance the outgrowth of brain metastatic tumour cells via enhanced proliferation and reduced apoptosis. Our findings demonstrate a remarkable plasticity of PTEN expression in metastatic tumour cells in response to different organ microenvironments, underpinning an essential role of co-evolution between the metastatic cells and their microenvironment during the adaptive metastatic outgrowth. Our findings signify the dynamic and reciprocal cross-talk between tumour cells and the metastatic niche; importantly, they provide new opportunities for effective anti-metastasis therapies, especially of consequence for brain metastasis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Lin -- Zhang, Siyuan -- Yao, Jun -- Lowery, Frank J -- Zhang, Qingling -- Huang, Wen-Chien -- Li, Ping -- Li, Min -- Wang, Xiao -- Zhang, Chenyu -- Wang, Hai -- Ellis, Kenneth -- Cheerathodi, Mujeeburahiman -- McCarty, Joseph H -- Palmieri, Diane -- Saunus, Jodi -- Lakhani, Sunil -- Huang, Suyun -- Sahin, Aysegul A -- Aldape, Kenneth D -- Steeg, Patricia S -- Yu, Dihua -- 5R00CA158066-05/CA/NCI NIH HHS/ -- P01-CA099031/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R00 CA158066/CA/NCI NIH HHS/ -- R01 CA194697/CA/NCI NIH HHS/ -- R01-CA112567-06/CA/NCI NIH HHS/ -- R01CA184836/CA/NCI NIH HHS/ -- England -- Nature. 2015 Nov 5;527(7576):100-4. doi: 10.1038/nature15376. Epub 2015 Oct 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. ; Cancer Biology Program, Graduate School of Biomedical Sciences, Houston, Texas 77030, USA. ; Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556, USA. ; Department of Neurosurgery, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. ; Woman's Malignancies Branch, National Cancer Institute, Bethesda, Maryland 20892, USA. ; The University of Queensland Centre for Clinical Research, Brisbane, Queensland 4029, Australia. ; The School of Medicine and Pathology Queensland, Brisbane, Queensland 4029, Australia. ; The Royal Brisbane and Women's Hospital, Brisbane, Queensland 4029, Australia. ; Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. ; Center for Molecular Medicine, China Medical University, Taichung 40402, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26479035" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/genetics ; Animals ; Astrocytes/cytology/metabolism ; Brain/metabolism/pathology ; Brain Neoplasms/metabolism/*pathology/*secondary ; Cell Proliferation/genetics ; Chemokine CCL2/secretion ; DNA-Binding Proteins/metabolism ; Down-Regulation/genetics ; Evolution, Molecular ; Exosomes/*genetics/metabolism/secretion ; Female ; *Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Male ; Mice ; MicroRNAs/*genetics ; PTEN Phosphohydrolase/*deficiency/genetics ; RNA, Messenger/analysis/genetics ; *Tumor Microenvironment/genetics ; Tumor Suppressor Proteins/deficiency/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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