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TABLE OF CONTENTS
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July 2018 Volume 24, Issue 7 |
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| Editorial News Feature Correspondence Q&A Research Highlights News & Views Review Articles Brief Communications Letters Articles | | Advertisement | | | | nature.com webcasts Nature Research Custom Media presents a webcast on: Combining scRNA-seq and Flow Analyses Date: Tuesday, July 24, 2018 Join our webcast to learn how fluorescence intensity information from flow parameters can be merged into a single-cell RNA expression matrix and analysed. This webcast has been produced on behalf of the sponsor who retains sole responsibility for content | | | |
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Harrington drug discovery research grants - awards up to $700,000 Harrington Discovery Institute at University Hospitals in Cleveland, Ohio invites Full Applications for the 2019 Harrington Scholar-Innovator Award, offering physician-scientists the resources to advance discoveries into medicines. Full Applications are accepted through May 10, 2018. Apply now at HarringtonDiscovery.org/Grant. | | |
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Editorial | |
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Actionable equality p881 doi:10.1038/s41591-018-0118-3 |
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News Feature | |
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Matching up pp882 - 884 Shraddha Chakradhar doi:10.1038/s41591-018-0113-8 |
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Homeward bound pp885 - 889 Shraddha Chakradhar doi:10.1038/s41591-018-0112-9 |
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Correspondence | |
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F508del-CFTR is not corrected by thymosin α1 pp890 - 891 Elizabeth Matthes, John W. Hanrahan & André M. Cantin doi:10.1038/s41591-018-0079-6 |
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Reply to ‘F508del-CFTR is not corrected by thymosin α1’ pp891 - 893 Luigina Romani, Claudia Stincardini, Stefano Giovagnoli, Maurizio Paci, Valeria R. Villella et al. doi:10.1038/s41591-018-0080-0 |
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Nature Outlook: The future of medicine Modern medicine is affording people longer and healthier lives. But researchers want to take improvements in health even further. With advances in gene editing, technology to overcome paralysis and efforts to address high drug costs, the future of medicine is bright. Get your free access >> Produced with support from Merck KGaA, Darmstadt, Germany | |
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Q&A | |
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Searching for Alzheimer’s disease therapies pp894 - 897 Hannah Stower doi:10.1038/s41591-018-0127-2 |
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Research Highlights | |
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News & Views | |
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A path to efficient gene editing pp899 - 900 Fyodor D. Urnov doi:10.1038/s41591-018-0110-y |
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Fire prevention in the Parkinson’s disease brain pp900 - 902 Lena Brundin, Liza Bergkvist & Patrik Brundin doi:10.1038/s41591-018-0109-4 |
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A treatment strategy for KRAS-driven tumors pp902 - 904 Trang T. Mai & Piro Lito doi:10.1038/s41591-018-0111-x |
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Predicting progression to AML pp904 - 906 Rob S. Sellar, Siddhartha Jaiswal & Benjamin L. Ebert doi:10.1038/s41591-018-0114-7 |
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Microbiome metabolomics reveals new drivers of human liver steatosis pp906 - 907 Nathalie M. Delzenne & Laure B. Bindels doi:10.1038/s41591-018-0126-3 |
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Review Articles | |
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Mechanisms of NAFLD development and therapeutic strategies pp908 - 922 Scott L. Friedman, Brent A. Neuschwander-Tetri, Mary Rinella & Arun J. Sanyal doi:10.1038/s41591-018-0104-9 Understanding of pathogenic mechanisms and clinical features of NAFLD is driving progress in therapeutic strategies now in clinical trials. |
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Brief Communications | |
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Rapid HIV RNA rebound after antiretroviral treatment interruption in persons durably suppressed in Fiebig I acute HIV infection pp923 - 926 Donn J. Colby, Lydie Trautmann, Suteeraporn Pinyakorn, Louise Leyre, Amélie Pagliuzza et al. doi:10.1038/s41591-018-0026-6 Initiation of antiretroviral therapy in the first 2 weeks of HIV infection fails to prevent resurgence of virus after stopping treatment, indicating early establishment of a resilient viral reservoir. |
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CRISPR–Cas9 genome editing induces a p53-mediated DNA damage response pp927 - 930 doi:10.1038/s41591-018-0049-z CRISPR–Cas9-induced DNA damage triggers p53 to limit the efficiency of gene editing in immortalized human retinal pigment epithelial cells. |
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Letters | |
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Block of A1 astrocyte conversion by microglia is neuroprotective in models of Parkinson’s disease pp931 - 938 Seung Pil Yun, Tae-In Kam, Nikhil Panicker, SangMin Kim, Yumin Oh et al. doi:10.1038/s41591-018-0051-5 Agonism of microglial glucagon-like peptide-1 receptor (GLP1R) using a brain-penetrant peptide prevents the generation of neurotoxic astrocytes and ameliorates disease progression in two rodent models of Parkinson’s disease. |
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p53 inhibits CRISPR–Cas9 engineering in human pluripotent stem cells pp939 - 946 Robert J. Ihry, Kathleen A. Worringer, Max R. Salick, Elizabeth Frias, Daniel Ho et al. doi:10.1038/s41591-018-0050-6 CRISPR–Cas9-induced DNA damage triggers p53 to limit the efficiency of gene editing in human pluripotent cells. |
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DNA repair processes are critical mediators of p53-dependent tumor suppression pp947 - 953 Ana Janic, Liz J. Valente, Matthew J. Wakefield, Leon Di Stefano, Liz Milla et al. doi:10.1038/s41591-018-0043-5 In vivo shRNA screens in sensitized genetic backgrounds identify p53-activated target genes involved in DNA repair that enable its tumor suppressor function. |
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Mutant KRAS-driven cancers depend on PTPN11/SHP2 phosphatase pp954 - 960 Dietrich A. Ruess, Guus J. Heynen, Katrin J. Ciecielski, Jiaoyu Ai, Alexandra Berninger et al. doi:10.1038/s41591-018-0024-8 The phosphatase SHP2 is required for mutant KRAS signaling in pancreatic and non-small-cell lung cancers and drives resistance to MEK inhibition. |
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SHP2 is required for growth of KRAS-mutant non-small-cell lung cancer in vivo pp961 - 967 Sara Mainardi, Antonio Mulero-Sánchez, Anirudh Prahallad, Giovanni Germano, Astrid Bosma et al. doi:10.1038/s41591-018-0023-9 Combined inhibition of SHP2 and MEK is an effective therapeutic approach in non-small-cell lung cancer. |
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Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition pp968 - 977 Gabrielle S. Wong, Jin Zhou, Jie Bin Liu, Zhong Wu, Xinsen Xu et al. doi:10.1038/s41591-018-0022-x Amplification of wild-type KRAS in a subset of gastroesophageal tumors drives intrinsic resistance to MAPK inhibition that can be overcome by combined targeting of MEK and SHP2. |
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Global characterization of T cells in non-small-cell lung cancer by single-cell sequencing pp978 - 985 Xinyi Guo, Yuanyuan Zhang, Liangtao Zheng, Chunhong Zheng, Jintao Song et al. doi:10.1038/s41591-018-0045-3 Deep single-cell RNA sequencing of tumor-infiltrating T cells in non-small-cell lung cancer identifies features associated with functional states and clinical outcome |
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Single-cell profiling of breast cancer T cells reveals a tissue-resident memory subset associated with improved prognosis pp986 - 993 Peter Savas, Balaji Virassamy, Chengzhong Ye, Agus Salim, Christopher P. Mintoff et al. doi:10.1038/s41591-018-0078-7 Extensive, high-dimensional characterization of T cells in breast cancer reveals activated TRM population and a gene signature associated with improved prognosis. |
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Articles | |
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A transcriptionally and functionally distinct PD-1+ CD8+ T cell pool with predictive potential in non-small-cell lung cancer treated with PD-1 blockade pp994 - 1004 Daniela S. Thommen, Viktor H. Koelzer, Petra Herzig, Andreas Roller, Marcel Trefny et al. doi:10.1038/s41591-018-0057-z Tumor-infiltrating CD8+ T cells with high expression of PD-1 in non-small-cell lung cancer are distinct from exhausted T cells in chronic virus infection, have high tumor reactivity and associate with response to PD-1-targeted immunotherapy. |
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A human anti-IL-2 antibody that potentiates regulatory T cells by a structure-based mechanism pp1005 - 1014 Eleonora Trotta, Paul H. Bessette, Stephanie L. Silveria, Lauren K. Ely, Kevin M. Jude et al. doi:10.1038/s41591-018-0070-2 A human anti-IL-2 antibody that selectively expands regulatory T cells is developed in this study for clinical applications aiming to mitigate autoimmune and inflammatory disorders and to promote transplant tolerance. |
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Somatic mutations precede acute myeloid leukemia years before diagnosis pp1015 - 1023 Pinkal Desai, Nuria Mencia-Trinchant, Oleksandr Savenkov, Michael S. Simon, Gloria Cheang et al. doi:10.1038/s41591-018-0081-z Somatic mutations detected years before diagnosis increase the odds of development of acute myeloid leukemia in women. |
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STAT3 labels a subpopulation of reactive astrocytes required for brain metastasis pp1024 - 1035 Neibla Priego, Lucía Zhu, Cátia Monteiro, Manon Mulders, David Wasilewski et al. doi:10.1038/s41591-018-0044-4 Reactive astrocytes expressing STAT3 support the metastatic growth of tumor cells colonizing the brain and can be pharmacologically targeted to improve the clinical management of patients with secondary brain tumors. |
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An inhibitor of oxidative phosphorylation exploits cancer vulnerability pp1036 - 1046 Jennifer R. Molina, Yuting Sun, Marina Protopopova, Sonal Gera, Madhavi Bandi et al. doi:10.1038/s41591-018-0052-4 A new inhibitor targeting the mitochondrial complex I shows antitumor activity in preclinical models of acute myeloid leukemia and glioblastoma relying on oxidative phosphorylation. |
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Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer pp1047 - 1057 Yonathan Lissanu Deribe, Yuting Sun, Christopher Terranova, Fatima Khan, Juan Martinez-Ledesma et al. doi:10.1038/s41591-018-0019-5 SMARCA4 loss in non-small-cell lung cancer creates a metabolic dependency on oxidative phosphorylation that can be targeted using a new small-molecule inhibitor. |
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Inactivating hepatic follistatin alleviates hyperglycemia pp1058 - 1069 Rongya Tao, Caixia Wang, Oliver Stöhr, Wei Qiu, Yue Hu et al. doi:10.1038/s41591-018-0048-0 Follistatin acts as a hepatokine to induce insulin resistance and can be targeted to improve diabetes in mice. |
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Molecular phenomics and metagenomics of hepatic steatosis in non-diabetic obese women pp1070 - 1080 Lesley Hoyles, José-Manuel Fernández-Real, Massimo Federici, Matteo Serino, James Abbott et al. doi:10.1038/s41591-018-0061-3 Metabolic activity of specific human gut microorganisms contributes to liver steatosis in obese women. |
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Focal Point on Japan's Designated National University Initiative Japan's radical new program to boost just a handful of universities has precedents across the world Access free online | | |
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