Institution
Novartis
Company•Basel, Switzerland•
About: Novartis is a company organization based out in Basel, Switzerland. It is known for research contribution in the topics: Alkyl & Population. The organization has 41930 authors who have published 50566 publications receiving 1978996 citations. The organization is also known as: Novartis International AG.
Topics: Alkyl, Population, Alkoxy group, Receptor, Cancer
Papers published on a yearly basis
Papers
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Novartis1, Icahn School of Medicine at Mount Sinai2, Emory University3, Children's Hospital of Philadelphia4, University of Utah5, Ghent University Hospital6, Oregon Health & Science University7, Kyoto University8, Oslo University Hospital9, Cincinnati Children's Hospital Medical Center10, University of Minnesota11
TL;DR: Mutations in the CD19 gene suggesting irreversible loss of its surface expression are identified in the majority of analyzed cases of CD19– relapse in two clinical trials of pediatric ALL CD19 CAR T therapy, offering considerations for the rational choice of follow-up therapies.
Abstract: We identified genetic mutations in CD19 and loss of heterozygosity at the time of CD19- relapse to chimeric antigen receptor (CAR) therapy. The mutations are present in the vast majority of resistant tumor cells and are predicted to lead to a truncated protein with a nonfunctional or absent transmembrane domain and consequently to a loss of surface antigen. This irreversible loss of CD19 advocates for an alternative targeting or combination CAR approach.
356 citations
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TL;DR: Jordi Barretina, Giordano Caponigro, Nicolas Stransky, Kavitha Venkatesan, Adam A. Golub, Michael P. Morais, Jodi Meltzer, Judit Jané-Valbuena, Felipa A. Mapa, Joseph Thibault, Eva Bric-Furlong, Pichai Raman, Aaron Shipway, Ingo H. Engels, Jill Cheng, Guoying K. Yu
Abstract: Jordi Barretina, Giordano Caponigro, Nicolas Stransky, Kavitha Venkatesan, Adam A. Margolin, Sungjoon Kim, Christopher J. Wilson, Joseph Lehár, Gregory V. Kryukov, Dmitriy Sonkin, Anupama Reddy, Manway Liu, Lauren Murray, Michael F. Berger, John E. Monahan, Paula Morais, Jodi Meltzer, Adam Korejwa, Judit Jané-Valbuena, Felipa A. Mapa, Joseph Thibault, Eva Bric-Furlong, Pichai Raman, Aaron Shipway, Ingo H. Engels, Jill Cheng, Guoying K. Yu, Jianjun Yu, Peter Aspesi Jr, Melanie de Silva, Kalpana Jagtap, Michael D. Jones, Li Wang, Charles Hatton, Emanuele Palescandolo, Supriya Gupta, Scott Mahan, Carrie Sougnez, Robert C. Onofrio, Ted Liefeld, Laura MacConaill, Wendy Winckler, Michael Reich, Nanxin Li, Jill P. Mesirov, Stacey B. Gabriel, Gad Getz, Kristin Ardlie, Vivien Chan, Vic E. Myer, Barbara L. Weber, Jeff Porter, Markus Warmuth, Peter Finan, Jennifer L. Harris, Matthew Meyerson, Todd R. Golub, Michael P. Morrissey, William R. Sellers, Robert Schlegel & Levi A. Garraway
356 citations
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TL;DR: Results indicate that Dot1L and H3K79 methylation play important roles in heterochromatin formation and in embryonic development.
Abstract: Dot1 is an evolutionarily conserved histone methyltransferase specific for lysine 79 of histone H3 (H3K79). In Saccharomyces cerevisiae, Dot1-mediated H3K79 methylation is associated with telomere silencing, meiotic checkpoint control, and DNA damage response. The biological function of H3K79 methylation in mammals, however, remains poorly understood. Using gene targeting, we generated mice deficient for Dot1L, the murine Dot1 homologue. Dot1L-deficient embryos show multiple developmental abnormalities, including growth impairment, angiogenesis defects in the yolk sac, and cardiac dilation, and die between 9.5 and 10.5 days post coitum. To gain insights into the cellular function of Dot1L, we derived embryonic stem (ES) cells from Dot1L mutant blastocysts. Dot1L-deficient ES cells show global loss of H3K79 methylation as well as reduced levels of heterochromatic marks (H3K9 di-methylation and H4K20 tri-methylation) at centromeres and telomeres. These changes are accompanied by aneuploidy, telomere elongation, and proliferation defects. Taken together, these results indicate that Dot1L and H3K79 methylation play important roles in heterochromatin formation and in embryonic development.
356 citations
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21 Dec 1993TL;DR: In this paper, a method of inhibiting matrix-degrading metalloproteinase (MDE) dependent conditions in mammals using such compounds is described. But this method is not suitable for humans.
Abstract: The invention relates to the compounds of formula I ##STR1## pharmaceutically acceptable prodrug derivatives and pharmaceutically acceptable salts thereof; methods for preparation thereof; pharmaceutical compositions comprising said compounds; and a method of inhibiting matrix-degrading metalloproteinase and of treating matrix-degrading metalloproteinase dependent conditions in mammals using such compounds.
355 citations
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TL;DR: The regional distribution of adenosine A2 receptors in the rat brain was determined using the A2-selective agonist ligand [3H](2-p-carboxyethyl)phenylamino)-5'-N- carboxamidoadenosine (CGS 21680) by quantitative receptor autoradiography to provide further evidence for a specific contribution of adenoine in the modulation of central neurotransmission.
354 citations
Authors
Showing all 41972 results
Name | H-index | Papers | Citations |
---|---|---|---|
Irving L. Weissman | 201 | 1141 | 172504 |
Peter J. Barnes | 194 | 1530 | 166618 |
Paul G. Richardson | 183 | 1533 | 155912 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Jie Zhang | 178 | 4857 | 221720 |
Lei Jiang | 170 | 2244 | 135205 |
Marc A. Pfeffer | 166 | 765 | 133043 |
Jorge E. Cortes | 163 | 2784 | 124154 |
Ian A. Wilson | 158 | 971 | 98221 |
Peter G. Schultz | 156 | 893 | 89716 |
Bruce D. Walker | 155 | 779 | 86020 |
Timothy P. Hughes | 145 | 831 | 91357 |
Kurt Wüthrich | 143 | 739 | 103253 |
Leonard Guarente | 143 | 352 | 80169 |
Christopher D.M. Fletcher | 138 | 674 | 82484 |