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  • Articles  (10)
  • Mice  (10)
  • Gene Expression Regulation, Neoplastic  (3)
  • 2010-2014  (10)
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  • 1
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    Intravascular danger signals guide neutrophils to sites of sterile inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, Braedon -- Pittman, Keir -- Menezes, Gustavo B -- Hirota, Simon A -- Slaba, Ingrid -- Waterhouse, Christopher C M -- Beck, Paul L -- Muruve, Daniel A -- Kubes, Paul -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):362-6. doi: 10.1126/science.1195491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947763" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion ; Chemokine CXCL2/metabolism ; Chemokines/metabolism ; Chemotaxis, Leukocyte ; Cues ; Endothelium, Vascular/physiology ; Inflammation/*immunology/metabolism/*pathology ; Kinetics ; Liver/blood supply/*immunology/metabolism/*pathology ; Liver Diseases/*immunology/metabolism/*pathology ; Macrophage-1 Antigen/physiology ; Mice ; Microscopy/methods ; Microscopy, Confocal ; Microvessels/physiology ; Necrosis ; *Neutrophil Infiltration ; Neutrophils/physiology ; Peptides/metabolism ; Receptors, Formyl Peptide/metabolism ; Receptors, Interleukin-8B/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7 ; Signal Transduction
    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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  • 2
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    The C-terminal domain of RNA polymerase II is modified by site-specific methylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-02
    Description: The carboxy-terminal domain (CTD) of RNA polymerase II (RNAPII) in mammals undergoes extensive posttranslational modification, which is essential for transcriptional initiation and elongation. Here, we show that the CTD of RNAPII is methylated at a single arginine (R1810) by the coactivator-associated arginine methyltransferase 1 (CARM1). Although methylation at R1810 is present on the hyperphosphorylated form of RNAPII in vivo, Ser2 or Ser5 phosphorylation inhibits CARM1 activity toward this site in vitro, suggesting that methylation occurs before transcription initiation. Mutation of R1810 results in the misexpression of a variety of small nuclear RNAs and small nucleolar RNAs, an effect that is also observed in Carm1(-/-) mouse embryo fibroblasts. These results demonstrate that CTD methylation facilitates the expression of select RNAs, perhaps serving to discriminate the RNAPII-associated machinery recruited to distinct gene types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773223/" 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/PMC3773223/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, Robert J 3rd -- Rojas, Luis Alejandro -- Beck, David -- Bonasio, Roberto -- Schuller, Roland -- Drury, William J 3rd -- Eick, Dirk -- Reinberg, Danny -- F32 GM071166/GM/NIGMS NIH HHS/ -- GM-37120/GM/NIGMS NIH HHS/ -- GM-71166/GM/NIGMS NIH HHS/ -- R01 GM037120/GM/NIGMS NIH HHS/ -- R37 GM037120/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):99-103. doi: 10.1126/science.1202663.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI), Department of Biochemistry, New York University School of Medicine, 522 First Avenue, Smilow 211, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/metabolism ; Cell Line ; HeLa Cells ; Humans ; Methylation ; Mice ; Mutation ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Protein-Arginine N-Methyltransferases/metabolism ; RNA Polymerase II/genetics/*metabolism ; RNA, Small Nuclear/metabolism ; RNA, Small Nucleolar/metabolism ; Recombinant Proteins
    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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  • 3
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    The structures of COPI-coated vesicles reveal alternate coatomer conformations and interactions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: Transport between compartments of eukaryotic cells is mediated by coated vesicles. The archetypal protein coats COPI, COPII, and clathrin are conserved from yeast to human. Structural studies of COPII and clathrin coats assembled in vitro without membranes suggest that coat components assemble regular cages with the same set of interactions between components. Detailed three-dimensional structures of coated membrane vesicles have not been obtained. Here, we solved the structures of individual COPI-coated membrane vesicles by cryoelectron tomography and subtomogram averaging of in vitro reconstituted budding reactions. The coat protein complex, coatomer, was observed to adopt alternative conformations to change the number of other coatomers with which it interacts and to form vesicles with variable sizes and shapes. This represents a fundamentally different basis for vesicle coat assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faini, Marco -- Prinz, Simone -- Beck, Rainer -- Schorb, Martin -- Riches, James D -- Bacia, Kirsten -- Brugger, Britta -- Wieland, Felix T -- Briggs, John A G -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1451-4. doi: 10.1126/science.1221443. Epub 2012 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural and Computational Biology Unit, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COP-Coated Vesicles/*chemistry/*ultrastructure ; Coat Protein Complex I/*chemistry ; Coatomer Protein/*chemistry ; Cryoelectron Microscopy ; Electron Microscope Tomography ; Image Processing, Computer-Assisted ; Mice ; Models, Molecular ; Protein Conformation
    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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  • 4
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    Molecular mechanics of cardiac myosin-binding protein C in native thick filaments (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-28
    Description: The heart's pumping capacity results from highly regulated interactions of actomyosin molecular motors. Mutations in the gene for a potential regulator of these motors, cardiac myosin-binding protein C (cMyBP-C), cause hypertrophic cardiomyopathy. However, cMyBP-C's ability to modulate cardiac contractility is not well understood. Using single-particle fluorescence imaging techniques, transgenic protein expression, proteomics, and modeling, we found that cMyBP-C slowed actomyosin motion generation in native cardiac thick filaments. This mechanical effect was localized to where cMyBP-C resides within the thick filament (i.e., the C-zones) and was modulated by phosphorylation and site-specific proteolytic degradation. These results provide molecular insight into why cMyBP-C should be considered a member of a tripartite complex with actin and myosin that allows fine tuning of cardiac muscle contraction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561468/" 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/PMC3561468/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Previs, M J -- Beck Previs, S -- Gulick, J -- Robbins, J -- Warshaw, D M -- 8P20GM103449/GM/NIGMS NIH HHS/ -- HL007647/HL/NHLBI NIH HHS/ -- HL059408/HL/NHLBI NIH HHS/ -- P01 HL059408/HL/NHLBI NIH HHS/ -- P20 GM103449/GM/NIGMS NIH HHS/ -- R01 HL086728/HL/NHLBI NIH HHS/ -- T32 HL007647/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 7;337(6099):1215-8. doi: 10.1126/science.1223602. Epub 2012 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923435" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology ; Actomyosin/metabolism ; Amino Acid Motifs ; Animals ; Carrier Proteins/chemistry/*metabolism ; Mice ; Mice, Transgenic ; *Myocardial Contraction ; Myocardium/*metabolism/ultrastructure ; Myofibrils/*metabolism ; Myosins/*metabolism ; Phosphorylation ; Proteolysis ; Sarcomeres/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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  • 5
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    Distinct stem cells contribute to mammary gland development and maintenance (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-11
    Description: The mammary epithelium is composed of several cell lineages including luminal, alveolar and myoepithelial cells. Transplantation studies have suggested that the mammary epithelium is maintained by the presence of multipotent mammary stem cells. To define the cellular hierarchy of the mammary gland during physiological conditions, we performed genetic lineage-tracing experiments and clonal analysis of the mouse mammary gland during development, adulthood and pregnancy. We found that in postnatal unperturbed mammary gland, both luminal and myoepithelial lineages contain long-lived unipotent stem cells that display extensive renewing capacities, as demonstrated by their ability to clonally expand during morphogenesis and adult life as well as undergo massive expansion during several cycles of pregnancy. The demonstration that the mammary gland contains different types of long-lived stem cells has profound implications for our understanding of mammary gland physiology and will be instrumental in unravelling the cells at the origin of breast cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Keymeulen, Alexandra -- Rocha, Ana Sofia -- Ousset, Marielle -- Beck, Benjamin -- Bouvencourt, Gaelle -- Rock, Jason -- Sharma, Neha -- Dekoninck, Sophie -- Blanpain, Cedric -- England -- Nature. 2011 Oct 9;479(7372):189-93. doi: 10.1038/nature10573.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21983963" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Differentiation ; *Cell Lineage ; Cell Transplantation ; Epithelium ; Female ; Homeostasis ; Lactation/physiology ; Mammary Glands, Animal/*cytology/*growth & development/physiology/transplantation ; Mice ; Multipotent Stem Cells/cytology ; Pregnancy ; Stem Cells/*cytology/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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  • 6
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    A vascular niche and a VEGF-Nrp1 loop regulate the initiation and stemness of skin tumours (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-21
    Description: Angiogenesis is critical during tumour initiation and malignant progression. Different strategies aimed at blocking vascular endothelial growth factor (VEGF) and its receptors have been developed to inhibit angiogenesis in cancer patients. It has become increasingly clear that in addition to its effect on angiogenesis, other mechanisms including a direct effect of VEGF on tumour cells may account for the efficiency of VEGF-blockade therapies. Cancer stem cells (CSCs) have been described in various cancers including squamous tumours of the skin. Here we use a mouse model of skin tumours to investigate the impact of the vascular niche and VEGF signalling on controlling the stemness (the ability to self renew and differentiate) of squamous skin tumours during the early stages of tumour progression. We show that CSCs of skin papillomas are localized in a perivascular niche, in the immediate vicinity of endothelial cells. Furthermore, blocking VEGFR2 caused tumour regression not only by decreasing the microvascular density, but also by reducing CSC pool size and impairing CSC renewal properties. Conditional deletion of Vegfa in tumour epithelial cells caused tumours to regress, whereas VEGF overexpression by tumour epithelial cells accelerated tumour growth. In addition to its well-known effect on angiogenesis, VEGF affected skin tumour growth by promoting cancer stemness and symmetric CSC division, leading to CSC expansion. Moreover, deletion of neuropilin-1 (Nrp1), a VEGF co-receptor expressed in cutaneous CSCs, blocked VEGF's ability to promote cancer stemness and renewal. Our results identify a dual role for tumour-cell-derived VEGF in promoting cancer stemness: by stimulating angiogenesis in a paracrine manner, VEGF creates a perivascular niche for CSCs, and by directly affecting CSCs through Nrp1 in an autocrine loop, VEGF stimulates cancer stemness and renewal. Finally, deletion of Nrp1 in normal epidermis prevents skin tumour initiation. These results may have important implications for the prevention and treatment of skin cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beck, Benjamin -- Driessens, Gregory -- Goossens, Steven -- Youssef, Khalil Kass -- Kuchnio, Anna -- Caauwe, Amelie -- Sotiropoulou, Panagiota A -- Loges, Sonja -- Lapouge, Gaelle -- Candi, Aurelie -- Mascre, Guilhem -- Drogat, Benjamin -- Dekoninck, Sophie -- Haigh, Jody J -- Carmeliet, Peter -- Blanpain, Cedric -- England -- Nature. 2011 Oct 19;478(7369):399-403. doi: 10.1038/nature10525.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IRIBHM, Universite Libre de Bruxelles, 808 route de Lennik, 1070 Brussels, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22012397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/*blood supply/*pathology ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Models, Animal ; Epithelial Cells/cytology ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Mice ; Neoplastic Stem Cells ; Neuropilin-1/genetics/*metabolism ; *Signal Transduction ; Skin Neoplasms/*blood supply/*pathology ; Vascular Endothelial Growth Factor A/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Defining the mode of tumour growth by clonal analysis (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-03
    Description: Recent studies using the isolation of a subpopulation of tumour cells followed by their transplantation into immunodeficient mice provide evidence that certain tumours, including squamous skin tumours, contain cells with high clonogenic potential that have been referred to as cancer stem cells (CSCs). Until now, CSC properties have only been investigated by transplantation assays, and their existence in unperturbed tumour growth is unproven. Here we make use of clonal analysis of squamous skin tumours using genetic lineage tracing to unravel the mode of tumour growth in vivo in its native environment. To this end, we used a genetic labelling strategy that allows individual tumour cells to be marked and traced over time at different stages of tumour progression. Surprisingly, we found that the majority of labelled tumour cells in benign papilloma have only limited proliferative potential, whereas a fraction has the capacity to persist long term, giving rise to progeny that occupy a significant part of the tumour. As well as confirming the presence of two distinct proliferative cell compartments within the papilloma, mirroring the composition, hierarchy and fate behaviour of normal tissue, quantitative analysis of clonal fate data indicates that the more persistent population has stem-cell-like characteristics and cycles twice per day, whereas the second represents a slower cycling transient population that gives rise to terminally differentiated tumour cells. Such behaviour is shown to be consistent with double-labelling experiments and detailed clonal fate characteristics. By contrast, measurements of clone size and proliferative potential in invasive squamous cell carcinoma show a different pattern of behaviour, consistent with geometric expansion of a single CSC population with limited potential for terminal differentiation. This study presents the first experimental evidence for the existence of CSCs during unperturbed solid tumour growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Driessens, Gregory -- Beck, Benjamin -- Caauwe, Amelie -- Simons, Benjamin D -- Blanpain, Cedric -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Aug 23;488(7412):527-30. doi: 10.1038/nature11344.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22854777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/genetics/pathology ; Cell Count ; Cell Differentiation ; *Cell Lineage ; Cell Proliferation ; *Cell Tracking ; Clone Cells/metabolism/pathology ; Disease Models, Animal ; Humans ; Mice ; Models, Biological ; Neoplastic Stem Cells/metabolism/pathology ; Skin Neoplasms/genetics/*pathology ; Stochastic Processes ; Tumor Microenvironment
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" 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/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    SOX2 controls tumour initiation and cancer stem-cell functions in squamous-cell carcinoma (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-06-10
    Description: Cancer stem cells (CSCs) have been reported in various cancers, including in skin squamous-cell carcinoma (SCC). The molecular mechanisms regulating tumour initiation and stemness are still poorly characterized. Here we find that Sox2, a transcription factor expressed in various types of embryonic and adult stem cells, was the most upregulated transcription factor in the CSCs of squamous skin tumours in mice. SOX2 is absent in normal epidermis but begins to be expressed in the vast majority of mouse and human pre-neoplastic skin tumours, and continues to be expressed in a heterogeneous manner in invasive mouse and human SCCs. In contrast to other SCCs, in which SOX2 is frequently genetically amplified, the expression of SOX2 in mouse and human skin SCCs is transcriptionally regulated. Conditional deletion of Sox2 in the mouse epidermis markedly decreases skin tumour formation after chemical-induced carcinogenesis. Using green fluorescent protein (GFP) as a reporter of Sox2 transcriptional expression (SOX2-GFP knock-in mice), we showed that SOX2-expressing cells in invasive SCC are greatly enriched in tumour-propagating cells, which further increase upon serial transplantations. Lineage ablation of SOX2-expressing cells within primary benign and malignant SCCs leads to tumour regression, consistent with the critical role of SOX2-expressing cells in tumour maintenance. Conditional Sox2 deletion in pre-existing skin papilloma and SCC leads to tumour regression and decreases the ability of cancer cells to be propagated upon transplantation into immunodeficient mice, supporting the essential role of SOX2 in regulating CSC functions. Transcriptional profiling of SOX2-GFP-expressing CSCs and of tumour epithelial cells upon Sox2 deletion uncovered a gene network regulated by SOX2 in primary tumour cells in vivo. Chromatin immunoprecipitation identified several direct SOX2 target genes controlling tumour stemness, survival, proliferation, adhesion, invasion and paraneoplastic syndrome. We demonstrate that SOX2, by marking and regulating the functions of skin tumour-initiating cells and CSCs, establishes a continuum between tumour initiation and progression in primary skin tumours.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boumahdi, Soufiane -- Driessens, Gregory -- Lapouge, Gaelle -- Rorive, Sandrine -- Nassar, Dany -- Le Mercier, Marie -- Delatte, Benjamin -- Caauwe, Amelie -- Lenglez, Sandrine -- Nkusi, Erwin -- Brohee, Sylvain -- Salmon, Isabelle -- Dubois, Christine -- del Marmol, Veronique -- Fuks, Francois -- Beck, Benjamin -- Blanpain, Cedric -- England -- Nature. 2014 Jul 10;511(7508):246-50. doi: 10.1038/nature13305. Epub 2014 Jun 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium. ; 1] Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium [2]. ; 1] Department of Pathology, Erasme Hospital, Universite Libre de Bruxelles, Brussels B-1070, Belgium [2] DIAPATH-Center for Microscopy and Molecular Imaging (CMMI), Gosselies B-6041, Belgium. ; Department of Pathology, Erasme Hospital, Universite Libre de Bruxelles, Brussels B-1070, Belgium. ; Laboratory of Cancer Epigenetics, Universite Libre de Bruxelles, Brussels B-1070, Belgium. ; Machine Learning Group, Computer Science Department, Faculte des Sciences, Universite Libre de Bruxelles, Brussels B-1050, Belgium. ; Department of Dermatology, Erasme Hospital, Universite Libre de Bruxelles, Brussels B-1070, Belgium. ; 1] Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium [2] WELBIO, Universite Libre de Bruxelles, Brussels B-1070, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24909994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinoma, Squamous Cell/genetics/pathology ; Cell Adhesion/genetics ; Cell Proliferation ; Cell Transformation, Neoplastic/*genetics/metabolism ; Disease Models, Animal ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Gene Regulatory Networks/genetics ; Mice ; Mice, Inbred Strains ; Neoplastic Stem Cells/*metabolism ; SOXB1 Transcription Factors/genetics/*metabolism ; *Skin Neoplasms/genetics/pathology
    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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  • 10
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    Spiroindolones, a potent compound class for the treatment of malaria (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Recent reports of increased tolerance to artemisinin derivatives--the most recently adopted class of antimalarials--have prompted a need for new treatments. The spirotetrahydro-beta-carbolines, or spiroindolones, are potent drugs that kill the blood stages of Plasmodium falciparum and Plasmodium vivax clinical isolates at low nanomolar concentration. Spiroindolones rapidly inhibit protein synthesis in P. falciparum, an effect that is ablated in parasites bearing nonsynonymous mutations in the gene encoding the P-type cation-transporter ATPase4 (PfATP4). The optimized spiroindolone NITD609 shows pharmacokinetic properties compatible with once-daily oral dosing and has single-dose efficacy in a rodent malaria model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050001/" 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/PMC3050001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rottmann, Matthias -- McNamara, Case -- Yeung, Bryan K S -- Lee, Marcus C S -- Zou, Bin -- Russell, Bruce -- Seitz, Patrick -- Plouffe, David M -- Dharia, Neekesh V -- Tan, Jocelyn -- Cohen, Steven B -- Spencer, Kathryn R -- Gonzalez-Paez, Gonzalo E -- Lakshminarayana, Suresh B -- Goh, Anne -- Suwanarusk, Rossarin -- Jegla, Timothy -- Schmitt, Esther K -- Beck, Hans-Peter -- Brun, Reto -- Nosten, Francois -- Renia, Laurent -- Dartois, Veronique -- Keller, Thomas H -- Fidock, David A -- Winzeler, Elizabeth A -- Diagana, Thierry T -- R01 AI059472/AI/NIAID NIH HHS/ -- R01 AI059472-04/AI/NIAID NIH HHS/ -- R01 AI059472-05/AI/NIAID NIH HHS/ -- R01AI059472/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1175-80. doi: 10.1126/science.1193225.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Tropical and Public Health Institute, Parasite Chemotherapy, CH-4002 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813948" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/antagonists & inhibitors/chemistry/genetics/metabolism ; Animals ; Antimalarials/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Cell Line ; Drug Discovery ; Drug Resistance ; Erythrocytes/parasitology ; Female ; Genes, Protozoan ; Humans ; Indoles/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Malaria/*drug therapy/parasitology ; Male ; Mice ; Models, Molecular ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Mutation ; Parasitic Sensitivity Tests ; Plasmodium berghei/*drug effects ; Plasmodium falciparum/*drug effects/genetics/growth & development ; Plasmodium vivax/*drug effects/growth & development ; Protein Synthesis Inhibitors/administration & ; dosage/chemistry/pharmacokinetics/pharmacology ; Protozoan Proteins/biosynthesis/chemistry/genetics/metabolism ; Rats ; Rats, Wistar ; Spiro Compounds/administration & dosage/chemistry/pharmacokinetics/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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