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  • 1
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    Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-21
    Description: The genetics of renal cancer is dominated by inactivation of the VHL tumour suppressor gene in clear cell carcinoma (ccRCC), the commonest histological subtype. A recent large-scale screen of approximately 3,500 genes by PCR-based exon re-sequencing identified several new cancer genes in ccRCC including UTX (also known as KDM6A), JARID1C (also known as KDM5C) and SETD2 (ref. 2). These genes encode enzymes that demethylate (UTX, JARID1C) or methylate (SETD2) key lysine residues of histone H3. Modification of the methylation state of these lysine residues of histone H3 regulates chromatin structure and is implicated in transcriptional control. However, together these mutations are present in fewer than 15% of ccRCC, suggesting the existence of additional, currently unidentified cancer genes. Here, we have sequenced the protein coding exome in a series of primary ccRCC and report the identification of the SWI/SNF chromatin remodelling complex gene PBRM1 (ref. 4) as a second major ccRCC cancer gene, with truncating mutations in 41% (92/227) of cases. These data further elucidate the somatic genetic architecture of ccRCC and emphasize the marked contribution of aberrant chromatin biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030920/" 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/PMC3030920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varela, Ignacio -- Tarpey, Patrick -- Raine, Keiran -- Huang, Dachuan -- Ong, Choon Kiat -- Stephens, Philip -- Davies, Helen -- Jones, David -- Lin, Meng-Lay -- Teague, Jon -- Bignell, Graham -- Butler, Adam -- Cho, Juok -- Dalgliesh, Gillian L -- Galappaththige, Danushka -- Greenman, Chris -- Hardy, Claire -- Jia, Mingming -- Latimer, Calli -- Lau, King Wai -- Marshall, John -- McLaren, Stuart -- Menzies, Andrew -- Mudie, Laura -- Stebbings, Lucy -- Largaespada, David A -- Wessels, L F A -- Richard, Stephane -- Kahnoski, Richard J -- Anema, John -- Tuveson, David A -- Perez-Mancera, Pedro A -- Mustonen, Ville -- Fischer, Andrej -- Adams, David J -- Rust, Alistair -- Chan-on, Waraporn -- Subimerb, Chutima -- Dykema, Karl -- Furge, Kyle -- Campbell, Peter J -- Teh, Bin Tean -- Stratton, Michael R -- Futreal, P Andrew -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- R01 CA113636/CA/NCI NIH HHS/ -- R01 CA134759/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):539-42. doi: 10.1038/nature09639. Epub 2011 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Renal Cell/*genetics ; Cell Line, Tumor ; Disease Models, Animal ; Gene Expression Regulation ; Gene Knockdown Techniques ; Humans ; Kidney Neoplasms/*genetics ; Mice ; Mutation/*genetics ; Nuclear Proteins/*genetics/*metabolism ; Pancreatic Neoplasms/genetics ; Transcription Factors/*genetics/*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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  • 2
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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
    Published by Nature Publishing Group (NPG)
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  • 3
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    The mutational landscapes of genetic and chemical models of Kras-driven lung cancer (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-11-05
    Description: Next-generation sequencing of human tumours has refined our understanding of the mutational processes operative in cancer initiation and progression, yet major questions remain regarding the factors that induce driver mutations and the processes that shape mutation selection during tumorigenesis. Here we performed whole-exome sequencing on adenomas from three mouse models of non-small-cell lung cancer, which were induced either by exposure to carcinogens (methyl-nitrosourea (MNU) and urethane) or by genetic activation of Kras (Kras(LA2)). Although the MNU-induced tumours carried exactly the same initiating mutation in Kras as seen in the Kras(LA2) model (G12D), MNU tumours had an average of 192 non-synonymous, somatic single-nucleotide variants, compared with only six in tumours from the Kras(LA2) model. By contrast, the Kras(LA2) tumours exhibited a significantly higher level of aneuploidy and copy number alterations compared with the carcinogen-induced tumours, suggesting that carcinogen-induced and genetically engineered models lead to tumour development through different routes. The wild-type allele of Kras has been shown to act as a tumour suppressor in mouse models of non-small-cell lung cancer. We demonstrate that urethane-induced tumours from wild-type mice carry mostly (94%) Kras Q61R mutations, whereas those from Kras heterozygous animals carry mostly (92%) Kras Q61L mutations, indicating a major role for germline Kras status in mutation selection during initiation. The exome-wide mutation spectra in carcinogen-induced tumours overwhelmingly display signatures of the initiating carcinogen, while adenocarcinomas acquire additional C 〉 T mutations at CpG sites. These data provide a basis for understanding results from human tumour genome sequencing, which has identified two broad categories of tumours based on the relative frequency of single-nucleotide variations and copy number alterations, and underline the importance of carcinogen models for understanding the complex mutation spectra seen in human cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304785/" 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/PMC4304785/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westcott, Peter M K -- Halliwill, Kyle D -- To, Minh D -- Rashid, Mamunur -- Rust, Alistair G -- Keane, Thomas M -- Delrosario, Reyno -- Jen, Kuang-Yu -- Gurley, Kay E -- Kemp, Christopher J -- Fredlund, Erik -- Quigley, David A -- Adams, David J -- Balmain, Allan -- 082356/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- A12401/Cancer Research UK/United Kingdom -- A13031/Cancer Research UK/United Kingdom -- A14356/Cancer Research UK/United Kingdom -- F31 CA180669/CA/NCI NIH HHS/ -- F31 CA180715/CA/NCI NIH HHS/ -- R01 CA111834/CA/NCI NIH HHS/ -- R01 CA184510/CA/NCI NIH HHS/ -- T32 GM007175/GM/NIGMS NIH HHS/ -- T32GM007175/GM/NIGMS NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA141455/CA/NCI NIH HHS/ -- U01 CA176287/CA/NCI NIH HHS/ -- U01 CA84244/CA/NCI NIH HHS/ -- UO1 CA176287/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jan 22;517(7535):489-92. doi: 10.1038/nature13898. Epub 2014 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California 94158, USA. ; Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA. ; Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK. ; Department of Pathology, University of California San Francisco, San Francisco, California 94143, USA. ; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Science for Life Laboratory, Department of Oncology-Pathology, Karolinska Institute, Stockholm 171 21, Sweden. ; 1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363767" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemically induced/genetics ; Animals ; Carcinogens/toxicity ; Carcinoma, Non-Small-Cell Lung/chemically induced/genetics ; Cell Transformation, Neoplastic/*chemically induced/*genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; Female ; Genes, ras/*genetics ; Genomic Instability/genetics ; Germ-Line Mutation/genetics ; Humans ; Lung Neoplasms/*chemically induced/*genetics ; Male ; Methylnitrosourea/toxicity ; Mice ; Models, Genetic ; Mutation/*genetics ; Oncogene Protein p21(ras)/*genetics ; Point Mutation/genetics ; Proto-Oncogene Proteins p21(ras)/*genetics ; Urethane/toxicity
    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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  • 4
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    The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: Pancreatic ductal adenocarcinoma (PDA) remains a lethal malignancy despite much progress concerning its molecular characterization. PDA tumours harbour four signature somatic mutations in addition to numerous lower frequency genetic events of uncertain significance. Here we use Sleeping Beauty (SB) transposon-mediated insertional mutagenesis in a mouse model of pancreatic ductal preneoplasia to identify genes that cooperate with oncogenic Kras(G12D) to accelerate tumorigenesis and promote progression. Our screen revealed new candidate genes for PDA and confirmed the importance of many genes and pathways previously implicated in human PDA. The most commonly mutated gene was the X-linked deubiquitinase Usp9x, which was inactivated in over 50% of the tumours. Although previous work had attributed a pro-survival role to USP9X in human neoplasia, we found instead that loss of Usp9x enhances transformation and protects pancreatic cancer cells from anoikis. Clinically, low USP9X protein and messenger RNA expression in PDA correlates with poor survival after surgery, and USP9X levels are inversely associated with metastatic burden in advanced disease. Furthermore, chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in human PDA cell lines, indicating a clinical approach for certain patients. The conditional deletion of Usp9x cooperated with Kras(G12D) to accelerate pancreatic tumorigenesis in mice, validating their genetic interaction. We propose that USP9X is a major tumour suppressor gene with prognostic and therapeutic relevance in PDA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376394/" 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/PMC3376394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perez-Mancera, Pedro A -- Rust, Alistair G -- van der Weyden, Louise -- Kristiansen, Glen -- Li, Allen -- Sarver, Aaron L -- Silverstein, Kevin A T -- Grutzmann, Robert -- Aust, Daniela -- Rummele, Petra -- Knosel, Thomas -- Herd, Colin -- Stemple, Derek L -- Kettleborough, Ross -- Brosnan, Jacqueline A -- Li, Ang -- Morgan, Richard -- Knight, Spencer -- Yu, Jun -- Stegeman, Shane -- Collier, Lara S -- ten Hoeve, Jelle J -- de Ridder, Jeroen -- Klein, Alison P -- Goggins, Michael -- Hruban, Ralph H -- Chang, David K -- Biankin, Andrew V -- Grimmond, Sean M -- Australian Pancreatic Cancer Genome Initiative -- Wessels, Lodewyk F A -- Wood, Stephen A -- Iacobuzio-Donahue, Christine A -- Pilarsky, Christian -- Largaespada, David A -- Adams, David J -- Tuveson, David A -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA122183/CA/NCI NIH HHS/ -- CA128920/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- K01 CA122183/CA/NCI NIH HHS/ -- K01 CA122183-05/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50CA62924/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Apr 29;486(7402):266-70. doi: 10.1038/nature11114.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Li Ka Shing Centre, Cambridge Research Institute, Cancer Research UK, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoikis/genetics ; Carcinoma, Pancreatic Ductal/*enzymology/genetics/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Endopeptidases ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/*enzymology/genetics/pathology ; U937 Cells ; Ubiquitin Thiolesterase/*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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  • 5
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    Magnetic clouds, helicity conservation, and intrinsic scale flux ropes (1995)
    In:  Other Sources
    Details
    Publication Date: 2019-07-17
    Description: An intrinsic-scale flux-rope model for interplanetary magnetic clouds, incorporating conservation of magnetic helicity, flux and mass is found to adequately explain clouds' average thermodynamic and magnetic properties. In spite their continuous expansion as they balloon into interplanetary space, magnetic clouds maintain high temperatures. This is shown to be due to magnetic energy dissipation. The temperature of an expanding cloud is shown to pass through a maximum above its starting temperature if the initial plasma beta in the cloud is less than 2/3. Excess magnetic pressure inside the cloud is not an important driver of the expansion as it is almost balanced by the tension in the helical field lines. It is conservation of magnetic helicity and flux that requires that clouds expand radially as they move away from the Sun. Comparison with published data shows good agreement between measured cloud properties and theory. Parameters determined from theoretical fits to the data, when extended back to the Sun, are consistent with the origin of interplanetary magnetic clouds in solar filament eruptions. A possible extension of the heating mechanism discussed here to heating of the solar corona is discussed.
    Keywords: Solar Physics
    Type: International Solar Wind 8 Conference; 46; NASA-CR-199940
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  • 6
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    Escape of magnetic toroids from the Sun (1995)
    In:  Other Sources
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    Publication Date: 2019-07-17
    Description: Analysis of heliospheric magnetic fields at 1 AU shows that 10(exp 24) Mx of net azimuthal flux escapes from the Sun per solar cycle. This rate is consistent with rates derived from other indicators of flux escape, including coronal mass ejections and filament eruptions. The toroidal flux escape rate is compared with the apparent rate of flux emergence at the solar surface, and it is concluded that escaping toroids will remove at least 20% of the emerging flux, and may remove as much as 100% of emerging flux if multiple eruptions occur on the toroids. The data imply that flux escapes the Sun with an efficiency far exceeding Parker's upper limit estimate of 3%. Toroidal flux escape is almost certainly the source of the observed overwinding of the interplanetary magnetic field spiral. Two mechanisms to facilitate net flux escape are discussed: helicity charging to push open the fields and flux transport with reconnection to close them off. We estimate the Sun will shed approximately 2 x 10(exp 45) of magnetic helicity per solar cycle, leading to a mean helicity density of 100 Mx(exp 2)cm(exp -3) at 1 AU, which agrees well with observations.
    Keywords: Solar Physics
    Type: International Solar Wind 8 Conference; 46; NASA-CR-199940
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  • 7
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    The Solar-B Mission (1997)
    In:  CASI
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    Publication Date: 2019-07-13
    Description: Solar-B, the next ISAS mission (with major NASA participation), is designed to address the fundamental question of how magnetic fields interact with plasma to produce solar variability. The mission has a number of unique capabilities that will enable it to answer the outstanding questions of solar magnetism. First, by escaping atmospheric seeing, it will deliver continuous observations of the solar surface with unprecedented spatial resolution. Second, Solar-B will deliver the first accurate measurements of all three components of the photospheric magnetic field. Solar-B will measure both the magnetic energy driving the photosphere and simultaneously its effects in the corona. Solar-B offers unique programmatic opportunities to NASA. It will continue an effective collaboration with our most reliable international partner. It will deliver images and data that will have strong public outreach potential. Finally, the science of Solar-B is clearly related to the themes of origins and plasma astrophysics, and contributes directly to the national space weather and global change programs.
    Keywords: Solar Physics
    Type: NASA-CR-204628 , NAS 1.26:204628
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  • 8
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    The Flare Genesis Experiment (2002)
    In:  CASI
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    Publication Date: 2019-07-13
    Description: Using the Flare Genesis Experiment (FGE), a balloon-borne observatory with an 80-cm solar telescope we observed the active region NOAA 8844 on January 25, 2000 for several hours. FGE was equipped with a vector polarimeter and a tunable Fabry-Perot narrow-band filter. It recorded time series of filtergrams, vector magnetograms, and Dopplergrams at the Ca(I) 6122.2 angstrom line, and H-alpha filtergrams with a cadence between 2.5 and 7.5 minutes. At the time of the observations, NOAA 8844 was located at approximately 5 N 30 W. The region was rapidly growing during the observations; new magnetic flux was constantly emerging in three supergranules near its center. We describe in detail how the FGE data were analyzed and report on the structure and behavior of peculiar moving dipolar features (MDFs) observed in the active region. In longitudinal magnetograms, the MDFs appeared to be small dipoles in the emerging fields. The east-west orientation of their polarities was opposite that of the sunspots. The dipoles were oriented parallel to their direction of motion, which was in most cases towards the sunspots. Previously, dipolar moving magnetic features have only been observed flowing out from sunspots. Vector magnetograms show that the magnetic field of each MDF negative part was less inclined to the local horizontal than the ones of the positive part. We identify the MDFs as undulations, or stitches, where the emerging flux ropes are still tied to the photosphere. We present a U-loop model that can account for their unusual structure and behavior, and it shows how emerging flux can shed its entrained mass.
    Keywords: Solar Physics
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