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  • 1
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    The causes and consequences of genetic heterogeneity in cancer evolution (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-21
    Description: Recent studies have revealed extensive genetic diversity both between and within tumours. This heterogeneity affects key cancer pathways, driving phenotypic variation, and poses a significant challenge to personalized cancer medicine. A major cause of genetic heterogeneity in cancer is genomic instability. This instability leads to an increased mutation rate and can shape the evolution of the cancer genome through a plethora of mechanisms. By understanding these mechanisms we can gain insight into the common pathways of tumour evolution that could support the development of future therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burrell, Rebecca A -- McGranahan, Nicholas -- Bartek, Jiri -- Swanton, Charles -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Sep 19;501(7467):338-45. doi: 10.1038/nature12625.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24048066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Progression ; *Genetic Heterogeneity ; Genomic Instability/genetics ; Humans ; Neoplasms/*genetics/metabolism/*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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  • 2
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    HELQ promotes RAD51 paralogue-dependent repair to avert germ cell loss and tumorigenesis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-06
    Description: Repair of interstrand crosslinks (ICLs) requires the coordinated action of the intra-S-phase checkpoint and the Fanconi anaemia pathway, which promote ICL incision, translesion synthesis and homologous recombination (reviewed in refs 1, 2). Previous studies have implicated the 3'-5' superfamily 2 helicase HELQ in ICL repair in Drosophila melanogaster (MUS301 (ref. 3)) and Caenorhabditis elegans (HELQ-1 (ref. 4)). Although in vitro analysis suggests that HELQ preferentially unwinds synthetic replication fork substrates with 3' single-stranded DNA overhangs and also disrupts protein-DNA interactions while translocating along DNA, little is known regarding its functions in mammalian organisms. Here we report that HELQ helicase-deficient mice exhibit subfertility, germ cell attrition, ICL sensitivity and tumour predisposition, with Helq heterozygous mice exhibiting a similar, albeit less severe, phenotype than the null, indicative of haploinsufficiency. We establish that HELQ interacts directly with the RAD51 paralogue complex BCDX2 and functions in parallel to the Fanconi anaemia pathway to promote efficient homologous recombination at damaged replication forks. Thus, our results reveal a critical role for HELQ in replication-coupled DNA repair, germ cell maintenance and tumour suppression in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836231/" 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/PMC3836231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adelman, Carrie A -- Lolo, Rafal L -- Birkbak, Nicolai J -- Murina, Olga -- Matsuzaki, Kenichiro -- Horejsi, Zuzana -- Parmar, Kalindi -- Borel, Valerie -- Skehel, J Mark -- Stamp, Gordon -- D'Andrea, Alan -- Sartori, Alessandro A -- Swanton, Charles -- Boulton, Simon J -- A3549/Cancer Research UK/United Kingdom -- R01 DK043889/DK/NIDDK NIH HHS/ -- R01-DK43889/DK/NIDDK NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2013 Oct 17;502(7471):381-4. doi: 10.1038/nature12565. Epub 2013 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24005329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenesis/genetics/pathology ; DNA Damage/genetics ; DNA Helicases/deficiency/genetics/*metabolism ; *DNA Repair/genetics ; DNA Replication/genetics ; Fanconi Anemia/metabolism ; Fanconi Anemia Complementation Group D2 Protein/deficiency/genetics/metabolism ; Female ; Gene Deletion ; Germ Cells/cytology/*metabolism/*pathology ; Male ; Mice ; Multiprotein Complexes/metabolism ; Ovarian Neoplasms/genetics/metabolism/pathology ; Ovary/metabolism/pathology ; Rad51 Recombinase/*metabolism ; Recombinational DNA Repair/genetics
    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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    Replication stress links structural and numerical cancer chromosomal instability (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-01
    Description: Cancer chromosomal instability (CIN) results in an increased rate of change of chromosome number and structure and generates intratumour heterogeneity. CIN is observed in most solid tumours and is associated with both poor prognosis and drug resistance. Understanding a mechanistic basis for CIN is therefore paramount. Here we find evidence for impaired replication fork progression and increased DNA replication stress in CIN(+) colorectal cancer (CRC) cells relative to CIN(-) CRC cells, with structural chromosome abnormalities precipitating chromosome missegregation in mitosis. We identify three new CIN-suppressor genes (PIGN (also known as MCD4), MEX3C (RKHD2) and ZNF516 (KIAA0222)) encoded on chromosome 18q that are subject to frequent copy number loss in CIN(+) CRC. Chromosome 18q loss was temporally associated with aneuploidy onset at the adenoma-carcinoma transition. CIN-suppressor gene silencing leads to DNA replication stress, structural chromosome abnormalities and chromosome missegregation. Supplementing cells with nucleosides, to alleviate replication-associated damage, reduces the frequency of chromosome segregation errors after CIN-suppressor gene silencing, and attenuates segregation errors and DNA damage in CIN(+) cells. These data implicate a central role for replication stress in the generation of structural and numerical CIN, which may inform new therapeutic approaches to limit intratumour heterogeneity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636055/" 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/PMC4636055/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burrell, Rebecca A -- McClelland, Sarah E -- Endesfelder, David -- Groth, Petra -- Weller, Marie-Christine -- Shaikh, Nadeem -- Domingo, Enric -- Kanu, Nnennaya -- Dewhurst, Sally M -- Gronroos, Eva -- Chew, Su Kit -- Rowan, Andrew J -- Schenk, Arne -- Sheffer, Michal -- Howell, Michael -- Kschischo, Maik -- Behrens, Axel -- Helleday, Thomas -- Bartek, Jiri -- Tomlinson, Ian P -- Swanton, Charles -- 090532/Wellcome Trust/United Kingdom -- A11590/Cancer Research UK/United Kingdom -- A17786/Cancer Research UK/United Kingdom -- A19310/Cancer Research UK/United Kingdom -- A4688/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Feb 28;494(7438):492-6. doi: 10.1038/nature11935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446422" target="_blank"〉PubMed〈/a〉
    Keywords: Aneuploidy ; Cell Line, Tumor ; Chromosomal Instability/drug effects/*genetics ; Chromosome Segregation/drug effects/genetics ; Chromosomes, Human, Pair 18/drug effects/genetics ; Colorectal Neoplasms/*genetics/pathology ; DNA Copy Number Variations/genetics ; DNA Damage/drug effects/genetics ; DNA Replication/drug effects/*genetics ; Gene Deletion ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Mitosis/drug effects ; Nucleosides/pharmacology ; Phosphotransferases/genetics ; RNA-Binding Proteins/genetics
    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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    Spatial and temporal diversity in genomic instability processes defines lung cancer evolution (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-11
    Description: Spatial and temporal dissection of the genomic changes occurring during the evolution of human non-small cell lung cancer (NSCLC) may help elucidate the basis for its dismal prognosis. We sequenced 25 spatially distinct regions from seven operable NSCLCs and found evidence of branched evolution, with driver mutations arising before and after subclonal diversification. There was pronounced intratumor heterogeneity in copy number alterations, translocations, and mutations associated with APOBEC cytidine deaminase activity. Despite maintained carcinogen exposure, tumors from smokers showed a relative decrease in smoking-related mutations over time, accompanied by an increase in APOBEC-associated mutations. In tumors from former smokers, genome-doubling occurred within a smoking-signature context before subclonal diversification, which suggested that a long period of tumor latency had preceded clinical detection. The regionally separated driver mutations, coupled with the relentless and heterogeneous nature of the genome instability processes, are likely to confound treatment success in NSCLC.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636050/" 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/PMC4636050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Bruin, Elza C -- McGranahan, Nicholas -- Mitter, Richard -- Salm, Max -- Wedge, David C -- Yates, Lucy -- Jamal-Hanjani, Mariam -- Shafi, Seema -- Murugaesu, Nirupa -- Rowan, Andrew J -- Gronroos, Eva -- Muhammad, Madiha A -- Horswell, Stuart -- Gerlinger, Marco -- Varela, Ignacio -- Jones, David -- Marshall, John -- Voet, Thierry -- Van Loo, Peter -- Rassl, Doris M -- Rintoul, Robert C -- Janes, Sam M -- Lee, Siow-Ming -- Forster, Martin -- Ahmad, Tanya -- Lawrence, David -- Falzon, Mary -- Capitanio, Arrigo -- Harkins, Timothy T -- Lee, Clarence C -- Tom, Warren -- Teefe, Enock -- Chen, Shann-Ching -- Begum, Sharmin -- Rabinowitz, Adam -- Phillimore, Benjamin -- Spencer-Dene, Bradley -- Stamp, Gordon -- Szallasi, Zoltan -- Matthews, Nik -- Stewart, Aengus -- Campbell, Peter -- Swanton, Charles -- 088340/Wellcome Trust/United Kingdom -- 091730/Wellcome Trust/United Kingdom -- 105104/Wellcome Trust/United Kingdom -- A11590/Cancer Research UK/United Kingdom -- A17786/Cancer Research UK/United Kingdom -- A19310/Cancer Research UK/United Kingdom -- A4688/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):251-6. doi: 10.1126/science.1253462.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London WC1E 6BT, UK. ; Cancer Research UK London Research Institute, London WC2A 3LY, UK. Centre for Mathematics and Physics in the Life Science and Experimental Biology (CoMPLEX), University College London, London WC1E 6BT, UK. ; Cancer Research UK London Research Institute, London WC2A 3LY, UK. ; Wellcome Trust Sanger Institute, Hinxton, CB10 1SA, UK. ; Wellcome Trust Sanger Institute, Hinxton, CB10 1SA, UK. University of Cambridge, Cambridge CB2 1TN, UK. ; Instituto de Biomedicina y Biotecnologia de Cantabria (CSIC-UC-Sodercan), Departamento de Biologia Molecular, Universidad de Cantabria, Santander, Spain. ; Wellcome Trust Sanger Institute, Hinxton, CB10 1SA, UK. Department of Human Genetics, University of Leuven, 3000 Leuven, Belgium. ; Papworth Hospital NHS Foundation Trust, Cambridge CB23 3RE, UK. ; Lungs for Living Research Centre, University College London, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London WC1E 6BT, UK. University College London Hospitals, London NW1 2BU, UK. ; University College London Hospitals, London NW1 2BU, UK. ; Thermo Fisher Scientific, Carlsbad, CA 92008, USA. ; Technical University of Denmark, 2800 Kongens Lyngby, Denmark. Children's Hospital Informatics Program, Harvard Medical School, Boston, MA 02115, USA. ; Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London WC1E 6BT, UK. Cancer Research UK London Research Institute, London WC2A 3LY, UK. charles.swanton@cancer.org.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301630" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinogens/toxicity ; Carcinoma, Non-Small-Cell Lung/chemically induced/*diagnosis/*genetics ; Cytidine Deaminase/genetics ; Evolution, Molecular ; Gene Dosage ; *Genetic Heterogeneity ; *Genomic Instability ; Humans ; Lung Neoplasms/chemically induced/*diagnosis/*genetics ; Mutation ; Neoplasm Recurrence, Local/genetics ; Prognosis ; Smoking/adverse effects ; Translocation, Genetic ; Tumor Cells, Cultured
    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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    Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-05
    Description: As tumors grow, they acquire mutations, some of which create neoantigens that influence the response of patients to immune checkpoint inhibitors. We explored the impact of neoantigen intratumor heterogeneity (ITH) on antitumor immunity. Through integrated analysis of ITH and neoantigen burden, we demonstrate a relationship between clonal neoantigen burden and overall survival in primary lung adenocarcinomas. CD8(+)tumor-infiltrating lymphocytes reactive to clonal neoantigens were identified in early-stage non-small cell lung cancer and expressed high levels of PD-1. Sensitivity to PD-1 and CTLA-4 blockade in patients with advanced NSCLC and melanoma was enhanced in tumors enriched for clonal neoantigens. T cells recognizing clonal neoantigens were detectable in patients with durable clinical benefit. Cytotoxic chemotherapy-induced subclonal neoantigens, contributing to an increased mutational load, were enriched in certain poor responders. These data suggest that neoantigen heterogeneity may influence immune surveillance and support therapeutic developments targeting clonal neoantigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGranahan, Nicholas -- Furness, Andrew J S -- Rosenthal, Rachel -- Ramskov, Sofie -- Lyngaa, Rikke -- Saini, Sunil Kumar -- Jamal-Hanjani, Mariam -- Wilson, Gareth A -- Birkbak, Nicolai J -- Hiley, Crispin T -- Watkins, Thomas B K -- Shafi, Seema -- Murugaesu, Nirupa -- Mitter, Richard -- Akarca, Ayse U -- Linares, Joseph -- Marafioti, Teresa -- Henry, Jake Y -- Van Allen, Eliezer M -- Miao, Diana -- Schilling, Bastian -- Schadendorf, Dirk -- Garraway, Levi A -- Makarov, Vladimir -- Rizvi, Naiyer A -- Snyder, Alexandra -- Hellmann, Matthew D -- Merghoub, Taha -- Wolchok, Jedd D -- Shukla, Sachet A -- Wu, Catherine J -- Peggs, Karl S -- Chan, Timothy A -- Hadrup, Sine R -- Quezada, Sergio A -- Swanton, Charles -- 12100/Cancer Research UK/United Kingdom -- 1R01CA155010-02/CA/NCI NIH HHS/ -- 1R01CA182461-01/CA/NCI NIH HHS/ -- 1R01CA184922-01/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1463-9. doi: 10.1126/science.aaf1490. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, London WC2A 3LY, UK. Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London (UCL), London WC1E 6BT, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Section for Immunology and Vaccinology, National Veterinary Institute, Technical University of Denmark, 1970 Frederiksberg C, Denmark. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; The Francis Crick Institute, London WC2A 3LY, UK. ; Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. Department of Cellular Pathology, UCL, London WC1E 6BT, UK. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium (DKTK), 69121 Heidelberg, Germany. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Hematology/Oncology Division, 177 Fort Washington Avenue, Columbia University, New York, NY 10032, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. Department of Internal Medicine, Brigham and Woman's Hospital, Boston, MA 02115, USA. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940869" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/drug therapy/genetics/*immunology ; Aged ; Aged, 80 and over ; Antigens, Neoplasm/genetics/*immunology ; Antineoplastic Agents/therapeutic use ; CD4-Positive T-Lymphocytes/*immunology ; CTLA-4 Antigen/immunology ; Carcinoma, Non-Small-Cell Lung/genetics/immunology ; Cell Cycle Checkpoints/immunology ; Female ; Humans ; *Immunologic Surveillance ; Lung Neoplasms/drug therapy/genetics/*immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma/immunology ; Middle Aged ; Mutation ; Programmed Cell Death 1 Receptor/immunology ; Skin Neoplasms/immunology
    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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  • 6
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    Metastasis as an evolutionary process (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-04-29
    Description: Therapeutic advances in oncology have not fully translated to the treatment of metastatic disease, which remains largely incurable. Metastatic subclones can emerge both early and late in the life of the primary tumor. A better understanding of the genetic evolution of metastatic disease has the potential to reveal differences in the therapeutic vulnerabilities of primary and metastatic tumors, shed light on the temporal patterns of and routes to metastatic colonization, and provide insight into the biology of the metastatic process. Here we review recent comparative studies of primary and metastatic tumors, including data suggesting that macroevolutionary shifts (the onset of chromosomal instability) contribute to the evolution of metastatic disease. We also discuss the practical challenges associated with these studies and how they might be overcome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turajlic, Samra -- Swanton, Charles -- C50947/A18176/Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):169-75. doi: 10.1126/science.aaf2784.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. Renal and Skin Units, The Royal Marsden Hospital, London SW3 6JJ, UK. ; The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY2, UK. University College London Hospitals and Cancer Institute, Cancer Research UK Lung Cancer Centre of Excellence, Huntley Street, London WC1, UK. charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124450" target="_blank"〉PubMed〈/a〉
    Keywords: Clone Cells/pathology ; *Evolution, Molecular ; Genetic Variation ; Humans ; Neoplasm Metastasis/*genetics/*pathology ; Neoplasms/classification/genetics/pathology ; Phylogeny
    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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  • 7
    Electronic Resource
    Electronic Resource
    The influence of temperature and relative humidity on the efficacy of glufosinate-ammonium (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Weed research 33 (1993), S. 0 
    Details
    ISSN: 1365-3180
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: The influence of temperature and relative humidity (r.h.) on the efficacy of glufosinate ammonium was investigated in controlled environment growth chambers using a tolerant species, barley (Hordeum vulgare L. cv. ‘Samson’), and a susceptible species, green foxtail (Setaria viridis (L.) Beauv.). The shoot ammonia concentration and visual injury of plants treated with glufosinate-ammonium doses of 100 and 800 g ha−1 were compared at day/night temperature regimes of 8/5,15/10 and 22/17°C at 60% r.h. The effect of relative humidity levels of 40% and 95% on the shoot ammonia concentration, visual injury and dry weight accumulation of glufosinate-ammonium treated plants was tested at temperature regimes of 15/10 and 22/17°C, with both species treated with 800 g ha−1. In addition, green foxtail treated with 100 g ha−1. was tested at both r.h. levels at 22/17°C. As the temperature de creased, less ammonia was produced in treated green foxtail plants. However, ammonia levels were comparable at all temperature regimes for barley. Lowest temperatures resulted in delayed injury to both species, but only small differences in injury existed among temperature regimes 288 h after spraying. The activity of glufosinate ammonium on both species was significantly de creased by low r.h. For example, when grown at 22/17°C, green foxtail survived the potentially lethal dose of 100 g ha−1 at 40% r.h. and accumulated 70% of the dry weight of control plants, but was killed at 95% r.h. Of the two environmental factors examined, r.h. had the most significant effect on the phytotoxic action of glufosinate-ammonium. L'influence de la température et de I'humidité relative sur I'efficacité du glufosinate-ammonium L'influence de la température et de 1'humidité relative (hr) sur I'efficacité du glufosinate ammonium a étéétudiée en chambre climatique en utilisant une espéce d'orge tolérante (Hor deum vulgare L. cv ‘Samson’) et une espéce sensible la svtaire verte (Setaria viridis L. Beauv).La concentration en ammoniaque des pieds et les dégats visuels des plantes traitérs avec des doses de glufosinate ammonium de 100 et 800 g/ ha−1 ont été comparés pour des régimes de températures jour/nuit de 8/5, 15/10 et 22/17°C à 60% hr. L'effet de taux d'humidité relative de 40 et 95% sur la teneur en ammoniaque des pieds, les dégats visuels et (l'accumulation de matiére séche chez des plantes traitéres au glufosinate ammonium a été testéà des régimes de températures de 15/10 et 22/17°C, pour les 2 espéces traitées à 800 g ha−1. En outre, la sétaire verte traitée à 100 g hr−1 a été testée aux 2 hr à 22/17°C. Quand la température diminue, il y a moins d'ammoniaque produit chez les sétaires vertes trailérs. Cependant les taux d'ammon iaque ont été comparables à toutes les tempéra tures chez 1'orge. Les températures les plus basses ont abouti à un retard de phytotoxicité ches les 2 espéces, mais à peu de différences entre les régimes de températures 288 h après 1'application. L'activité du glufosinate ammon ium chez les deux espèces a été significative ment réduite par des faibles hr. Par exemple cul tivée à 22/17°C, la sétaire verte a survécu à des doses potentiellement léthales de 100 g ha−1à 40% d'hr et a accumulé 70% de la matière sèche des témoins mais a été détruite à 95% d'hr. Sur les 2 facteurs environnementaux étudiés, l'hr a l'effet le plus important sur l'activité phytotoxique du glufosinate ammonium. Einfluβ von Temperatur und relativer Feuchte auf die Wirksamkeit von Glufosinat-ammonium Der Einfluß von Temperatur und relativer Feuchte (rF) auf die Wirksamkeit von Glufosinat-ammonium wurde in Klimakammern anhand einer toleranten Art, der Gersten-Sorte ‘Samson’ (Hordeum vulgare L.), und einer empfindlichen Art, der Grünen Borstenhirse (Setaria viridis (L.) Beauv.), untersucht. Die Ammonium-Konzentration im Sproß und sichtbare Schädigungen der Pflanzen, die mit Dosen von 100 und 800 g ha−1 behandelt worden waren, wurden bei Tag/Nacht-Temperaturen von 8/5, 15/10 und 22/17 °C bei 60% rF verglichen. Die Wirkung von 40 oder 95% rF auf die Ammonium-Konzentrationen im Sproß, sichtbare Pflanzenschädigungen und die Trockenmassebildung wurde bei 15/10 und 22/17°C und bei 800 g ha−1 Glufosinat-ammonium untersucht. Zusätzlich wurde die Grüne Borstenhirse mit 100 g ha−1 behandelt und bei den beiden Feuchtegraden und 22/17 °C untersucht. Mit abnehmender Temperatur bildete die Grüne Borstenhirse weniger Ammonium, dessen Gehalt bei der Gerste jedoch bei allen Temperaturen gleich war. Geringere Temperaturen verzögerten bei beiden Arten die Schädigungen, doch ließen sich 288 h nach der Behandlung nur noch geringe Unterschiede bei den verschiedenen Temperaturen beobachten. Die Wirkung von Glufosinat-ammonium war bei niedriger rF bei beiden Arten signifikant schwächer. Z. B. überlebte die Grüne Borstenhirse die potentiell letale Dosis von 100 g ha−1 bei 22/17 °C und 40% rF und bildete 70% der Trockenmasse von Kontrollpflanzen, wurde jedoch bei 95% rF abgetötet. Die rF war von den beiden untersuchten Umweltfakoren der signkfikantere für die phytotoxische Wirkung des Glufosinat-ammoniums.
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    URL: http://dx.doi.org/10.1111/j.1365-3180.1993.tb01927.x
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  • 8
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    Basis for the selective action of fluroxypyr (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Weed research 34 (1994), S. 0 
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    ISSN: 1365-3180
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: The dose-response, foliar uptake, translocation and metabolism of the methylheptyl ester (MHE) of fluroxypyr were examined in lambs-quarters (Chenopodium album L.), wild buckwheat (Polygonum convolvulus L.), Canada thistle (Cirsium arvense L. Scop.) and field bindweed (Convolvulus arvensis L.). Under controlled environment growth room conditions, E50 values, determined from shoot dry weights of the susceptible species, wild buckwheat (16 g ha−1) and field bindweed (40 g ha−1), were markedly different than those of the tolerant species, lambsquarters (331 g ha−1) and Canada thistle (〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:00431737:WRE333:ges" location="ges.gif"/〉800 g ha−1). Regardless of species, more than 80% of applied [14C]fluroxypyr-MHE was absorbed by foliar surfaces 120 h after treatment. Translocation of radioactivity out of the treated leaves of susceptible species was significantly greater than that of tolerant species. For example, 120 h after treatment with [14C]-fluroxypyr-MHE, the proportion of applied radioactivity translocated in tolerant Canada thistle and lambsquarters was 15 and 10%, respectively, whereas in susceptible wild buckwheat and field bindweed it was 41 and 40% of applied radioactivity, respectively. High-performance liquid chromatography (HPLC) of plant extracts indicated four distinct chroma-tographic peaks common to all four species. More fluroxypyr was recovered in the susceptible species (70%) than in the tolerant species (30%), 120 h after application. Selectivity differences between the tolerant and susceptible species may be the result of enhanced metabolic transformation of the herbicide to more polar, non-phytotoxic compounds with limited mobility within the tolerant species. Les bases de la sélectivité du fluroxypyr La courbe dose effet, la pénétration foliaire, la migration et le métabolisme de Tester méthyle-heptyle (MHE) du fluroxypyr ont étéétudiés chez le chénopode blanc (Chenopodium album L.), la renouée faux-liseron (Polygonum con-vulvulus L.), le chardon des champs (Cirsium arvense L. Scop.) et le liseron des champs (Convolvulus arvensis L.). En conditions de crois-sance contrôlées, les valeurs ED50, déterminées à partir du poids de matière sèche des parties aériennes étaient nettement différentes chez les plantes sensibles et chez les plantes résistan-tes:renouée faux-liseron, 16 g ha−1; liseron des champs, 40 g ha−1; chénopode blanc, 331 g ha−1; chardon des champs, 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:00431737:WRE333:ges" location="ges.gif"/〉800 g ha−1. Quelle que soit 1'espèce, plus de 80% du [14C]fluroxypyr-MHE pénétrait dans les feuilles en 120 h. La migration de la radioactivité hors des feuilles traitérs était significativement plus importante chez les plantes sensibles que chez les plantes tolérantes. Par exemple, 120 h après le traite-ment avec du [14C]fluroxypyr-MHE, la proportion de radioactivité appliquée qui avait migré dans le chardon des champs et le chénopode, tolérants, était respectivement 15 et 10%, alors que chez la renouée faux-liseron et le liseron des champs, sensibles, elle était respectivement 41 et 40%. Des analyses par HPLC des extraits de plantes montraient quatre pics chro-matographiques distincts dans chacune des quatre espèces. Davantage de fluroxypyr était retrouvé 120 h après 1'application chez les plantes sensibles que chez les plantes résistantes (70% contre 30%). Les différences de sensibilité entre espèces pourraient être dues chez les plantes tolérantes à un métabolisme plus important de l'herbicide en composés plus polaires, non phytotoxiques et peu mobiles. Grundlagen für die selektive Wirkung von Fluroxypyr Die Dosis/Wirkungs-Beziehung, Blattaufnahme, Translokation und Metabolismus des Methylheptyl-Esters (MHE) von Fluroxypyr wurden bei Weißem Gänsefuß (Chenopodium album L.), Gemeinem Windenknöterich (Polygonum convolvulus L.), Acker-Kratzdistel (Cirsium arvense (L.) Scop.) und Gemeiner Ackerwinde (Convolvulus arvensis L.) untersucht. Unter den kontrollierten Umweltbedingungen eines Phytotrons wurden anhand des Trockengewichts die ED50-Werte bestimmt, die bei den empfindlichen Arten Polygonum convolvulus mit 16 g ha−1 und Convolvulus arvensis mit 40 g ha−1 sich deutlich von denen der toleranten Arten Chenopodium album mit 331 g ha−1 und Cirsium arvense mit 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:00431737:WRE333:ges" location="ges.gif"/〉800 g ha−1 unterschieden. Unabhängig von der Art waren mehr als 80 % der Aufwandmenge von [14C]-Fluroxypyr-MHE durch die Blattoberflächen 120 h nach der Behandlung aufgenommen. Die Translokation der Radioaktivität aus den behandelten Blättern war bei den empfindlichen Arten signifikant größer als bei den toleranten. Z. B. waren 120 h nach der Behandlung bei den toleranten Arten Cirsium arvense und Chenopodium album 15 bzw. 10 % der Radioaktivität transloziert, während es bei den empfindlichen Arten Polygonum convolvulus und Convolvulus arvensis 41 bzw. 40 % waren. Bei allen 4 Arten ergab eine HPLC-Untersuchung der Pflanzenextrakte 4 distinkte Peaks. Bei den empfindlichen Arten wurde 120 h nach der Anwendung mit 70 % mehr Fluroxypyr wiedergefunden als bei den toleranten (30 %). Die Selektivitätsunterschiede zwischen den toleranten und empfindlichen Arten könnten auf einen beschleunigten Metabolismus des Herbizids zu stärker polaren, nichphytotoxischen Stoffen mit eingeschränkter Mobilität bei den toleranten Arten zurückgeführt werden.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3180.1994.tb02002.x
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    Effect of tillage, cover crop and crop rotation on the composition of weed flora in a sandy soil (2002)
    Oxford UK : Blackwell Science Ltd.
    Weed research 42 (2002), S. 0 
    Details
    ISSN: 1365-3180
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: The development of integrated weed management strategies requires knowledge of mechanisms that influence compositional changes in weed flora. A 9-year study was initiated in 1988 at Delhi, Canada, on a loamy sand soil to evaluate the effect of tillage systems [conventional (CT) and no-till (NT)] and cover crops (only in NT) on weed density, species composition and associations, and crop yield in a winter wheat (Triticum aestivum L.)/bean/winter wheat rotation. Three bean types: soyabean (Glycine max L. Merr.), white bean (Phaseolus vulgaris L.) and kidney bean (P. vulgaris L.) were included. The NT system included variations: rye (Secale cereale L.) or maize (Zea mays L.) cover crop, volunteer wheat disked after harvest and wheat stubble. Data were collected in 1994, 1995 and 1996. Tillage systems, cover crops and crop type had differential effects on weed densities, species composition and associations. Weed densities were not affected by tillage or cover crops in wheat but, in the beans, densities were greater in the CT than in the NT systems. Various associations of weed species with tillage system, cover crop and crop type were observed. Crop yields were not affected by tillage type or cover crop, except that soyabean yields were highest in plots with cover crops.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3180.2002.00264.x
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  • 10
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    Comparison of empirical models depicting density of Amaranthus retroflexus L. and relative leaf area as predictors of yield loss in maize (Zea mays L.) (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Weed research 35 (1995), S. 0 
    Details
    ISSN: 1365-3180
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: The outcome of crop-weed competition should be predicted as early as possible in order to allow time for weed control measures. Maize grain yield losses caused by interference from Amaranthus retroflexus L. (redroot pigweed) were determined in 1991 and 1992. The performance of three empirical models of crop-weed competition were evaluated. Damage functions were calculated based on the weed density or relative leaf area of the weed. In the yield loss-weed density model, values of I (percentage yield loss at low weed density) were relatively stable for similar emergence dates of A. retroflexus across years and locations. Estimated maximum yield loss (A) was more variable between locations and may reflect environmental variation and its effect on crop-weed competition, at least in 1991. The two-parameter yield loss-relative leaf area model, based on m (maximum yield loss caused by weeds) and q (the relative damage coefficient) gave a better fit than the single-parameter version of the model (which includes only q). In both relative leaf area models, the values of q varied between years and locations. Attempts to stabilize the value of q by using the relative growth rate of the leaves of the crop and weed were successful; however, the practical application of such relative leaf area models may still be limited owing to the lack of a method to estimate leaf area index quickly and accurately.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3180.1995.tb01783.x
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