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  • 1
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    Activating mutations in ALK provide a therapeutic target in neuroblastoma (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-17
    Description: Neuroblastoma, an embryonal tumour of the peripheral sympathetic nervous system, accounts for approximately 15% of all deaths due to childhood cancer. High-risk neuroblastomas are rapidly progressive; even with intensive myeloablative chemotherapy, relapse is common and almost uniformly fatal. Here we report the detection of previously unknown mutations in the ALK gene, which encodes a receptor tyrosine kinase, in 8% of primary neuroblastomas. Five non-synonymous sequence variations were identified in the kinase domain of ALK, of which three were somatic and two were germ line. The most frequent mutation, F1174L, was also identified in three different neuroblastoma cell lines. ALK complementary DNAs encoding the F1174L and R1275Q variants, but not the wild-type ALK cDNA, transformed interleukin-3-dependent murine haematopoietic Ba/F3 cells to cytokine-independent growth. Ba/F3 cells expressing these mutations were sensitive to the small-molecule inhibitor of ALK, TAE684 (ref. 4). Furthermore, two human neuroblastoma cell lines harbouring the F1174L mutation were also sensitive to the inhibitor. Cytotoxicity was associated with increased amounts of apoptosis as measured by TdT-mediated dUTP nick end labelling (TUNEL). Short hairpin RNA (shRNA)-mediated knockdown of ALK expression in neuroblastoma cell lines with the F1174L mutation also resulted in apoptosis and impaired cell proliferation. Thus, activating alleles of the ALK receptor tyrosine kinase are present in primary neuroblastoma tumours and in established neuroblastoma cell lines, and confer sensitivity to ALK inhibition with small molecules, providing a molecular rationale for targeted therapy of this disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587486/" 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/PMC2587486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, Rani E -- Sanda, Takaomi -- Hanna, Megan -- Frohling, Stefan -- Luther, William 2nd -- Zhang, Jianming -- Ahn, Yebin -- Zhou, Wenjun -- London, Wendy B -- McGrady, Patrick -- Xue, Liquan -- Zozulya, Sergey -- Gregor, Vlad E -- Webb, Thomas R -- Gray, Nathanael S -- Gilliland, D Gary -- Diller, Lisa -- Greulich, Heidi -- Morris, Stephan W -- Meyerson, Matthew -- Look, A Thomas -- CA21765/CA/NCI NIH HHS/ -- CA69129/CA/NCI NIH HHS/ -- K08 NS047983/NS/NINDS NIH HHS/ -- K08 NS047983-03/NS/NINDS NIH HHS/ -- K08 NS047983-04/NS/NINDS NIH HHS/ -- K08 NS047983-05/NS/NINDS NIH HHS/ -- England -- Nature. 2008 Oct 16;455(7215):975-8. doi: 10.1038/nature07397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18923525" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Enzyme Activation/genetics ; Genome, Human/genetics ; Humans ; In Situ Hybridization, Fluorescence ; In Situ Nick-End Labeling ; Mice ; Mutation/*genetics ; Neuroblastoma/enzymology/*genetics/pathology/*therapy ; Polymorphism, Single Nucleotide/genetics ; Protein Structure, Tertiary/genetics ; Protein-Tyrosine Kinases/*antagonists & inhibitors/chemistry/*genetics/metabolism ; Receptor Protein-Tyrosine Kinases ; Sequence Analysis, DNA
    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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    Targeting transcription regulation in cancer with a covalent CDK7 inhibitor (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: Tumour oncogenes include transcription factors that co-opt the general transcriptional machinery to sustain the oncogenic state, but direct pharmacological inhibition of transcription factors has so far proven difficult. However, the transcriptional machinery contains various enzymatic cofactors that can be targeted for the development of new therapeutic candidates, including cyclin-dependent kinases (CDKs). Here we present the discovery and characterization of a covalent CDK7 inhibitor, THZ1, which has the unprecedented ability to target a remote cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7. Cancer cell-line profiling indicates that a subset of cancer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensitivity to THZ1. Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects transcription of RUNX1 and suggests that sensitivity to THZ1 may be due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core transcriptional regulatory circuitry of these tumour cells. Pharmacological modulation of CDK7 kinase activity may thus provide an approach to identify and treat tumour types that are dependent on transcription for maintenance of the oncogenic state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244910/" 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/PMC4244910/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwiatkowski, Nicholas -- Zhang, Tinghu -- Rahl, Peter B -- Abraham, Brian J -- Reddy, Jessica -- Ficarro, Scott B -- Dastur, Anahita -- Amzallag, Arnaud -- Ramaswamy, Sridhar -- Tesar, Bethany -- Jenkins, Catherine E -- Hannett, Nancy M -- McMillin, Douglas -- Sanda, Takaomi -- Sim, Taebo -- Kim, Nam Doo -- Look, Thomas -- Mitsiades, Constantine S -- Weng, Andrew P -- Brown, Jennifer R -- Benes, Cyril H -- Marto, Jarrod A -- Young, Richard A -- Gray, Nathanael S -- CA109901/CA/NCI NIH HHS/ -- CA178860-01/CA/NCI NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- P01 NS047572/NS/NINDS NIH HHS/ -- P01 NS047572-10/NS/NINDS NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- R01 CA130876/CA/NCI NIH HHS/ -- R01 CA130876-04/CA/NCI NIH HHS/ -- R01 CA179483/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R21 CA178860/CA/NCI NIH HHS/ -- T32 GM008042/GM/NIGMS NIH HHS/ -- U54 HG006097/HG/NHGRI NIH HHS/ -- U54 HG006097-02/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Jul 31;511(7511):616-20. doi: 10.1038/nature13393. Epub 2014 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA [4]. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA [3]. ; Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; 1] Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA [2] Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA. ; Department of Medicine Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA. ; 1] Department of Medicine Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA [2] Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; 1] Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia V5Z 1L3, Canada. ; 1] Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Cancer Science Institute of Singapore, National University of Singapore, 117599 Singapore. ; Chemical Kinomics Research Center, Korea Institute of Science and Technology, 39-1, Hawolgok-dong, Seongbuk-gu, Seoul 136-791, Korea, and KU-KIST Graduate School of Converging Science and Technology, 145, Anam-ro, Seongbuk-gu, Seoul 136-713, Korea. ; Daegu-Gyeongbuk Medical Innovation Foundation, 2387 dalgubeol-daero, Suseong-gu, Daegu 706-010, Korea. ; 1] Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Division of Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115 USA. ; 1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043025" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Core Binding Factor Alpha 2 Subunit/metabolism ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Cysteine/metabolism ; Enzyme Inhibitors/*pharmacology ; Gene Expression Regulation, Neoplastic/*drug effects ; Humans ; Jurkat Cells ; Phenylenediamines/*pharmacology ; Phosphorylation/drug effects ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*enzymology ; Pyrimidines/*pharmacology
    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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    Oncogene regulation. An oncogenic super-enhancer formed through somatic mutation of a noncoding intergenic element (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-15
    Description: In certain human cancers, the expression of critical oncogenes is driven from large regulatory elements, called super-enhancers, that recruit much of the cell's transcriptional apparatus and are defined by extensive acetylation of histone H3 lysine 27 (H3K27ac). In a subset of T-cell acute lymphoblastic leukemia (T-ALL) cases, we found that heterozygous somatic mutations are acquired that introduce binding motifs for the MYB transcription factor in a precise noncoding site, which creates a super-enhancer upstream of the TAL1 oncogene. MYB binds to this new site and recruits its H3K27 acetylase-binding partner CBP, as well as core components of a major leukemogenic transcriptional complex that contains RUNX1, GATA-3, and TAL1 itself. Additionally, most endogenous super-enhancers found in T-ALL cells are occupied by MYB and CBP, which suggests a general role for MYB in super-enhancer initiation. Thus, this study identifies a genetic mechanism responsible for the generation of oncogenic super-enhancers in malignant cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720521/" 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/PMC4720521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mansour, Marc R -- Abraham, Brian J -- Anders, Lars -- Berezovskaya, Alla -- Gutierrez, Alejandro -- Durbin, Adam D -- Etchin, Julia -- Lawton, Lee -- Sallan, Stephen E -- Silverman, Lewis B -- Loh, Mignon L -- Hunger, Stephen P -- Sanda, Takaomi -- Young, Richard A -- Look, A Thomas -- 1R01CA176746-01/CA/NCI NIH HHS/ -- 5P01CA109901-08/CA/NCI NIH HHS/ -- 5P01CA68484/CA/NCI NIH HHS/ -- CA114766/CA/NCI NIH HHS/ -- CA120215/CA/NCI NIH HHS/ -- CA167124/CA/NCI NIH HHS/ -- CA29139/CA/NCI NIH HHS/ -- CA30969/CA/NCI NIH HHS/ -- CA98413/CA/NCI NIH HHS/ -- CA98543/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1373-7. doi: 10.1126/science.1259037. Epub 2014 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Department of Haematology, UCL Cancer Institute, University College London, London WC1E 6BT, UK. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Division of Pediatric Hematology-Oncology, Boston Children's Hospital, MA 02115, USA. ; Department of Pediatrics, Benioff Children's Hospital, University of California San Francisco, CA 94143, USA. ; Pediatric Hematology/Oncology/BMT, University of Colorado School of Medicine and Children's Hospital Colorado, Aurora, CO 80045, USA. ; Cancer Science Institute of Singapore, National University of Singapore, and Department of Medicine, Yong Loo Lin School of Medicine, 117599, Singapore. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. thomas_look@dfci.harvard.edu young@wi.mit.edu. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Division of Pediatric Hematology-Oncology, Boston Children's Hospital, MA 02115, USA. thomas_look@dfci.harvard.edu young@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25394790" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Base Sequence ; Basic Helix-Loop-Helix Transcription Factors/*genetics ; Binding Sites ; Cell Line, Tumor ; *DNA, Intergenic ; *Enhancer Elements, Genetic ; *Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Humans ; *INDEL Mutation ; Molecular Sequence Data ; *Mutation ; Oncogenes ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics ; Protein Interaction Domains and Motifs ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-myb/metabolism
    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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  • 4
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    Testosterone regulates lymphocyte differentiation [Immunology] (2014)
    National Academy of Sciences
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    Publication Date: 2014-07-09
    Description: The hormonal milieu influences immune tolerance and the immune response against viruses and cancer, but the direct effect of androgens on cellular immunity remains largely uncharacterized. We therefore sought to evaluate the effect of androgens on murine and human T cells in vivo and in vitro. We found that murine...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
    Electronic Resource
    Electronic Resource
    A new method for digital power spectrum analysis
    Amsterdam : Elsevier
    Nuclear Instruments and Methods 108 (1973), S. 243-252 
    Details
    ISSN: 0029-554X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0029-554X(73)90595-8
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  • 6
    Electronic Resource
    Electronic Resource
    Microstructures of Ni/Cu and Ni-Co/Cu Multilayers Produced by Electrodeposition Method (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Advanced materials research Vol. 26-28 (Oct. 2007), p. 1321-1324 
    Details
    ISSN: 1662-8985
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Microstructures of Ni/Cu and Ni-Co/Cu multilayers were investigated by X-ray diffractionanalysis. These multilayered structures were fabricated on copper substrates using electrodepositiontechnique. At an as-deposited Ni/Cu multilayer with the layer thickness of h=5nm, a single diffractionpeak appeared, although the multilayer of h=100nm exhibited the diffractions splitting into two peakswhich resulted from both the Ni and Cu layers. In the Ni-Co/Cu multilayers, it was found thatcomposition of the Ni-Co layer depended on an electric potential applied during deposition. The fccand hcp structures were detected at the Ni-rich and the Co-rich deposits, respectively. The Vickershardness of the Co-Ni/Cu multilayer was higher than that of the Ni/Cu multilayer
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/01/40/transtech_doi~10.4028%252Fwww.scientific.net%252FAMR.26-28.1321.pdf
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  • 7
    Electronic Resource
    Electronic Resource
    Fatigue Life Enhancement by Surface Coating of Ni/Cu Multilayered Films (2007)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 561-565 (Oct. 2007), p. 2393-2398 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Effect of Ni/Cu multilayer coating on fatigue durability was investigated. The Ni/Cumultilayered films were coated on cylindrical copper specimens by electroplating technique.Thickness of individual component layers was h=20nm and 100nm and the total thickness was 5μm.The specimens with a conventional nickel coating and uncoated specimens were also prepared.Push-pull fatigue tests were carried out in air at room temperature. It was found that the specimenswith the Ni/Cu multilayered coatings exhibited the fatigue lives longer than those of the conventionalnickel coating. In particular, the fatigue life with the h=100nm multilayer was at least ten times longerthan that with the nickel coating at the stress amplitude of 90MPa. From the electron channellingcontrast imaging (ECCI) observation of subsurface areas of the copper specimens, dislocationstructures peculiar to fatigue deformation was suppressed by the surface coatings
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/18/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.561-565.2393.pdf
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  • 8
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    A new method for digital power spectrum analysis (1973)
    Elsevier
    Details
    Publication Date: 1973-04-01
    Print ISSN: 0029-554X
    Electronic ISSN: 1878-3759
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Physics
    Published by Elsevier
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  • 9
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    The transcription factor SP3 drives TNF-{alpha} expression in response to Smac mimetics (2019)
    The American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2019
    Description: 〈p〉The controlled production and downstream signaling of the inflammatory cytokine tumor necrosis factor–α (TNF-α) are important for immunity and its anticancer effects. Although chronic stimulation with TNF-α is detrimental to the health of the host in several autoimmune and inflammatory disorders, TNF-α—contrary to what its name implies—leads to cancer formation by promoting cell proliferation and survival. Smac mimetic compounds (SMCs), small-molecule antagonists of inhibitor of apoptosis proteins (IAPs), switch the TNF-α signal from promoting survival to promoting death in cancer cells. Using a genome-wide siRNA screen to identify factors required for SMC–to–TNF-α–mediated cancer cell death, we identified the transcription factor SP3 as a critical molecule in both basal and SMC-induced production of TNF-α by engaging the nuclear factor B (NF-B) transcriptional pathway. Moreover, the promotion of TNF-α expression by SP3 activity confers differential sensitivity of cancer versus normal cells to SMC treatment. The key role of SP3 in TNF-α production and signaling will help us further understand TNF-α biology and provide insight into mechanisms relevant to cancer and inflammatory disease.〈/p〉
    Print ISSN: 1945-0877
    Electronic ISSN: 1937-9145
    Topics: Biology , Medicine
    Published by The American Association for the Advancement of Science (AAAS)
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  • 10
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    Runoff formation in a humid, temperate headwater catchment using a combined hydrological, hydrochemical and isotopic approach (Jizera Mountains, Czech Republic) (2013)
    Wiley
    Details
    Publication Date: 2013-04-29
    Description: The formation of baseflow and stormflow was examined in the 1.18 km 2 part of the headwater catchment Uhlířská, Jizera Mts., Czech Republic, over the period 2007–2011, by means of runoff data and environmental tracers 18 O and SiO 2 . The baseflow, computed using the digital filter approach BFLOW, contributes 67% to total streamflow and has a mean residence time of 12.3 months. It is formed by groundwater discharge from the valley deluviofluvial granitic sediments, in combination with soil water in weathered layers on hillslopes during rainfall and snowmelt periods. The prevailing source of the groundwater is the infiltration of snowmelt water. Analysis of 20 runoff events and their hysteretic patterns demonstrated that the stormflow water has a residence time of about 4 months and is generated by preferential flow on hillslopes combined by soil matrix drainage. Due to slower flow in the soil matrix the enrichment of pore water in SiO 2 is more pronounced. The stormflow and snowmelt water flowing via preferential pathways of upslope minerals soils pushes the pre-event groundwater through the pathways in wetlands to the stream, and the wetland can be therefore considered as groundwater-supplied. This mechanism has found to be typical for the groundwater-supplied headwater catchments of the Jizera Mountains and can be also assumed in other mountainous headwaters of the granitic massif in Central Europe. The main methodological contribution of this study are the residence time calculations stratified by baseflow and event flow, identifying runoff components of different travel times to streams and linking them with geochemical runoff sources. This achievement was possible due to a comprehensive dataset on hydrology, stable isotopes and silica hydrochemistry in all relevant runoff generation components. This concept indicates that a possible long term change in snowmelt may affect the runoff regime of headwater catchments to climate or land use changes. This article is protected by copyright. All rights reserved.
    Print ISSN: 0885-6087
    Electronic ISSN: 1099-1085
    Topics: Architecture, Civil Engineering, Surveying , Geography
    Published by Wiley
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