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  • 1
    Publication Date: 2012-06-23
    Description: Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA, TP53, AKT1, GATA3 and MAP3K1, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3-AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148686/" 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/PMC4148686/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerji, Shantanu -- Cibulskis, Kristian -- Rangel-Escareno, Claudia -- Brown, Kristin K -- Carter, Scott L -- Frederick, Abbie M -- Lawrence, Michael S -- Sivachenko, Andrey Y -- Sougnez, Carrie -- Zou, Lihua -- Cortes, Maria L -- Fernandez-Lopez, Juan C -- Peng, Shouyong -- Ardlie, Kristin G -- Auclair, Daniel -- Bautista-Pina, Veronica -- Duke, Fujiko -- Francis, Joshua -- Jung, Joonil -- Maffuz-Aziz, Antonio -- Onofrio, Robert C -- Parkin, Melissa -- Pho, Nam H -- Quintanar-Jurado, Valeria -- Ramos, Alex H -- Rebollar-Vega, Rosa -- Rodriguez-Cuevas, Sergio -- Romero-Cordoba, Sandra L -- Schumacher, Steven E -- Stransky, Nicolas -- Thompson, Kristin M -- Uribe-Figueroa, Laura -- Baselga, Jose -- Beroukhim, Rameen -- Polyak, Kornelia -- Sgroi, Dennis C -- Richardson, Andrea L -- Jimenez-Sanchez, Gerardo -- Lander, Eric S -- Gabriel, Stacey B -- Garraway, Levi A -- Golub, Todd R -- Melendez-Zajgla, Jorge -- Toker, Alex -- Getz, Gad -- Hidalgo-Miranda, Alfredo -- Meyerson, Matthew -- CA089393/CA/NCI NIH HHS/ -- CA122099/CA/NCI NIH HHS/ -- R01 CA122099/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 20;486(7403):405-9. doi: 10.1038/nature11154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722202" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Breast Neoplasms/*classification/*genetics/pathology ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor beta Subunit/genetics ; DNA Mutational Analysis ; Exome/genetics ; Female ; Gene Fusion/genetics ; Humans ; Membrane Proteins/genetics ; Mexico ; Mutation/*genetics ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/metabolism ; Translocation, Genetic/*genetics ; Vietnam
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Nature Publishing Group (NPG)
    Publication Date: 2014-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Polyak, Kornelia -- Marusyk, Andriy -- England -- Nature. 2014 Apr 3;508(7494):52-3. doi: 10.1038/508052a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24695309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*metabolism/*pathology ; Female ; Wnt1 Protein/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-08-01
    Description: Cancers arise through a process of somatic evolution that can result in substantial sub-clonal heterogeneity within tumours. The mechanisms responsible for the coexistence of distinct sub-clones and the biological consequences of this coexistence remain poorly understood. Here we used a mouse xenograft model to investigate the impact of sub-clonal heterogeneity on tumour phenotypes and the competitive expansion of individual clones. We found that tumour growth can be driven by a minor cell subpopulation, which enhances the proliferation of all cells within a tumour by overcoming environmental constraints and yet can be outcompeted by faster proliferating competitors, resulting in tumour collapse. We developed a mathematical modelling framework to identify the rules underlying the generation of intra-tumour clonal heterogeneity. We found that non-cell-autonomous driving of tumour growth, together with clonal interference, stabilizes sub-clonal heterogeneity, thereby enabling inter-clonal interactions that can lead to new phenotypic traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184961/" 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/PMC4184961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marusyk, Andriy -- Tabassum, Doris P -- Altrock, Philipp M -- Almendro, Vanessa -- Michor, Franziska -- Polyak, Kornelia -- U54 CA143798/CA/NCI NIH HHS/ -- U54CA143798/CA/NCI NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):54-8. doi: 10.1038/nature13556. Epub 2014 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA [3] Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] BBS Program, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115, USA [3] Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115, USA. ; 1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA [3] Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA [4] BBS Program, Harvard Medical School, Boston, Massachusetts 02115, USA [5] Harvard Stem Cell Institute and the Broad Institute, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Proliferation ; Clone Cells/*metabolism/*pathology ; Epigenesis, Genetic/genetics ; Female ; Interleukin-11/metabolism ; Mice ; Models, Biological ; Neoplasm Metastasis ; Neoplasms/*genetics/metabolism/*pathology ; Phenotype ; 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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  • 4
    Publication Date: 2016-01-07
    Description: Triple-negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. BET bromodomain inhibitors, which have shown efficacy in several models of cancer, have not been evaluated in TNBC. These inhibitors displace BET bromodomain proteins such as BRD4 from chromatin by competing with their acetyl-lysine recognition modules, leading to inhibition of oncogenic transcriptional programs. Here we report the preferential sensitivity of TNBCs to BET bromodomain inhibition in vitro and in vivo, establishing a rationale for clinical investigation and further motivation to understand mechanisms of resistance. In paired cell lines selected for acquired resistance to BET inhibition from previously sensitive TNBCs, we failed to identify gatekeeper mutations, new driver events or drug pump activation. BET-resistant TNBC cells remain dependent on wild-type BRD4, which supports transcription and cell proliferation in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify strong association with MED1 and hyper-phosphorylation of BRD4 attributable to decreased activity of PP2A, identified here as a principal BRD4 serine phosphatase. Together, these studies provide a rationale for BET inhibition in TNBC and present mechanism-based combination strategies to anticipate clinical drug resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shu, Shaokun -- Lin, Charles Y -- He, Housheng Hansen -- Witwicki, Robert M -- Tabassum, Doris P -- Roberts, Justin M -- Janiszewska, Michalina -- Huh, Sung Jin -- Liang, Yi -- Ryan, Jeremy -- Doherty, Ernest -- Mohammed, Hisham -- Guo, Hao -- Stover, Daniel G -- Ekram, Muhammad B -- Peluffo, Guillermo -- Brown, Jonathan -- D'Santos, Clive -- Krop, Ian E -- Dillon, Deborah -- McKeown, Michael -- Ott, Christopher -- Qi, Jun -- Ni, Min -- Rao, Prakash K -- Duarte, Melissa -- Wu, Shwu-Yuan -- Chiang, Cheng-Ming -- Anders, Lars -- Young, Richard A -- Winer, Eric P -- Letai, Antony -- Barry, William T -- Carroll, Jason S -- Long, Henry W -- Brown, Myles -- Liu, X Shirley -- Meyer, Clifford A -- Bradner, James E -- Polyak, Kornelia -- CA080111/CA/NCI NIH HHS/ -- CA103867/CA/NCI NIH HHS/ -- CA120184/CA/NCI NIH HHS/ -- CA168504/CA/NCI NIH HHS/ -- P50 CA168504/CA/NCI NIH HHS/ -- R01 CA103867/CA/NCI NIH HHS/ -- England -- Nature. 2016 Jan 21;529(7586):413-7. doi: 10.1038/nature16508. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; Department of Medicine, Brigham and Women's Hospital, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, and Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02115, USA. ; Princess Margaret Cancer Center/University Health Network, Toronto, Ontario M5G1L7, Canada. ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G2M9, Canada. ; Harvard University, Cambridge, Massachusetts 02138, USA. ; Cancer Research UK, Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, UK. ; Department of Pathology, Brigham and Women's Hospital, and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; Simmons Comprehensive Cancer Center, Departments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA. ; Broad Institute, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735014" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-04-18
    Description: Centrosome amplification has long been recognized as a feature of human tumours; however, its role in tumorigenesis remains unclear. Centrosome amplification is poorly tolerated by non-transformed cells and, in the absence of selection, extra centrosomes are spontaneously lost. Thus, the high frequency of centrosome amplification, particularly in more aggressive tumours, raises the possibility that extra centrosomes could, in some contexts, confer advantageous characteristics that promote tumour progression. Using a three-dimensional model system and other approaches to culture human mammary epithelial cells, we find that centrosome amplification triggers cell invasion. This invasive behaviour is similar to that induced by overexpression of the breast cancer oncogene ERBB2 (ref. 4) and indeed enhances invasiveness triggered by ERBB2. Our data indicate that, through increased centrosomal microtubule nucleation, centrosome amplification increases Rac1 activity, which disrupts normal cell-cell adhesion and promotes invasion. These findings demonstrate that centrosome amplification, a structural alteration of the cytoskeleton, can promote features of malignant transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061398/" 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/PMC4061398/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godinho, Susana A -- Picone, Remigio -- Burute, Mithila -- Dagher, Regina -- Su, Ying -- Leung, Cheuk T -- Polyak, Kornelia -- Brugge, Joan S -- Thery, Manuel -- Pellman, David -- 310472/European Research Council/International -- GM083299-1/GM/NIGMS NIH HHS/ -- R01 GM083299/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jun 5;510(7503):167-71. doi: 10.1038/nature13277. Epub 2014 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.). ; 1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France [2] Hopital Saint Louis, Institut Universitaire d'Hematologie, U1160 INSERM/AP-HP/Universite Paris Diderot, Paris 75010, France [3] CYTOO SA, Grenoble 38054, France. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.). ; Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France [2] Hopital Saint Louis, Institut Universitaire d'Hematologie, U1160 INSERM/AP-HP/Universite Paris Diderot, Paris 75010, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739973" target="_blank"〉PubMed〈/a〉
    Keywords: Aneuploidy ; Breast/cytology/pathology ; Breast Neoplasms/genetics/*pathology ; Cell Adhesion ; Cell Line ; Cell Transformation, Neoplastic/genetics/*pathology ; Centrosome/*pathology ; Disease Progression ; Enzyme Activation ; Epithelial Cells/cytology/pathology ; *Genes, erbB-2 ; Humans ; Microtubules/chemistry/metabolism/pathology ; Neoplasm Invasiveness/pathology ; Receptor, ErbB-2/genetics/metabolism ; rac1 GTP-Binding Protein/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marusyk, Andriy -- Polyak, Kornelia -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):528-9. doi: 10.1126/science.1234415.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23372002" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Shape ; Clonal Evolution ; Clone Cells ; Colorectal Neoplasms/classification/*pathology/*prevention & control ; *Disease Eradication ; Drug Resistance, Neoplasm/genetics ; Epigenesis, Genetic ; Humans ; Phenotype
    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
    Keywords: RNA ; PATIENT ; TISSUES ; BREAST-CANCER ; IN-SITU ; resistance ; EVOLUTION ; SINGLE CELLS ; INTRATUMOR HETEROGENEITY ; CHALLENGE
    Abstract: The extent of tumor heterogeneity is an emerging theme that researchers are only beginning to understand. How genetic and epigenetic heterogeneity affects tumor evolution and clinical progression is unknown. The precise nature of the environmental factors that influence this heterogeneity is also yet to be characterized. Nature Medicine, Nature Biotechnology and the Volkswagen Foundation organized a meeting focused on identifying the obstacles that need to be overcome to advance translational research in and tumor heterogeneity. Once these key questions were established, the attendees devised potential solutions. Their ideas are presented here.
    Type of Publication: Journal article published
    PubMed ID: 26248267
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  • 8
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Airborne dusts were collected by a two-stage sampler on an electrically activated filter at different working places. Inhalable size (particles are less than 5 μm) and course fractions were separated by a cyclone. The particle size distribution of three minerals (quartz, calcite, albite) and four metals (Pb, Cd, Cr, Co) was determined. Infrared spectroscopic and AAS methods were applied. The quartz concentrated in the course fractions while the calcite in the inhalable ones. No direct relation to the size fractions was found for albite. The toxic metals were extremely enriched in the fine fractions, in some cases 5–12 times more than in the course fractions. Since only the fine particles might be deposited in the deepest parts of the lung the importance of elimination of pollution sources should be taken into account.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1436-5073
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Zusammenfassung Das Verhalten verschiedener Quecksilber-Verbindungen im Graphitrohr bei der Bestimmung der Atomabsorption wurde untersucht. Bei wasserlöslichen, flüchtigen Quecksilberverbindungen (Nitrat, Chlorid) tritt schon bei dem Eintrocknen des Tropfens ein erheblicher Quecksilberverlust auf. Quecksilber kann aber in Form des kolloidalen Quecksilbersulfids bei ca. 200° C und Versprühung bei relativ niedriger Temperatur bestimmt werden. Einige Störungen begrenzen die Verwendbarkeit des Verfahrens in der Praxis (mit Quecksilber flüchtige Verbindungen, Anwesenheit anderer Metalle als Sulfide), aber die Verwendung von Quecksilber-Dithizonat beseitigt diese Störungen.
    Notes: Summary The atomic-absorption behaviour of different mercury compounds in the graphite tube was investigated. It was established that in the case of water-soluble volatile mercury compounds (nitrate, chloride) there is a considerable mercury loss even during the drying of the drop. The mercury can be determined, however, in the form of colloidal mercury sulphide atca. 200° C and with atomization at a relatively low temperature. Some interferences limit the use of the method in practice (compounds evaporating together with the mercury, presence of other metals producing sulphide precipitates) but the use of mercury dithizonate overcomes these limitations. The method was applied for determination of the mercury content of waste water and waste water sludge.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1572-8943
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Résumé Méthode thermométrique rapide pour le dosage du Cr(VI) en présence d'autres substances oxydantes [par ex. le Fe(III)]. Le peroxyde d'hydrogène utilisé comme réactif réduit le Cr(VI) en Cr(III) sans que le Fe(III) gêne.
    Abstract: Zusammenfassung Es wurde ein thermometrisches Schnellverfahren zur Bestimmung von Cr(VI) neben anderen reduzierbaren Stoffen [z. B. Fe(III)] ausgearbeitet, wie es z. B. bei der Analyse von Chromerzen der Fall ist. Reagenz ist Wasserstoffperoxid, welches die Reduktion des Chroms ohne Störung des Eisens ermöglicht.
    Notes: Abstract A rapid thermometric method has been developed for the determination of dichromate ions. The method can also be applied in the presence of other oxidizing agents [e.g. Fe(III)in chromium ore analysis]. Hydrogen peroxide was used as reagent which permits the reduction of dichromate ions to chromium(III) without the reduction of Fe(III).
    Type of Medium: Electronic Resource
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