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  1. Book ; Thesis: Aurorakinase-Inhibitor ZM447439 induziert Polyploidie und Apoptose bei kolorektalen Tumorzelllinien in vitro

    Jung, Anke Christina

    2012  

    Author's details vorgelegt von Anke Christina Jung
    Language German
    Size 102 S. : Ill., graph. Darst.
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Tübingen, Univ., Diss., 2012
    HBZ-ID HT017495125
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Thesis: Einsatz von Kohlenstoff-Nanomaterialien als neuartige Katalysatorträger

    Jung, Anke

    am Beispiel von Hydrierreaktionen und der Fischer-Tropsch-Synthese

    (Berichte aus der Verfahrenstechnik)

    2009  

    Author's details Anke Jung
    Series title Berichte aus der Verfahrenstechnik
    Keywords Trägerkatalysator ; Fischer-Tropsch-Synthese ; Funktionalisierung ; Herstellung ; Katalytische Hydrierung ; Kohlenstofffaser ; Nanostrukturiertes Material ; Kohlenstoff-Nanoröhre
    Language German
    Size VIII, 249 S, Ill., graph. Darst, 21 cm, 398 gr.
    Publisher Shaker
    Publishing place Aachen
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Univ., Diss.--Bayreuth, 2009
    ISBN 9783832280383 ; 3832280383
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  3. Book ; Online ; Thesis: Einsatz von Kohlenstoff-Nanomaterialien als neuartige Katalysatorträger

    Jung, Anke [Verfasser]

    am Beispiel von Hydrierreaktionen und der Fischer-Tropsch-Synthese

    2009  

    Author's details Anke Jung
    Keywords Technische Chemie ; Technical Chemistry
    Subject code sg660
    Language German
    Publisher Shaker
    Publishing place Aachen
    Document type Book ; Online ; Thesis
    ISBN 978-3-8322-8038-3 ; 3-8322-8038-3
    Database Digital theses on the web

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  4. Article ; Online: Aurora kinase inhibitor ZM447439 induces apoptosis via mitochondrial pathways.

    Li, Minglun / Jung, Anke / Ganswindt, Ute / Marini, Patrizia / Friedl, Anna / Daniel, Peter T / Lauber, Kirsten / Jendrossek, Verena / Belka, Claus

    Biochemical pharmacology

    2010  Volume 79, Issue 2, Page(s) 122–129

    Abstract: ZM447439 (ZM) is a potent and selective inhibitor of aurora-A and -B kinase with putative anti-tumoral activity. Inhibitors of aurora kinases were shown to induce apoptosis in vitro and in vivo. To investigate the underlying mechanisms, cell death ... ...

    Abstract ZM447439 (ZM) is a potent and selective inhibitor of aurora-A and -B kinase with putative anti-tumoral activity. Inhibitors of aurora kinases were shown to induce apoptosis in vitro and in vivo. To investigate the underlying mechanisms, cell death pathways triggered by ZM was analysed in HCT-116 colorectal cancer cells. Through correlation of polyploidization and apoptosis in different knockout cells, the interrelation of these cellular responses to ZM was investigated. ZM induced apoptosis in a concentration- and time-dependent manner. ZM-induced apoptosis was associated with an upregulation of p53, breakdown of the mitochondrial membrane potential (DeltaPsim) and activation of caspase-3. To precisely define key components for ZM-induced apoptosis, knockout cells lacking p53, Bak, Bax or both Bak and Bax were used. Lack of p53 reduced ZM-induced apoptosis and breakdown of DeltaPsim, while lack of Bak, Bax or both almost completely inhibited apoptosis and breakdown of DeltaPsim. Since no difference in apoptosis induction was detectable between HCT-116 cells lacking Bak, Bax or both, apoptosis induction depended non-redundantly on both Bak and Bax. Phenomenally, ZM induced notable polyploidization in all examined cells, especially in p53-/- cells. A correlation between polyploidization and apoptosis was observed in wild-type, and also in p53-/- cells, albeit with a modest extent of apoptosis. Moreover, in Bak-/-, Bax-/- and Bak/Bax-/- cells apoptosis was totally inhibited in spite of the strongest polyploidization, suggesting apoptosis may be a secondary event following polyploidization in HCT-116 cells. Thus ZM-induced apoptosis depends not only on polyploidization, but also on the intracellular apoptotic signaling.
    MeSH term(s) Apoptosis/drug effects ; Aurora Kinases ; Benzamides/pharmacology ; Cell Line, Tumor ; Flow Cytometry ; Humans ; Mitochondria/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Quinazolines/pharmacology
    Chemical Substances 4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline ; Benzamides ; Protein Kinase Inhibitors ; Quinazolines ; Aurora Kinases (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2010-01-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2009.08.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A variant affecting a putative miRNA target site in estrogen receptor (ESR) 1 is associated with breast cancer risk in premenopausal women.

    Tchatchou, Sandrine / Jung, Anke / Hemminki, Kari / Sutter, Christian / Wappenschmidt, Barbara / Bugert, Peter / Weber, Bernhard H F / Niederacher, Dieter / Arnold, Norbert / Varon-Mateeva, Raymonda / Ditsch, Nina / Meindl, Alfons / Schmutzler, Rita K / Bartram, Claus R / Burwinkel, Barbara

    Carcinogenesis

    2009  Volume 30, Issue 1, Page(s) 59–64

    Abstract: MicroRNAs (miRNAs) negatively regulate expression of target transcripts by hybridization to complementary sites of their messenger RNA targets. Chen et al. have described several putative functional single nucleotide polymorphisms (SNPs) in miRNA target ... ...

    Abstract MicroRNAs (miRNAs) negatively regulate expression of target transcripts by hybridization to complementary sites of their messenger RNA targets. Chen et al. have described several putative functional single nucleotide polymorphisms (SNPs) in miRNA target sites. Here, we selected 11 miRNA target site SNPs located in 3' untranslated regions of genes involved in cancer and breast cancer to analyze their impact on breast cancer risk using a large familial study population. Whereas no association was observed for 10 SNPs, a significant association was revealed for the variant affecting a miRNA target site in the estrogen receptor (ESR) 1. Age stratification showed that the association was stronger in premenopausal women [C versus T: odds ratio (OR) = 0.60, confidence interval (CI) = 0.41-0.89, P = 0.010]. Furthermore, the effect was stronger in high-risk familial cases (C versus T: OR = 0.42, CI = 0.25-0.71, P = 0.0009). Clinical studies have shown that elimination of ESR1 significantly reduces breast cancer risk. Thus, therapies that inhibit ESR1 are used for breast cancer treatment. According to in silico analysis, ESR1_rs2747648 affects the binding capacity of miR-453, which is stronger when the C allele is present. In contrast, the T allele attenuates the binding of miR-453, which might lead to a reduced miRNA-mediated ESR1 repression, in consequence higher ESR1 protein levels and an increased breast cancer risk. Thus, the breast cancer protective effect observed for the C allele in premenopausal women is biologically reasonable. The analysis of large study populations in multicentre collaboration will be needed to verify the association and answer questions regarding the possible impact of this variant on therapeutic and clinical outcome.
    MeSH term(s) Adult ; Breast Neoplasms/genetics ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Humans ; MicroRNAs/genetics ; Middle Aged ; Polymorphism, Single Nucleotide ; Premenopause
    Chemical Substances Estrogen Receptor alpha ; MicroRNAs
    Language English
    Publishing date 2009-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgn253
    Database MEDical Literature Analysis and Retrieval System OnLINE

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