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  1. Book: Mitochondria

    Neužil, Jiří / Pervaiz, Shazib / Fulda, Simone

    the anti-cancer target for the third millennium

    2014  

    Author's details Jiri Neuzil ; Shazib Pervaiz ; Simone Fulda ed
    Keywords Mitochondria
    Subject code 571.657
    Language English
    Size VIII, 382 S. : Ill., graph. Darst., 24 cm
    Publisher Springer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    Note Includes bibliographical references
    HBZ-ID HT018319416
    ISBN 978-94-017-8983-7 ; 9789401789844 ; 94-017-8983-5 ; 9401789843
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2014 A 2702 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: HIF-1-regulated glucose metabolism in the control of apoptosis signaling.

    Fulda, Simone

    Expert review of endocrinology & metabolism

    2019  Volume 3, Issue 3, Page(s) 303–308

    Abstract: Resistance of human cancers to current treatment approaches remains a major concern in oncology. Therefore, much effort has been focused on identifying molecular pathways that are responsible for primary or acquired resistance of cancers in order to ... ...

    Abstract Resistance of human cancers to current treatment approaches remains a major concern in oncology. Therefore, much effort has been focused on identifying molecular pathways that are responsible for primary or acquired resistance of cancers in order to overcome resistance. Hypoxia is one of the hallmarks of solid tumors and usually correlates with poor prognosis. Under hypoxic conditions, cancer cells undergo a variety of adoptive changes, including the activation of signaling pathways, which promote cancer cell survival and block cell death. Hypoxia inducible factor (HIF)-1 is the key transcription factor that mediates adaptation of cancer cells to the hypoxic environment. There is increasing evidence that HIF-1 promotes tumor growth, at least in part, by upregulating genes that are involved in cellular energy metabolism. Thus, HIF-1 and hypoxia-inducible genes represent attractive targets for the design of molecular targeted therapies, which may offer new therapeutic options for a wide range of malignancies.
    Language English
    Publishing date 2019-02-12
    Publishing country England
    Document type Journal Article
    ISSN 1744-8417
    ISSN (online) 1744-8417
    DOI 10.1586/17446651.3.3.303
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book ; Online: Biology-Driven Targeted Therapy of Pediatric Soft-Tissue and Bone Tumors: Current Opportunities and Future Challenges

    Grunewald, Thomas G. P. / Fulda, Simone

    2016  

    Abstract: Recent advances in the understanding of the biological basis of pediatric soft-tissue and bone tumors, especially owing to the advent of "omics" technologies, have led to an exponential increase in the current knowledge on the genetic and cellular patho- ... ...

    Abstract Recent advances in the understanding of the biological basis of pediatric soft-tissue and bone tumors, especially owing to the advent of "omics" technologies, have led to an exponential increase in the current knowledge on the genetic and cellular patho-mechanisms that drive these diseases. This offers the unprecedented opportunity to develop and implement targeted therapies such as monoclonal antibodies, small molecules, oncolytic viruses, and immunotherapies in standard and/or personalized treatment regimens. However, to date only a few examples document a successful translation of discoveries from the bench to the bedside. Recent international expert congresses such as the "Pediatric Cancer Translational Genomics" conference (Phoenix, Arizona, 2012), the ESF-EMBO workshop on "Molecular Biology and Innovative Therapies in Sarcomas" (Pultusk, Poland, 2012), and the AACR special meeting on "Pediatric Cancer at the Crossroads - Translating Discovery into Improved Outcomes" (San Diego, California, 2013) further emphasize the urgent need for a more rapid and especially more successful translational process. Hence, we strongly believe that a Frontiers Research Topic aiming at this aspect would fit just in time and that it would have great potential to receive numerous contributions of outstanding experts of the field. The proposed Frontiers Research Topic shall provide a platform for active and interdisciplinary discussion, summarize current state-of-the-art knowledge on all basic research and translational aspects in pediatric soft-tissue and bone tumors, and offer new perspectives of how to further promote and accelerate the translational process. We welcome high-quality original research articles, brief reports, as well as opinion, hypothesis, and review articles, and especially encourage submissions from early-career scientists
    Keywords Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; Medicine (General)
    Size 1 electronic resource (147 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020090542
    ISBN 9782889198191 ; 2889198197
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  4. Article ; Online: Cell death-based treatment of glioblastoma.

    Fulda, Simone

    Cell death & disease

    2018  Volume 9, Issue 2, Page(s) 121

    Abstract: Cancer cells including glioblastoma have typically evolved multiple mechanisms to escape programmed cell death in order to maintain their survival. Defects in cell death mechanisms not only facilitate tumorigenesis but also ensure resistance to current ... ...

    Abstract Cancer cells including glioblastoma have typically evolved multiple mechanisms to escape programmed cell death in order to maintain their survival. Defects in cell death mechanisms not only facilitate tumorigenesis but also ensure resistance to current anticancer therapies. This emphasizes that targeting cell death pathways may provide a means to tackle one of the Achilles' heels of cancer. Over the last decades several approaches have been developed to selectively target cell death pathways for therapeutic purposes. Some of these concepts have already been transferred into clinical application in oncology and may open new perspectives for the treatment of cancer.
    MeSH term(s) Apoptosis Regulatory Proteins/metabolism ; Cell Death ; Glioblastoma/pathology ; Glioblastoma/therapy ; Humans ; Molecular Targeted Therapy ; Signal Transduction ; Systems Biology
    Chemical Substances Apoptosis Regulatory Proteins
    Language English
    Publishing date 2018-01-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-017-0021-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Targeting autophagy for the treatment of cancer.

    Fulda, Simone

    Biological chemistry

    2018  Volume 399, Issue 7, Page(s) 673–677

    Abstract: Macroautophagy (herein termed autophagy) is evolutionarily highly conserved across eukaryotic cells and represents an intracellular catabolic process that targets damaged macromolecules and organelles for degradation. Autophagy is dysregulated in various ...

    Abstract Macroautophagy (herein termed autophagy) is evolutionarily highly conserved across eukaryotic cells and represents an intracellular catabolic process that targets damaged macromolecules and organelles for degradation. Autophagy is dysregulated in various human diseases including cancer. In addition, many drugs currently used for the treatment of cancer can engage autophagy, which typically promotes cancer cell survival by mitigating cellular stress. However, under certain circumstances activation of autophagy upon anticancer drug treatment can also trigger a lethal type of autophagy termed autophagic cell death (ACD). This may pave new avenues for exploiting the autophagic circuitry in oncology. This review presents the concept and some examples of anticancer drug-induced ACD.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Humans ; Neoplasms/drug therapy ; Neoplasms/pathology
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2018-02-26
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1334659-3
    ISSN 1437-4315 ; 1431-6730 ; 1432-0355
    ISSN (online) 1437-4315
    ISSN 1431-6730 ; 1432-0355
    DOI 10.1515/hsz-2018-0105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.50: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Repurposing anticancer drugs for targeting necroptosis.

    Fulda, Simone

    Cell cycle (Georgetown, Tex.)

    2018  Volume 17, Issue 7, Page(s) 829–832

    Abstract: Necroptosis represents a form of programmed cell death that can be engaged by various upstream signals, for example by ligation of death receptors, by viral sensors or by pattern recognition receptors. It depends on several key signaling proteins, ... ...

    Abstract Necroptosis represents a form of programmed cell death that can be engaged by various upstream signals, for example by ligation of death receptors, by viral sensors or by pattern recognition receptors. It depends on several key signaling proteins, including the kinases Receptor-Interacting Protein (RIP)1 and RIP3 and the pseudokinase mixed-lineage kinase domain-like protein (MLKL). Necroptosis has been implicated in a number of physiological and pathophysiological conditions and is disturbed in many human diseases. Thus, targeted interference with necroptosis signaling may offer new opportunities for the treatment of human diseases. Besides structure-based drug design, in recent years drug repositioning has emerged as a promising alternative to develop drug-like compounds. There is accumulating evidence showing that multi-targeting kinase inhibitors, for example Dabrafenib, Vemurafenib, Sorafenib, Pazopanib and Ponatinib, used for the treatment of cancer also display anti-necroptotic activity. This review summarizes recent evidence indicating that some anticancer kinase inhibitors also negatively affect necroptosis signaling. This implies that some cancer therapeutics may be repurposed for other pathologies, e.g. ischemic or inflammatory diseases.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Antineoplastic Agents/pharmacology ; Antioxidants/pharmacology ; Apoptosis/drug effects ; Apoptosis/genetics ; Drug Repositioning ; Humans ; Imidazoles/pharmacology ; Necrosis/genetics ; Necrosis/metabolism ; Necrosis/pathology ; Necrosis/prevention & control ; Oximes/pharmacology ; Pyridazines/pharmacology ; Pyrimidines/pharmacology ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reperfusion Injury/prevention & control ; Sorafenib/pharmacology ; Sulfonamides/pharmacology ; Systemic Inflammatory Response Syndrome/drug therapy ; Systemic Inflammatory Response Syndrome/genetics ; Systemic Inflammatory Response Syndrome/metabolism ; Systemic Inflammatory Response Syndrome/pathology ; Vemurafenib/pharmacology
    Chemical Substances Anti-Inflammatory Agents ; Antineoplastic Agents ; Antioxidants ; Imidazoles ; Oximes ; Pyridazines ; Pyrimidines ; Sulfonamides ; Vemurafenib (207SMY3FQT) ; ponatinib (4340891KFS) ; pazopanib (7RN5DR86CK) ; Sorafenib (9ZOQ3TZI87) ; dabrafenib (QGP4HA4G1B)
    Language English
    Publishing date 2018-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2018.1442626
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: Autophagy in Cancer Therapy.

    Fulda, Simone

    Frontiers in oncology

    2017  Volume 7, Page(s) 128

    Abstract: Autophagy represents a catabolic program involved in the degradation of cellular ... ...

    Abstract Autophagy represents a catabolic program involved in the degradation of cellular components
    Language English
    Publishing date 2017-06-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2017.00128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Therapeutic opportunities based on caspase modulation.

    Fulda, Simone

    Seminars in cell & developmental biology

    2017  Volume 82, Page(s) 150–157

    Abstract: Caspases are a family of proteolytic enzymes that play a critical role in the regulation of programmed cell death via apoptosis. Activation of caspases is frequently impaired in human cancers, contributing to cancer formation, progression and therapy ... ...

    Abstract Caspases are a family of proteolytic enzymes that play a critical role in the regulation of programmed cell death via apoptosis. Activation of caspases is frequently impaired in human cancers, contributing to cancer formation, progression and therapy resistance. A better understanding of the molecular mechanisms regulating caspase activation in cancer cells is therefore highly important. Thus, targeted modulation of caspase activation and apoptosis represents a promising approach for the development of new therapeutic options to elucidate cancer cell death.
    MeSH term(s) Caspases/pharmacology ; Caspases/therapeutic use ; Humans
    Chemical Substances Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2017-12-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2017.12.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2918: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Book ; Thesis: Apoptosemechanismen bei zytotoxischer Therapie

    Fulda, Simone

    2001  

    Author's details vorgelegt von Simone Fulda
    Language German ; English
    Size 38, [222] S., Ill., graph. Darst., 30 cm
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Ulm, Univ., Habil.-Schr., 2001
    Note Enth. außerdem 30 Sonderabdr. aus verschiedenen Zeitschr. - Beitr. teilw. dt., teilw. engl.
    HBZ-ID HT013334828
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2002 E 1416 order to use in reading room Magazin

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  10. Article ; Online: Mitochondria, redox signaling and cell death in cancer.

    Fulda, Simone

    Biological chemistry

    2016  Volume 397, Issue 7, Page(s) 583

    Language English
    Publishing date 2016-07-01
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1334659-3
    ISSN 1437-4315 ; 1431-6730 ; 1432-0355
    ISSN (online) 1437-4315
    ISSN 1431-6730 ; 1432-0355
    DOI 10.1515/hsz-2016-0199
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.50: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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