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Berlin Brandenburg

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  • 1
    Language: English
    In: Journal of medicinal chemistry, 10 May 2012, Vol.55(9), pp.4099-100
    Keywords: Antineoplastic Agents -- Pharmacology ; Inhibitor of Apoptosis Proteins -- Antagonists & Inhibitors ; Thiadiazoles -- Pharmacology
    ISSN: 00222623
    E-ISSN: 1520-4804
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  • 2
    Language: English
    In: Cancer Research, 04/15/2013, Vol.73(8 Supplement), pp.SY24-03-SY24-03
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 3
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 01 August 2014, Vol.20(15), pp.3915-20
    Description: Inhibitor of apoptosis (IAP) proteins are overexpressed in multiple human malignancies, an event that is associated with poor prognosis and treatment resistance. Therefore, IAP proteins represent relevant targets for therapeutic intervention. Second mitochondrial activator of caspases (Smac) is a mitochondrial protein that is released into the cytosol upon the induction of programmed cell death and promotes apoptosis by neutralizing IAP proteins. On the basis of this property, a variety of small-molecule inhibitors have been developed that mimic the binding domain of the native Smac protein to IAP proteins. Evaluation of these Smac mimetics in preclinical studies revealed that they particularly synergize together with agents that trigger the death receptor pathway of apoptosis. Such combinations might therefore be of special interest for being included in the ongoing evaluation of Smac mimetics in early clinical trials.
    Keywords: Biomimetic Materials -- Chemistry ; Inhibitor of Apoptosis Proteins -- Metabolism ; Intracellular Signaling Peptides and Proteins -- Antagonists & Inhibitors ; Mitochondrial Proteins -- Antagonists & Inhibitors ; Neoplasms -- Drug Therapy ; Oligopeptides -- Chemistry ; Receptors, Death Domain -- Antagonists & Inhibitors ; Signal Transduction -- Drug Effects
    ISSN: 1078-0432
    E-ISSN: 15573265
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  • 4
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 15 January 2014, Vol.20(2), pp.289-95
    Description: Inhibitor of apoptosis (IAP) proteins play a critical role in the control of survival and cell death by regulating key signaling events such as caspase activation and NF-κB signaling. Because aberrantly high expression of IAP proteins represents a frequent oncogenic event in human cancers, therapeutic targeting of IAP proteins is considered as a promising approach. Several small-molecule pharmacologic inhibitors of IAP proteins that mimic the binding domain of the endogenous IAP antagonist second mitochondrial activator of caspases (Smac) to IAP proteins have been developed over the past few years. IAP antagonists have been shown in various preclinical cancer models to either directly initiate cell death or, alternatively, to prime cancer cells for cytotoxic therapies by lowering the threshold for cell death induction. IAP antagonists (i.e., GDC-0917/CUDC-427, LCL161, AT-406, HGS1029, and TL32711) are currently under evaluation in early clinical trials alone or in combination regimens. Thus, the concept to therapeutically target IAP proteins in human cancer has in principle been successfully transferred into a clinical setting and warrants further evaluation as a treatment approach.
    Keywords: Signal Transduction ; Inhibitor of Apoptosis Proteins -- Metabolism ; Neoplasms -- Metabolism
    ISSN: 1078-0432
    E-ISSN: 15573265
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  • 5
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 15 November 2015, Vol.21(22), pp.5030-6
    Description: Inhibitor of Apoptosis (IAP) proteins block programmed cell death and are expressed at high levels in various human cancers, thus making them attractive targets for cancer drug development. Second mitochondrial activator of caspases (Smac) mimetics are small-molecule inhibitors that mimic Smac, an endogenous antagonist of IAP proteins. Preclinical studies have shown that Smac mimetics can directly trigger cancer cell death or, even more importantly, sensitize tumor cells for various cytotoxic therapies, including conventional chemotherapy, radiotherapy, or novel agents. Currently, several Smac mimetics are under evaluation in early clinical trials as monotherapy or in rational combinations (i.e., GDC-0917/CUDC-427, LCL161, AT-406/Debio1143, HGS1029, and TL32711/birinapant). This review discusses the promise as well as some challenges at the translational interface of exploiting Smac mimetics as cancer therapeutics.
    Keywords: Antineoplastic Agents -- Therapeutic Use ; Apoptosis -- Drug Effects ; Intracellular Signaling Peptides and Proteins -- Therapeutic Use ; Mitochondrial Proteins -- Therapeutic Use ; Neoplasms -- Drug Therapy
    ISSN: 1078-0432
    E-ISSN: 15573265
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  • 6
    Language: English
    In: Experimental Cell Research, 01 July 2012, Vol.318(11), pp.1208-1212
    Description: Evasion of apoptosis represents a key mechanism leading to treatment resistance of human cancers. Abnormal regulation of chromatin remodeling has been implied in tumorigenesis as well as treatment resistance. Acetylation of histones represents one of the key posttranslational modifications that contribute to the regulation of chromatin remodeling. Histone acetylation is governed by the balance between enzymes that put acetyl groups on histone tails or, alternatively, remove them. Since a disturbed regulation of histone acetylation plays an important role in cancer formation and progression, a variety of histone deacetylase (HDAC) inhibitors have been developed in recent years to target aberrant HDAC activity. HDAC inhibitors also represent a promising strategy to lower the threshold of cancer cells for apoptosis induction. For example, synergistic induction of apoptosis has been documented for the concomitant use of HDAC inhibitors together with the death receptor ligand TRAIL in a panel of human cancers. Understanding the molecular mechanism that mediates this synergistic drug interaction will be critical to further optimize this approach in order to successfully translate it into a clinical setting.
    Keywords: Apoptosis ; Hdac ; Trail ; Biology
    ISSN: 0014-4827
    E-ISSN: 1090-2422
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  • 7
    Language: English
    In: Mitochondrion, May 2013, Vol.13(3), pp.195-198
    Description: Most anticancer therapies exert their action by triggering programmed cell death (apoptosis) in cancer cells. The mitochondrial pathway of apoptosis is initiated by mitochondrial outer membrane permeabilization, leading to the release of apoptogenic factors such as cytochrome c or Smac from the mitochondrial intermembrane space into the cytosol. Mitochondrial outer membrane permeabilization is tightly controlled, for example by pro- and anti-apoptotic proteins of the Bcl-2 family. Recent evidence indicates that inhibition of the PI3K/Akt/mTOR pathway by small-molecule PI3K inhibitors primes cancer cells to mitochondrial apoptosis by tipping the balance towards pro-apoptotic Bcl-2 proteins, resulting in increased mitochondrial outer membrane permeabilization. Thus, mitochondrial apoptotic events play an important role in PI3K inhibitor-mediated sensitization for apoptosis.
    Keywords: Mitochondria ; Apoptosis ; Pi3k ; Biology
    ISSN: 1567-7249
    E-ISSN: 1872-8278
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  • 8
    Language: English
    In: Cancer Letters, 28 May 2013, Vol.332(2), pp.369-373
    Description: Evasion of apoptosis (programmed cell death) is a characteristic feature of human cancers including childhood malignancies. Since cytotoxic therapies such as chemotherapy or radiotherapy trigger apoptosis as a primary mechanism of action, resistance to apoptosis can also lead to treatment resistance. Studies on apoptosis pathways in childhood malignancies yielded a series of key molecules that can now be exploited as molecular targets for the development of targeted therapies. This strategy is anticipated to open novel perspectives for more effective treatment options for children with cancer.
    Keywords: Apoptosis ; Childhood Cancer ; Trail ; Bcl-2 ; Iaps ; Medicine
    ISSN: 0304-3835
    E-ISSN: 1872-7980
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  • 9
    Language: English
    In: Cancer Letters, 10 September 2013, Vol.338(1), pp.168-173
    Description: Cancer stem cell are considered to represent a population within the bulk tumor that share many similarities to normal stem cells as far as their capacities to self-renew, differentiate, proliferate and to reconstitute the entire tumor upon serial transplantation are concerned. Since cancer stem cells have been shown to be critical for maintaining tumor growth and have been implicated in treatment resistance and tumor progression, they constitute relevant targets for therapeutic intervention. Indeed, it has been postulated that eradication of cancer stem cells will be pivotal in order to achieve long-term relapse-free survival. However, one of the hallmarks of cancer stem cells is their high resistance to undergo cell death including apoptosis in response to environmental cues or cytotoxic stimuli. Since activation of apoptosis programs in tumor cells underlies the antitumor activity of most currently used cancer therapeutics, it will be critical to develop strategies to overcome the intrinsic resistance to apoptosis of cancer stem cells. Thus, a better understanding of the molecular mechanisms that are responsible for the ability of cancer stem cells to evade apoptosis will likely open new avenues to target this critical pool of cells within the tumor in order to develop more efficient treatment options for patients suffering from cancer.
    Keywords: Cancer Stem Cells ; Apoptosis ; Death Receptors ; Bcl-2 ; Iap Proteins ; Medicine
    ISSN: 0304-3835
    E-ISSN: 1872-7980
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  • 10
    Language: English
    In: Cancer Treatment Reviews, October 2012, Vol.38(6), pp.760-766
    Description: Radiotherapy initiates a variety of signaling events in cancer cells that eventually lead to cell death in case the DNA damage cannot be repaired. However, the signal transduction pathways that mediate cell death in response to radiation-inflicted DNA damage are frequently disturbed in human cancers, contributing to radioresistance. For example, aberrant activation of antiapoptotic programs such as high expression of Inhibitor of Apoptosis (IAP) proteins has been shown to interfere with the efficacy of radiotherapy. Since IAP proteins have been linked to radioresistance in several malignancies, therapeutic targeting of IAP proteins may open new perspectives to overcome radioresistance. Therefore, molecular targeting of IAP proteins may provide novel opportunities to reactivate cell death pathways that mediate radiation-induced cytotoxicity. A number of strategies have been developed in recent years to antagonize IAP proteins for the treatment of cancers. Some of these approaches have already been translated into a clinical application. While IAP protein-targeting agents are currently being evaluated in early clinical trials alone or in combination with conventional chemotherapy, they have not yet been tested in combination with radiation therapy. Therefore, it is a timely subject to discuss the opportunities of antagonizing IAP proteins for radiosensitization. Preclinical studies demonstrating the potential of this concept in relevant and models underscore that this combination approach warrants further clinical investigation. Thus, combination protocols using IAP antagonists together with radiotherapy may pave the avenue to more effective radiation-based treatment options for cancer patients.
    Keywords: Iap Proteins ; Smac ; Apoptosis ; Radiotherapy ; Medicine
    ISSN: 0305-7372
    E-ISSN: 1532-1967
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