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  • 1
    Keywords: CELLS ; CELL ; Germany ; THERAPY ; PROTEIN ; MOLECULES ; TISSUE ; MICE ; MECHANISM ; TISSUES ; mechanisms ; HEALTH ; Drosophila ; GLUTATHIONE ; PLASMA ; STRESS ; AGE ; NECROSIS-FACTOR-ALPHA ; DAMAGE ; LIFE-SPAN ; CAENORHABDITIS-ELEGANS ; MUSCLE ; PARAMETERS ; SKELETAL-MUSCLE ; DIET ; LIPID-PEROXIDATION ; OXIDATIVE STRESS ; OXYGEN ; antioxidants ; reactive oxygen species ; signaling ; OXIDATIVE-STRESS ; INCREASE ; INSULIN-RECEPTOR ; WEIGHT ; clinical trials ; LIFE ; REACTIVE OXYGEN ; LEVEL ; PROTEIN-TYROSINE PHOSPHATASES ; AGE-RELATED-CHANGES ; function ; LOSSES ; ROS ; PRECURSOR ; age-related decrease in ; ageing related functions ; CALORIE RESTRICTION ; cysteine deficit and ageing ; cysteine supplementation ; GLUTATHIONE REDOX STATE ; improvement of ; insulin receptor signaling and ageing ; limiting availability in old age ; oxidative shift in redox status ; redox signaling 'and ageing ; thiols
    Abstract: The popular use of antioxidative vitamins illustrates the growing awareness of oxidative stress as an important hazard to our health and as an important factor in the ageing process. Superoxide radicals and superoxide-derived reactive oxygen species (ROS) are constantly formed in most cells and tissues. To ensure that ROS can function as biological signaling molecules without excessive tissue damage, ROS are typically scavenged by antioxidants such as glutathione and the vitamins A, C, and E. "Oxidative stress" occurs if the production of ROS is abnormally increased or antioxidant concentrations are decreased. Genetic studies in mice, Drosophila, and Celegans suggested that ageing may be mechanistically linked to oxidative stress. Several manifestations of oxidative stress were shown to increase with age, whereas tissue levels of vitamin E, plasma concentrations of vitamin C, and intracellular glutathione concentrations decrease with age. In at least two independent studies, cysteine supplementation on top of the normal protein diet has shown significant beneficial effects on each of several different parameters relevant to ageing, including skeletal muscle functions. As the quality of life in old age is severely compromised by the loss of skeletal muscle function, and as muscle function can be measured with satisfactory precision, loss of muscle function is one of the most attractive surrogate parameters of ageing. The mechanisms by which a deficit in glutathione and its precursor cysteine contributes to various ageing-related degenerative processes appears to be related largely but not exclusively to the dysregulation of redox-regulated biological signaling cascades
    Type of Publication: Journal article published
    PubMed ID: 17100590
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  • 2
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; EXPRESSION ; IN-VIVO ; GENE ; GENE-EXPRESSION ; DIFFERENTIATION ; MECHANISM ; INDUCTION ; CYCLE ; ACID ; DNA methylation ; POLYPHENOLS ; RECEPTORS ; chemoprevention ; histone deacetylase inhibitor ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; HYPERMETHYLATION ; RETINOIC ACID ; HYPOMETHYLATION ; INHIBITORS ; SUPPRESSOR GENES ; HISTONE ACETYLATION ; high-throughput analysis ; CPG-ISLAND METHYLATION ; chemopreventive agents ; TUMOR-SUPPRESSOR GENES ; epigenetic ; histone modifications ; DNA METHYLTRANSFERASE INHIBITORS ; chromatin modifications ; HISTONE METHYLATION ; ABERRANT CRYPT FORMATION ; DNA methyltransferase (DNMT) ; epigenomic ; GREEN TEA POLYPHENOLS ; histone acetyl transferase (HAT) ; histone deacetylase (HDAC) ; NORDIHYDROGUAIARETIC ACID NDGA ; sirtuins ; SMALL-MOLECULE ACTIVATORS
    Abstract: The term "epigenetics" refers to modifications in gene expression caused by heritable, but potentially reversible, changes in DNA methylation and chromatin structure. Given the fact that epigenetic modifications occur early in carcinogenesis and represent potentially initiating events in cancer development, they have been identified as promising new targets for prevention strategies. The present review will give a comprehensive overview of the current literature on chemopreventive agents and their influence on major epigenetic mechanisms, that is DNA methylation, histone acetylation and methylation, and microRNAs, both in vitro and in rodent and human studies, taking into consideration specific mechanisms of action, target sites, concentrations, methods used for analysis, and outcome. Chemopreventive agents with reported mechanisms targeting the epigenome include micronutrients (folate, selenium, retinoic acid, Vit. E), butyrate, polyphenols (from green tea, apples, coffee, and other dietary sources), genistein and soy isoflavones, parthenolide, curcumin, ellagitannin, indol-3-carbinol (I3C) and diindolylmethane (DIM), mahanine, nordihydroguaiaretic acid (NDGA), lycopene, sulfur-containing compounds from Allium and cruciferous vegetables (sulforaphane, phenylethyl isothiocyanate (PEITC), phenylhexyl isothiocyanate (PHI), diallyldisulfide (DADS), allyl mercaptan (AM)), antibiotics (mithramycin A, apicidin), pharmacological agents (celecoxib, DFMO, 5-aza-2'-deoxycytidine and zebularine), compounds affecting sirtuin activity (resveratrol, dihydrocoumarin, cambinol), inhibitors of histone acetyl transferases (anacardic acid, garcinol, ursodeoxycholic acid), and relatively unexplored modulators of histone lysine methylation (chaetocin, polyamine analogues, n-3 polyunsaturated fatty acids). Their effects on global DNA methylation, tumor suppressor genes silenced by promoter methylation, histone modifications, and miRNAs deregulated during carcinogenesis have potential impact on multiple mechanisms relevant for chemoprevention, including signal transduction mediated by nuclear receptors and transcription factors such as NF-kappaB, cell cycle progression, cellular differentiation, apoptosis induction, senescence and others. In vivo studies that demonstrate the functional relevance of epigenetic mechanisms for chemopreventive efficacy are still limited. Future research will need to identify best strategies for chemopreventive intervention, taking into account the importance of epigenetic mechanisms for gene regulation.
    Type of Publication: Journal article published
    PubMed ID: 21158707
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  • 3
    Keywords: CANCER ; Germany ; THERAPY ; DRUG ; MOLECULES ; MOLECULE ; TARGET ; TARGETS ; chemoprevention ; CANCER-THERAPY ; ORIGIN ; RE ; cancer therapy ; pharmacology
    Type of Publication: Journal article published
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  • 4
    Keywords: CANCER ; Germany ; THERAPY ; DRUG ; MOLECULES ; MOLECULE ; TARGET ; TARGETS ; chemoprevention ; CANCER-THERAPY ; ORIGIN ; RE ; cancer therapy ; pharmacogenomics ; pharmacology
    Type of Publication: Journal article published
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  • 5
    Keywords: ANGIOGENESIS ; APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; IN-VITRO ; tumor ; AGENTS ; CELL ; Germany ; GENE ; GENES ; PROTEIN ; DRUG ; MOLECULES ; MECHANISM ; INDUCTION ; mechanisms ; GROWTH-FACTOR RECEPTOR ; METABOLITES ; MOLECULE ; TARGET ; resistance ; STRESS ; DERIVATIVES ; CANCER-CELLS ; ONCOGENE ; TARGETS ; OXIDATIVE STRESS ; MULTIDRUG-RESISTANCE ; SWEET ; PLASMODIUM-FALCIPARUM ; multidrug resistance ; antitumor agents ; traditional Chinese medicine ; RE ; OXIDATIVE-STRESS ; PRODUCTS ; TUMOR-SUPPRESSOR ; SUPPRESSOR GENE ; SURFACE GLYCOPROTEIN ; tumor suppressor gene ; ANTIMALARIAL ARTESUNATE ; pharmacogenomics ; sesquiterpene lactones ; TRIOXANE DIMERS ; pharmacology ; oncogenes ; COMPOUND ; ANTITUMOR ; ANTITUMOR ACTIVITIES ; ANTITUMOR AGENT ; CONTROLLED TUMOR PROTEIN ; QINGHAOSU ARTEMISININ ; TRANSFERRIN RECEPTORS ; tumor suppressor genes
    Abstract: Secondary metabolites from plants can serve as defense against herbivores, microbes, viruses or competing plants. Many compounds from medicinal plants have pharmacological activities and thus may be a source for novel antitumor agents. We have analyzed natural products from traditional Chinese medicine during the past decade and focused our interest oil the compound artemisinin from Artemisia annua L. (qinghao, sweet wormwood) and its derivatives. In addition to their anti-malarial properties, artemisinins are cytotoxic for cancer cells. The present review focuses on the mechanisms of action of artemisinins in cancer cells relating to: 1. anti-proliferative and anti-angiogenic effects, 2. induction of apoptosis, 3. oxidative stress, 4. oncogenes and tumor suppressor genes, and 5. multidrug resistance. Data on putative target molecules of artemisinins are presented and discussed, e.g. the translationally controlled tumor protein (TCTP). Emphasis is given to pharmacogenomic approaches to analyze the pleiotropic nature of mechanisms of artemisinins in cancer cells
    Type of Publication: Journal article published
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  • 6
    Keywords: CANCER ; CELL LUNG-CANCER ; IN-VIVO ; microarray ; PROTEIN ; BREAST-CANCER ; Molecular targets ; prostate-specific antigen ; SUPERPARAMAGNETIC IRON-OXIDE ; ALBUMIN-BOUND PACLITAXEL ; COLORIMETRIC SILVER DETECTION ; Nanotechnology ; RESONANCE LIGHT-SCATTERING ; SELF-ASSEMBLED NANOPARTICLES ; SEMICONDUCTOR QUANTUM DOTS
    Abstract: Nanoparticles are sphere-like biocompatible materials made of inert silica, metal or crystals of a few nanometers in size. They are emerging as a novel class of therapeutics for cancer treatment. Being more selective and specific toward their targets, nanoparticles have the ability to enhance the anticancer effects and to simultaneously reduce systemic toxicity compared with conventional therapeutics. Furthermore, they offer the potential to overcome drug resistance leading to higher intracellular drug accumulation. Nowadays, nanotechnologies are applied to molecular diagnostics and incorporated in cutting-edge molecular diagnostic methods, such as DNA and protein microarray biochips. Nanotechnologies enable diagnosis at the single-cell and single-molecule levels. Recent progress in cancer nanotechnology raises exciting opportunities for specific drug delivery. The purpose of this review is to give an overview about different types of nanoparticles and to summarize the latest results regarding their diagnostic and therapeutic applications in the clinic with more focus on cancer treatment. Furthermore, we discuss opportunities, limitations, and challenges faced by therapeutic nanoparticles
    Type of Publication: Journal article published
    PubMed ID: 20955146
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