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    Keywords: CANCER ; CELLS ; IN-VITRO ; tumor ; CELL ; COMBINATION ; evaluation ; human ; VITRO ; CLASSIFICATION ; screening ; EPIDEMIOLOGY ; EXPOSURE ; POPULATION ; MECHANISM ; CARCINOGENESIS ; mechanisms ; TARGET ; VERIFICATION ; IDENTIFICATION ; PROGRESSION ; etiology ; STEPS ; POPULATIONS ; STRATEGIES ; CARCINOGENS ; CANCER-RESEARCH ; ASBESTOS ; molecular epidemiology ; AGENT ; molecular biology ; CARCINOGEN ; animal bioassays
    Abstract: Rapid identification of human carcinogens before their dissemination into society, and exposure of worker and lay populations is an important goal of cancer research. Retroactively, verification of in-placehuman carcinogens is also required to target their removal, and other preventive and therapeutic strategies. The hierarchy of methods used historically for evaluation of carcinogenic potential is epidemiology 〉 animal bioassays 〉 mechanistic studies, and the focus has been on single agents that are genotoxic. However, mechanistic research has revealed several obligatory steps in carcinogenesis, tumor promotion, and progression that can now be used in screening studies with human cells in vitro and animal bioassays. These approaches should be combined with molecular epidemiology and molecular pathology to identify human carcinogens with more emphasis on evaluating combinations of suspect agents and mechanisms of action of epigenetic carcinogens. (C) 2004 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15489138
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    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; Germany ; IN-VIVO ; THERAPY ; VITRO ; VIVO ; INFORMATION ; screening ; SYSTEM ; SYSTEMS ; TOOL ; CLONES ; GENE ; GENES ; GENOME ; PROTEIN ; PROTEINS ; MOLECULES ; LINES ; DNA ; INFECTION ; primary ; DOMAIN ; ANTIGEN ; ANTIGENS ; T cell ; T cells ; T-CELL ; T-CELLS ; CELL-LINES ; chromosome ; MOLECULE ; RECOGNITION ; PARTICLES ; virus ; MUTANT ; IDENTIFICATION ; VECTORS ; ESCHERICHIA-COLI ; VECTOR ; CELL-LINE ; LINE ; MODULATION ; EFFICIENT ; VACCINES ; VIRUS-LIKE PARTICLES ; B-CELLS ; VACCINE ; STRATEGIES ; REPLICATION ; CD8(+) ; immune response ; IMMUNE-RESPONSE ; specificity ; HERPES-SIMPLEX-VIRUS ; EPSTEIN-BARR-VIRUS ; DOMAINS ; CD4(+) T-CELLS ; Epstein-Barr virus ; ONCOLOGY ; RECOMBINANT ; review ; RE ; THERAPIES ; INFECTED-CELLS ; analysis ; NUCLEAR ; MUTANTS ; EBV ; B-CELL ; TOOLS ; ENGLAND ; EXPANSION ; viral ; GENOMES ; genetic analysis ; bacterial ; response ; Escherichia coli ; IMMUNE EVASION ; HELPER-CELLS ; STRAIN ; viral proteins ; in vitro ; tumours ; BACTERIAL ARTIFICIAL CHROMOSOME ; HOST SHUTOFF ; LYTIC PROTEIN BHRF1 ; NUCLEAR ANTIGEN-1
    Abstract: Over the past two decades, Epstein-Barr virus (EBV) mutants have become valuable tools for the analysis of viral functions. Several experimental strategies are currently used to generate recombinant mutant genomes that carry alterations in one or several viral genes. The probably most versatile approach utilizes bacterial artificial chromosomes (BAC) carrying parts or the whole EBV genome, which permits extensive genetic manipulations in Escherichia coli cells. The 'mini-EBVs', for example, which contain roughly half of the wild type viral information, efficiently transform primary B cells and have been used as gene vectors for foreign antigens. After expression in lymphoblastoid cell lines (LCLs), these antigens are efficiently presented on MHC molecules and recognized by antigen-specific T cells. These vectors, however, cannot undergo lytic replication and require a helper cell line for efficient replication and DNA packaging. Further experimental systems include the complete viral genome cloned onto a BAC. These mutants can typically be complemented by expression plasmids, some of which are expressed on EBV-derived vectors and can be propagated without requirement of a helper cell line. Over the last years, these viral recombinants have been utilized increasingly to analyse different aspects of the immune response against EBV. Immunological applications are manifold and steadily growing and include crude screening of T cell clones for their specificity towards latent versus lytic antigens, or more detailed analyses in which the exact specificity of T cells is determined using EBV mutants that lack a single viral antigen. Other applications include detailed analysis of protein domains important for immune recognition, e.g. Gly-Ala repeats in the EBV nuclear antigen 1 (EBNA1) protein, expansion of T cell clones directed against virion structures using virus-like particles and phenotypic analysis of virus mutants defective in infection. Future developments might include the genetic identification and characterization of viral proteins involved in the modulation of the immune response and, in particular, immune evasion. Recombinant viral strains are already being used experimentally for the expansion of T cells in vitro prior to in vivo cellular therapy and have been proposed as potential prophylactic vaccines. (C) 2008 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18938248
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    Keywords: CELLS ; PATHWAYS ; GENOME ; BREAST-CANCER ; PREDICTION ; RECONSTRUCTION ; TUMOR-SUPPRESSOR ; GLYCOLYSIS ; FLUX ANALYSIS ; ENRICHMENT ANALYSIS
    Abstract: Metabolism is the functional phenotype of a cell, at a given condition, resulting from an intricate interplay of various regulatory processes. The study of these dynamic metabolic processes and their capabilities help to identify the fundamental properties of living systems. Metabolic deregulation is an emerging hallmark of cancer cells. This deregulation results in rewiring of the metabolic circuitry conferring an exploitative metabolic advantage for the tumor cells which leads to a distinct benefit in survival and lays the basis for unbound progression. Metabolism can be considered as a thermodynamic open-system in which source substrates of high value are being processed through a well established interconnected biochemical conversion system, strictly obeying physiochemical principles, generating useful intermediates and finally resulting in the release of byproducts. Based on this basic principle of an input-output balance, various models have been developed to interrogate metabolism elucidating its underlying functional properties. However, only a few modeling approaches have proved computationally feasible in elucidating the metabolic nature of cancer at a systems level. Besides this, statistical approaches have been set up to identify biochemical pathways being more relevant for specific types of tumor cells. In this review, we are briefly introducing the basic statistical approaches followed by the major modeling concepts. We have put an emphasis on the methods and their applications that have been used to a greater extent in understanding the metabolic remodeling of cancer.
    Type of Publication: Journal article published
    PubMed ID: 23680724
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    Keywords: PROSTATE-CANCER ; ACUTE PROMYELOCYTIC LEUKEMIA ; RETINOIC ACID ; DOUBLE-STRAND BREAKS ; ACUTE MYELOID-LEUKEMIA ; EPITHELIAL-MESENCHYMAL TRANSITION ; DNA-DAMAGE RESPONSE ; TUMOR-INITIATING CELLS ; SIDE-POPULATION CELLS ; ALDEHYDE-DEHYDROGENASE
    Abstract: Similar to normal tissue, many tumors have a hierarchical organization where tumorigenic cancer stem cells (CSCs) differentiate into non-tumorigenic progenies. A host of studies have demonstrated that although CSCs and their non-tumorigenic progenies within the same clone can share common genotype, they display different epigenetic profiles that results in changes of multiple signaling pathways. Many of these pathways confer cell adaptation to the microenvironmental stresses including inflammation, hypoxia, low pH, shortage in nutrients and anti-cancer therapies. Treatment strategies based on combination of conventional therapies targeting bulk tumor cells and CSC-specific pathway inhibition bear a promise to improve cancer cure compared to monotherapies. In this review we describe the mechanisms of CSC-related therapy resistance including drug efflux by ABC transporters, activation of aldehyde dehydrogenase and developmental pathways, enhanced DNA damage response, autophagy and microenvironmental conditions, and discuss possible therapeutic strategies for improving cancer treatment.
    Type of Publication: Journal article published
    PubMed ID: 24956577
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    Keywords: SQUAMOUS-CELL CARCINOMA ; N-TERMINAL KINASE ; EPIDERMAL-GROWTH-FACTOR ; HUMAN GLIOBLASTOMA CELLS ; MINIMAL RESIDUAL DISEASE ; MOUSE SKIN CARCINOGENESIS ; INTEGRIN-LINKED KINASE ; SMALL-MOLECULE INHIBITOR ; MEDIATED DRUG-RESISTANCE ; CHEMOTHERAPY-INDUCED APOPTOSIS
    Abstract: Interlocking gene mutations, epigenetic alterations and microenvironmental features perpetuate tumor development, growth, infiltration and spread. Consequently, intrinsic and acquired therapy resistance arises and presents one of the major goals to solve in oncologic research today. Among the myriad of microenvironmental factors impacting on cancer cell resistance, cell adhesion to the extracellular matrix (ECM) has recently been identified as key determinant. Despite the differentiation between cell adhesion-mediated drug resistance (CAMDR) and cell adhesion-mediated radioresistance (CAMRR), the underlying mechanisms share great overlap in integrin and focal adhesion hub signaling and differ further downstream in the complexity of signaling networks between tumor entities. Intriguingly, cell adhesion to ECM is per se also essential for cancer cells similar to their normal counterparts. However, based on the overexpression of focal adhesion hub signaling receptors and proteins and a distinct addiction to particular integrin receptors, targeting of focal adhesion proteins has been shown to potently sensitize cancer cells to different treatment regimes including radiotherapy, chemotherapy and novel molecular therapeutics. In this review, we will give insight into the role of integrins in carcinogenesis, tumor progression and metastasis. Additionally, literature and data about the function of focal adhesion molecules including integrins, integrin-associated proteins and growth factor receptors in tumor cell resistance to radio- and chemotherapy will be elucidated and discussed.
    Type of Publication: Journal article published
    PubMed ID: 25117005
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    Abstract: Myelodysplastic syndrome (MDS) is a clonal bone marrow disorder, typically of older adults, which is characterized by ineffective hematopoiesis, peripheral blood cytopenias and risk of progression to acute myeloid leukemia. Juvenile myelomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm occurring in young children. The common denominator of these malignant myeloid disorders is the limited benefit of conventional chemotherapy and a particular responsiveness to epigenetic therapy with the DNA-hypomethylating agents 5-azacytidine (azacitidine) or decitabine. However, hypomethylating therapy does not eradicate the malignant clone in MDS or JMML and allogeneic hematopoietic stem cell transplantation (HSCT) remains the only curative treatment option. An emerging concept with intriguing potential is the combination of hypomethylating therapy and HSCT. Possible advantages include disease control with good tolerability during donor search and HSCT preparation, improved antitumoral alloimmunity, and reduced risk of relapse even with non-myeloablative regimens. Herein we review the current role of pre- and post-transplant therapy with hypomethylating agents in MDS and JMML.
    Type of Publication: Journal article published
    PubMed ID: 29129488
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