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Articles 1 - 4 of 4
Full-Text Articles in Medicine and Health Sciences
Ido1 Is An Integral Mediator Of Inflammatory Neovascularization., Arpita Mondal, Courtney Smith, James B. Duhadaway, Erika Sutanto-Ward, George C. Prendergast, Arturo Bravo-Nuevo, Alexander J. Muller
Ido1 Is An Integral Mediator Of Inflammatory Neovascularization., Arpita Mondal, Courtney Smith, James B. Duhadaway, Erika Sutanto-Ward, George C. Prendergast, Arturo Bravo-Nuevo, Alexander J. Muller
Kimmel Cancer Center Papers, Presentations, and Grand Rounds
The immune tolerogenic effects of IDO1 (indoleamine 2,3-dioxygenase 1) have been well documented and genetic studies in mice have clearly established the significance of IDO1 in tumor promotion. Dichotomously, the primary inducer of IDO1, the inflammatory cytokine IFNγ (interferon-γ), is a key mediator of immune-based tumor suppression. One means by which IFNγ can exert an anti-cancer effect is by decreasing tumor neovascularization. We speculated that IDO1 might contribute to cancer promotion by countering this anti-neovascular effect of IFNγ, possibly through IDO1-potentiated elevation of the pro-tumorigenic inflammatory cytokine IL6 (interleukin-6). In this study, we investigated how genetic loss of IDO1 affects …
Celecoxib Inhibits Proliferation And Survival Of Chronic Myelogeous Leukemia (Cml) Cells Via Ampk-Dependent Regulation Of Β-Catenin And Mtorc1/2., Beatrice Riva, Marco De Dominici, Ilaria Gnemmi, Samanta A. Mariani, Alberto Minassi, Valentina Minieri, Paolo Salomoni, Pier Luigi Canonico, Armando A Genazzani, Bruno Calabretta, Fabrizio Condorelli
Celecoxib Inhibits Proliferation And Survival Of Chronic Myelogeous Leukemia (Cml) Cells Via Ampk-Dependent Regulation Of Β-Catenin And Mtorc1/2., Beatrice Riva, Marco De Dominici, Ilaria Gnemmi, Samanta A. Mariani, Alberto Minassi, Valentina Minieri, Paolo Salomoni, Pier Luigi Canonico, Armando A Genazzani, Bruno Calabretta, Fabrizio Condorelli
Kimmel Cancer Center Papers, Presentations, and Grand Rounds
CML is effectively treated with tyrosine kinase inhibitors (TKIs). However, the efficacy of these drugs is confined to the chronic phase of the disease and development of resistance to TKIs remains a pressing issue. The anti-inflammatory COX2 inhibitor celecoxib has been utilized as anti-tumour drug due to its anti-proliferative activity. However, its effects in hematological malignancies, in particular CML, have not been investigated yet. Thus, we tested biological effects and mechanisms of action of celecoxib in Philadelphia-positive (Ph+) CML and ALL cells.We show here that celecoxib suppresses the growth of Ph+ cell lines by increasing G1-phase and apoptotic cells and …
Repurposing Atovaquone: Targeting Mitochondrial Complex Iii And Oxphos To Eradicate Cancer Stem Cells., Marco Fiorillo, Rebecca Lamb, Herbert B Tanowitz, Luciano Mutti, Marija Krstic-Demonacos, Anna Rita Cappello, Ubaldo E. Martinez-Outshoorn, Federica Sotgia, Michael P Lisanti
Repurposing Atovaquone: Targeting Mitochondrial Complex Iii And Oxphos To Eradicate Cancer Stem Cells., Marco Fiorillo, Rebecca Lamb, Herbert B Tanowitz, Luciano Mutti, Marija Krstic-Demonacos, Anna Rita Cappello, Ubaldo E. Martinez-Outshoorn, Federica Sotgia, Michael P Lisanti
Kimmel Cancer Center Papers, Presentations, and Grand Rounds
Atovaquone is an FDA-approved anti-malarial drug, which first became clinically available in the year 2000. Currently, its main usage is for the treatment of pneumocystis pneumonia (PCP) and/or toxoplasmosis in immune-compromised patients. Atovaquone is a hydroxy-1,4-naphthoquinone analogue of ubiquinone, also known as Co-enzyme Q10 (CoQ10). It is a well-tolerated drug that does not cause myelo-suppression. Mechanistically, it is thought to act as a potent and selective OXPHOS inhibitor, by targeting the CoQ10-dependence of mitochondrial complex III. Here, we show for the first time that atovaquone also has anti-cancer activity, directed against Cancer Stem-like Cells (CSCs). More specifically, we demonstrate that …
Cancer Stem Cell Metabolism., Maria Peiris-Pagès, Ubaldo E. Martinez-Outshoorn, Richard G. Pestell, Federica Sotgia, Michael P Lisanti
Cancer Stem Cell Metabolism., Maria Peiris-Pagès, Ubaldo E. Martinez-Outshoorn, Richard G. Pestell, Federica Sotgia, Michael P Lisanti
Kimmel Cancer Center Papers, Presentations, and Grand Rounds
Cancer is now viewed as a stem cell disease. There is still no consensus on the metabolic characteristics of cancer stem cells, with several studies indicating that they are mainly glycolytic and others pointing instead to mitochondrial metabolism as their principal source of energy. Cancer stem cells also seem to adapt their metabolism to microenvironmental changes by conveniently shifting energy production from one pathway to another, or by acquiring intermediate metabolic phenotypes. Determining the role of cancer stem cell metabolism in carcinogenesis has become a major focus in cancer research, and substantial efforts are conducted towards discovering clinical targets.