Groupement des Hopitaux Paris Center

Paris, France

Groupement des Hopitaux Paris Center

Paris, France
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Thomas-Schoemann A.,University of Paris Descartes | Batteux F.,University of Paris Descartes | Mongaret C.,University of Paris Descartes | Nicco C.,University of Paris Descartes | And 9 more authors.
Journal of Immunology | Year: 2012

Immunotherapy is a promising antitumor strategy that can successfully be combined with current anticancer treatment. In this study, arsenic trioxide (As2O3) was shown to increase the antitumor immune response in CT26 colon tumor-bearing mice through the modulation of regulatory T cell (Treg) numbers. As2O3 induced Treg- selective depletion in vitro. In vivo, tumor-bearing mice injected with 1 mg/kg As2O3 showed a significant decrease in the T reg/CD4 cell ratio and in absolute Treg count versus controls. As2O3 exerted antitumor effects only in immunocompetent mice and enhanced adoptive immunotherapy effects. Inhibition of As 2O3-induced Treg depletion by the NO synthase inhibitor NG-nitro-L-arginine methyl ester and the superoxide dismutase mimic manganese [III] tetrakis-(5, 10, 15, 20)-benzoic acid porphyrin suggested that it was mediated by oxidative and nitrosative stress. The differential effect of As2O3 on Treg versus other CD4 cells may be related to differences in the cells' redox status, as indicated by significant differences in 2′7′dichlorodihydrofluorescein diacetate and 4,5-diaminofluorescein diacetate fluorescence levels. In conclusion, these results show for the first time, to our knowledge, that low doses As 2O3 can delay solid tumor growth by depleting T regs through oxidative and nitrosative bursts, and suggest that As2O3 could be used to enhance the antitumor activity of adoptive immunotherapy strategies in human cancer. Copyright © 2012 by The American Association of Immunologists, Inc.


Thomas-Schoemann A.,Center Detude Et Of Recours Aux Inhibiteurs Of Langiogenese | Thomas-Schoemann A.,Groupement des Hopitaux Paris Center | Blanchet B.,Center Detude Et Of Recours Aux Inhibiteurs Of Langiogenese | Blanchet B.,Groupement des Hopitaux Paris Center | And 9 more authors.
Critical Reviews in Oncology/Hematology | Year: 2014

Drug interactions are an on-going concern in the treatment of cancer, especially when targeted therapies, such as tyrosine kinase inhibitors (TKI) or mammalian target of rapamycin (mTOR) inhibitors, are being used. The emergence of elderly patients and/or patients with both cancer and other chronic co-morbidities leads to polypharmacy. Therefore, the risk of drug-drug interactions (DDI) becomes a clinically relevant issue, all the more so as TKIs and mTOR inhibitors are essentially metabolised by cytochrome P450 enzymes. These DDIs can result in variability in anticancer drug exposure, thus favouring the selection of resistant cellular clones or the occurrence of toxicity. This review provides a comprehensive overview of DDIs that involve targeted therapies approved by the FDA for the treatment of solid tumours for more than 3 years (sorafenib, sunitinib, erlotinib, gefitinib, imatinib, lapatinib, everolimus, temsirolimus) and medicinal herb or drugs. This review also provides some guidelines to help oncologists and pharmacists in their clinical practice. © 2013 Elsevier Ireland Ltd.


Thomas-Schoemann A.,University of Paris Descartes | Batteux F.,University of Paris Descartes | Alexandre J.,University of Paris Descartes | Alexandre J.,Groupement des Hopitaux Paris Center
OncoImmunology | Year: 2013

The depletion of regulatory T cells (Tregs) is a promising therapeutic strategy to enhance antitumor immune responses.Our recent findings indicate that low doses of arsenic trioxide can delay tumor growth in murine models of colon and breast cancer by depleting Tregs through oxidative and nitrosative bursts. © 2013 Landes Bioscience.


PubMed | Center Detude Et Of Recours Aux Inhibiteurs Of Langiogenese, University of Paris Descartes and Groupement des Hopitaux Paris Center
Type: Journal Article | Journal: Critical reviews in oncology/hematology | Year: 2013

Drug interactions are an on-going concern in the treatment of cancer, especially when targeted therapies, such as tyrosine kinase inhibitors (TKI) or mammalian target of rapamycin (mTOR) inhibitors, are being used. The emergence of elderly patients and/or patients with both cancer and other chronic co-morbidities leads to polypharmacy. Therefore, the risk of drug-drug interactions (DDI) becomes a clinically relevant issue, all the more so as TKIs and mTOR inhibitors are essentially metabolised by cytochrome P450 enzymes. These DDIs can result in variability in anticancer drug exposure, thus favouring the selection of resistant cellular clones or the occurrence of toxicity. This review provides a comprehensive overview of DDIs that involve targeted therapies approved by the FDA for the treatment of solid tumours for more than 3 years (sorafenib, sunitinib, erlotinib, gefitinib, imatinib, lapatinib, everolimus, temsirolimus) and medicinal herb or drugs. This review also provides some guidelines to help oncologists and pharmacists in their clinical practice.

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