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  1. Article ; Online: [No title information]

    Carrier, Alice

    Bulletin du cancer

    2020  Volume 107, Issue 2, Page(s) 281–282

    Title translation Actualités sur le lien métabolisme et cancers, l’essentiel du Congrès international Métabolisme & Cancer 2019.
    Language French
    Publishing date 2020-01-24
    Publishing country France
    Document type Clinical Conference
    ZDB-ID 213270-9
    ISSN 1769-6917 ; 0007-4551
    ISSN (online) 1769-6917
    ISSN 0007-4551
    DOI 10.1016/j.bulcan.2020.01.006
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  2. Article ; Online: A novel anticancer pharmacological agent targeting mitochondrial complex I.

    Reyes-Castellanos, Gabriela / Carrier, Alice

    Trends in pharmacological sciences

    2022  Volume 43, Issue 9, Page(s) 706–708

    Abstract: Targeting metabolic reprogramming has proven successful in oncology, but this field requires better identification of drugs that inhibit mitochondrial metabolism in cancer cells. Recent work from Dr Wolf's group reveals that the primary target of the ... ...

    Abstract Targeting metabolic reprogramming has proven successful in oncology, but this field requires better identification of drugs that inhibit mitochondrial metabolism in cancer cells. Recent work from Dr Wolf's group reveals that the primary target of the antitumor compound SMIP004-7 is mitochondrial complex I (NDUFS2 subunit), inhibition of which promotes anticancer immune surveillance.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Electron Transport Complex I/metabolism ; Humans ; Mitochondria/metabolism ; Neoplasms/pathology
    Chemical Substances Antineoplastic Agents ; Electron Transport Complex I (EC 7.1.1.2)
    Language English
    Publishing date 2022-04-02
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2022.03.007
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  3. Article ; Online: Metabolic Syndrome and Oxidative Stress: A Complex Relationship.

    Carrier, Alice

    Antioxidants & redox signaling

    2017  Volume 26, Issue 9, Page(s) 429–431

    Abstract: The worldwide epidemic of obesity is a major public health concern. Obesity is a major risk factor for noncommunicable diseases such as type 2 diabetes and cardiovascular diseases, clustered in the so-called metabolic syndrome (MS). Other main chronic ... ...

    Abstract The worldwide epidemic of obesity is a major public health concern. Obesity is a major risk factor for noncommunicable diseases such as type 2 diabetes and cardiovascular diseases, clustered in the so-called metabolic syndrome (MS). Other main chronic illnesses are promoted by excessive body weight, including cancer and neurodegenerative pathologies, both affecting a number of people worldwide. In recent years, the primary role of an excess of reactive oxygen species (oxidative stress) resulting from altered redox control in the etiology of all of these pathologies has been unveiled. Interestingly, it appears that oxidative stress is both the cause and the consequence of obesity and associated disorders. This Forum features reviews that recapitulate the current knowledge on the link between oxidative stress and MS in the physiopathology of different biological systems. Antioxid. Redox Signal. 26, 429-431.
    MeSH term(s) Animals ; Disease Susceptibility ; Humans ; Inflammation/complications ; Inflammation/metabolism ; Metabolic Syndrome/etiology ; Metabolic Syndrome/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2017-03-20
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2016.6929
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  4. Article ; Online: Autophagy Contributes to Metabolic Reprogramming and Therapeutic Resistance in Pancreatic Tumors.

    Reyes-Castellanos, Gabriela / Abdel Hadi, Nadine / Carrier, Alice

    Cells

    2022  Volume 11, Issue 3

    Abstract: Metabolic reprogramming is a feature of cancers for which recent research has been particularly active, providing numerous insights into the mechanisms involved. It occurs across the entire cancer process, from development to resistance to therapies. ... ...

    Abstract Metabolic reprogramming is a feature of cancers for which recent research has been particularly active, providing numerous insights into the mechanisms involved. It occurs across the entire cancer process, from development to resistance to therapies. Established tumors exhibit dependencies for metabolic pathways, constituting vulnerabilities that can be targeted in the clinic. This knowledge is of particular importance for cancers that are refractory to any therapeutic approach, such as Pancreatic Ductal Adenocarcinoma (PDAC). One of the metabolic pathways dysregulated in PDAC is autophagy, a survival process that feeds the tumor with recycled intracellular components, through both cell-autonomous (in tumor cells) and nonautonomous (from the local and distant environment) mechanisms. Autophagy is elevated in established PDAC tumors, contributing to aberrant proliferation and growth even in a nutrient-poor context. Critical elements link autophagy to PDAC including genetic alterations, mitochondrial metabolism, the tumor microenvironment (TME), and the immune system. Moreover, high autophagic activity in PDAC is markedly related to resistance to current therapies. In this context, combining autophagy inhibition with standard chemotherapy, and/or drugs targeting other vulnerabilities such as metabolic pathways or the immune response, is an ongoing clinical strategy for which there is still much to do through translational and multidisciplinary research.
    MeSH term(s) Autophagy/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Drug Resistance, Neoplasm ; Humans ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Tumor Microenvironment ; Pancreatic Neoplasms
    Language English
    Publishing date 2022-01-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11030426
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  5. Article ; Online: A pharmacological strategy to recapitulate exercise-induced antitumoral immunity.

    Rébillard, Amélie / Nunès, Jacques A / Carrier, Alice

    Trends in pharmacological sciences

    2022  Volume 43, Issue 12, Page(s) 1001–1003

    Abstract: The antitumor activity of exercise by means of enhanced immune activation is documented, but better identification of the underlying mechanisms is required to develop new therapeutic strategies. Recent work from the Dr Bar-Sagi group reveals that ... ...

    Abstract The antitumor activity of exercise by means of enhanced immune activation is documented, but better identification of the underlying mechanisms is required to develop new therapeutic strategies. Recent work from the Dr Bar-Sagi group reveals that exercise engages IL-15 signaling and pharmacological activation of the IL-15/IL-15R axis mimics the exercise-driven immune cell-mediated cytotoxicity in pancreatic cancer.
    MeSH term(s) Humans ; Interleukin-15 ; Signal Transduction
    Chemical Substances Interleukin-15
    Language English
    Publishing date 2022-08-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2022.08.004
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  6. Article ; Online: Targeting Redox Metabolism in Pancreatic Cancer.

    Abdel Hadi, Nadine / Reyes-Castellanos, Gabriela / Carrier, Alice

    International journal of molecular sciences

    2021  Volume 22, Issue 4

    Abstract: Cell metabolism is reprogrammed in cancer cells to meet their high bioenergetics and biosynthetic demands. This metabolic reprogramming is accompanied by alterations in redox metabolism, characterized by accumulation of reactive oxygen species (ROS). ... ...

    Abstract Cell metabolism is reprogrammed in cancer cells to meet their high bioenergetics and biosynthetic demands. This metabolic reprogramming is accompanied by alterations in redox metabolism, characterized by accumulation of reactive oxygen species (ROS). Elevated production of ROS, mostly by mitochondrial respiration, is counteracted by higher production of antioxidant defenses (mainly glutathione and antioxidant enzymes). Cancer cells are adapted to a high concentration of ROS, which contributes to tumorigenesis, metastasis formation, resistance to therapy and relapse. Frequent genetic alterations observed in pancreatic ductal adenocarcinoma (PDAC) affect KRAS and p53 proteins, which have a role in ROS production and control, respectively. These observations led to the proposal of the use of antioxidants to prevent PDAC development and relapse. In this review, we focus on the therapeutic strategies to further increase ROS level to induce PDAC cell death. Combining the promotion of ROS production and inhibition of antioxidant capacity is a promising avenue for pancreatic cancer therapy in the clinic.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Antioxidants/metabolism ; Biomarkers, Tumor ; Clinical Studies as Topic ; Disease Management ; Disease Susceptibility ; Drug Evaluation, Preclinical ; Energy Metabolism/drug effects ; Humans ; Mitochondria/drug effects ; Mitochondria/metabolism ; Molecular Targeted Therapy ; Oxidation-Reduction/drug effects ; Oxidative Stress/drug effects ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/etiology ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Treatment Outcome
    Chemical Substances Antineoplastic Agents ; Antioxidants ; Biomarkers, Tumor ; Reactive Oxygen Species
    Language English
    Publishing date 2021-02-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22041534
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  7. Article: Mitochondrial Metabolism in PDAC: From Better Knowledge to New Targeting Strategies.

    Reyes-Castellanos, Gabriela / Masoud, Rawand / Carrier, Alice

    Biomedicines

    2020  Volume 8, Issue 8

    Abstract: Cancer cells reprogram their metabolism to meet bioenergetics and biosynthetic demands. The first observation of metabolic reprogramming in cancer cells was made a century ago ("Warburg effect" or aerobic glycolysis), leading to the classical view that ... ...

    Abstract Cancer cells reprogram their metabolism to meet bioenergetics and biosynthetic demands. The first observation of metabolic reprogramming in cancer cells was made a century ago ("Warburg effect" or aerobic glycolysis), leading to the classical view that cancer metabolism relies on a glycolytic phenotype. There is now accumulating evidence that most cancers also rely on mitochondria to satisfy their metabolic needs. Indeed, the current view of cancer metabolism places mitochondria as key actors in all facets of cancer progression. Importantly, mitochondrial metabolism has become a very promising target in cancer therapy, including for refractory cancers such as Pancreatic Ductal AdenoCarcinoma (PDAC). In particular, mitochondrial oxidative phosphorylation (OXPHOS) is an important target in cancer therapy. Other therapeutic strategies include the targeting of glutamine and fatty acids metabolism, as well as the inhibition of the TriCarboxylic Acid (TCA) cycle intermediates. A better knowledge of how pancreatic cancer cells regulate mitochondrial metabolism will allow the identification of metabolic vulnerabilities and thus novel and more efficient therapeutic options for the benefit of each patient.
    Language English
    Publishing date 2020-08-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines8080270
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  8. Article ; Online: Pesticides and pancreatic adenocarcinoma: A transversal epidemiological, environmental and mechanistic narrative review.

    Brugel, Mathias / Carlier, Claire / Reyes-Castellanos, Gabriela / Callon, Sidonie / Carrier, Alice / Bouché, Olivier

    Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

    2022  Volume 54, Issue 12, Page(s) 1605–1613

    Abstract: Pancreatic adenocarcinoma (PA) incidence is rising worldwide, especially in France. The evolution of known risk factors such as tobacco smoking, obesity, type 2 diabetes, chronic pancreatitis, or constitutional mutations is not sufficient to explain this ...

    Abstract Pancreatic adenocarcinoma (PA) incidence is rising worldwide, especially in France. The evolution of known risk factors such as tobacco smoking, obesity, type 2 diabetes, chronic pancreatitis, or constitutional mutations is not sufficient to explain this trend. Pesticides are known risk factors in other malignancies. Previous studies have outlined pesticides' influence in PA, such as dichlorodiphenyltrichloroethane as plausible risk factors. The general population is directly or indirectly exposed to pesticides through air, food or water. Some of these chemicals may accumulate in the body all along lifetime and may harm carriers. The toxic mixing effects of these chemicals are not well documented. Several hypotheses have been put forward to explain how pesticides can induce indirect (fatty pancreas, induced diabetes) or direct (oxidative stress, cell damage) carcinogenesis in pancreatic cells through inflammation. A strong corpus exists acknowledging pesticides as a PA risk factor. However, published studies do not provide a sufficient level of evidence to prove causality and current prospective case-control studies are still ongoing.
    MeSH term(s) Humans ; Pancreatic Neoplasms/chemically induced ; Pancreatic Neoplasms/epidemiology ; Pesticides/toxicity ; Adenocarcinoma/chemically induced ; Adenocarcinoma/epidemiology ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/complications ; Pancreatic Neoplasms
    Chemical Substances Pesticides
    Language English
    Publishing date 2022-09-09
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1459373-7
    ISSN 1878-3562 ; 1125-8055
    ISSN (online) 1878-3562
    ISSN 1125-8055
    DOI 10.1016/j.dld.2022.08.023
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  9. Article ; Online: Thymus-specific serine protease, a protease that shapes the CD4 T cell repertoire.

    Guerder, Sylvie / Hassel, Chervin / Carrier, Alice

    Immunogenetics

    2018  Volume 71, Issue 3, Page(s) 223–232

    Abstract: The lifespan of T cells is determined by continuous interactions of their T cell receptors (TCR) with self-peptide-MHC (self-pMHC) complexes presented by different subsets of antigen-presenting cells (APC). In the thymus, developing thymocytes are ... ...

    Abstract The lifespan of T cells is determined by continuous interactions of their T cell receptors (TCR) with self-peptide-MHC (self-pMHC) complexes presented by different subsets of antigen-presenting cells (APC). In the thymus, developing thymocytes are positively selected through recognition of self-pMHC presented by cortical thymic epithelial cells (cTEC). They are subsequently negatively selected by medullary thymic epithelial cells (mTEC) or thymic dendritic cells (DC) presenting self-pMHC complexes. In the periphery, the homeostasis of mature T cells is likewise controlled by the interaction of their TCR with self-pMHC complexes presented by lymph node stromal cells while they may be tolerized by DC presenting tissue-derived self-antigens. To perform these tasks, the different subsets of APC are equipped with distinct combination of antigen processing enzymes and consequently present specific repertoire of self-peptides. Here, we discuss one such antigen processing enzyme, the thymus-specific serine protease (TSSP), which is predominantly expressed by thymic stromal cells. In thymic DC and TEC, TSSP edits the repertoire of peptide presented by class II molecules and thus shapes the CD4 T cell repertoire.
    MeSH term(s) Animals ; Antigen Presentation/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Humans ; Serine Proteases/immunology ; Serine Proteases/metabolism ; Thymus Gland/enzymology ; Thymus Gland/immunology
    Chemical Substances Serine Proteases (EC 3.4.-)
    Language English
    Publishing date 2018-09-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 186560-2
    ISSN 1432-1211 ; 0093-7711
    ISSN (online) 1432-1211
    ISSN 0093-7711
    DOI 10.1007/s00251-018-1078-y
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  10. Article: A novel actor in antitumoral immunity: The thymus-specific serine protease TSSP/PRSS16 involved in CD4

    Brisson, Lydie / Carrier, Alice

    Oncoimmunology

    2015  Volume 4, Issue 9, Page(s) e1026536

    Abstract: The maturation of a specific subset of ... ...

    Abstract The maturation of a specific subset of CD4
    Language English
    Publishing date 2015-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.1080/2162402X.2015.1026536
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