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  1. Article ; Online: Metabolic oscillations during cell-cycle progression.

    Icard, Philippe / Simula, Luca

    Trends in endocrinology and metabolism: TEM

    2022  Volume 33, Issue 7, Page(s) 447–450

    Abstract: We discuss how metabolism changes during different phases of the cell cycle to sustain biosynthesis and replication in normal and cancer cells. We also highlight how several master regulators of cell cycle, such as cyclin-cyclin-dependent kinases (cyc- ... ...

    Abstract We discuss how metabolism changes during different phases of the cell cycle to sustain biosynthesis and replication in normal and cancer cells. We also highlight how several master regulators of cell cycle, such as cyclin-cyclin-dependent kinases (cyc-CDK complexes) and E3 proteasome ligases, modulate key metabolic enzymes to support cell-cycle progression.
    MeSH term(s) Cell Cycle/genetics ; Cyclin-Dependent Kinases/metabolism ; Humans ; Proteasome Endopeptidase Complex
    Chemical Substances Cyclin-Dependent Kinases (EC 2.7.11.22) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2022-05-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2022.04.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2999: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: The potential for citrate to reinforce epigenetic therapy by promoting apoptosis.

    Icard, Philippe / Alifano, Marco / Simula, Luca

    Trends in endocrinology and metabolism: TEM

    2023  Volume 34, Issue 10, Page(s) 586–589

    Abstract: Epigenetic drugs induce ATP depletion, promoting a glycolysis-to-oxidative phosphorylation (OXPHOS) shift which sometimes favors tumor growth by promoting necroptosis over apoptosis. To restore effective apoptosis in tumors, we propose that the ... ...

    Abstract Epigenetic drugs induce ATP depletion, promoting a glycolysis-to-oxidative phosphorylation (OXPHOS) shift which sometimes favors tumor growth by promoting necroptosis over apoptosis. To restore effective apoptosis in tumors, we propose that the administration of citrate could inhibit ATP production, activate caspase-8 (a key necroptosis inhibitor), and downregulate key anti-apoptotic proteins (Bcl-xL and MCL1).
    MeSH term(s) Humans ; Citric Acid/pharmacology ; bcl-X Protein/genetics ; bcl-X Protein/metabolism ; bcl-X Protein/pharmacology ; Apoptosis/genetics ; Citrates/pharmacology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Adenosine Triphosphate ; Epigenesis, Genetic/genetics
    Chemical Substances Citric Acid (2968PHW8QP) ; bcl-X Protein ; Citrates ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-08-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2023.07.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2999: Show issues Location:
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  3. Article: How Phosphofructokinase-1 Promotes PI3K and YAP/TAZ in Cancer: Therapeutic Perspectives.

    Simula, Luca / Alifano, Marco / Icard, Philippe

    Cancers

    2022  Volume 14, Issue 10

    Abstract: PI3K/AKT is one of the most frequently altered signaling pathways in human cancers, supporting the activation of many proteins sustaining cell metabolism, proliferation, and aggressiveness. Another important pathway frequently altered in cancer cells is ... ...

    Abstract PI3K/AKT is one of the most frequently altered signaling pathways in human cancers, supporting the activation of many proteins sustaining cell metabolism, proliferation, and aggressiveness. Another important pathway frequently altered in cancer cells is the one regulating the YAP/TAZ transcriptional coactivators, which promote the expression of genes sustaining aerobic glycolysis (such as WNT, MYC, HIF-1), EMT, and drug resistance. Of note, the PI3K/AKT pathway can also regulate the YAP/TAZ one. Unfortunately, although PI3K and YAP inhibitors are currently tested in highly resistant cancers (both solid and hematologic ones), several resistance mechanisms may arise. Resistance mechanisms to PI3K inhibitors may involve the stimulation of alternative pathways (such as RAS, HER, IGFR/AKT), the inactivation of PTEN (the physiologic inhibitor of PI3K), and the expression of anti-apoptotic Bcl-xL and MCL1 proteins. Therefore, it is important to improve current therapeutic strategies to overcome these limitations. Here, we want to highlight how the glycolytic enzyme PFK1 (and its product F-1,6-BP) promotes the activation of both PI3K/AKT and YAP/TAZ pathways by several direct and indirect mechanisms. In turn, PI3K/AKT and YAP/TAZ can promote PFK1 activity and F-1,6-BP production in a positive feedback loop, thus sustaining the Warburg effect and drug resistance. Thus, we propose that the inhibition of PFK1 (and of its key activator PFK2/PFKFB3) could potentiate the sensitivity to PI3K and YAP inhibitors currently tested. Awaiting the development of non-toxic inhibitors of these enzymes, we propose to test the administration of citrate at a high dosage, because citrate is a physiologic inhibitor of both PFK1 and PFK2/PFKFB3. Consistently, in various cultured cancer cells (including melanoma, sarcoma, hematologic, and epithelial cancer cells), this "citrate strategy" efficiently inhibits the IGFR1/AKT pathway, promotes PTEN activity, reduces Bcl-xL and MCL1 expression, and increases sensitivity to standard chemotherapy. It also inhibits the development of sarcoma, pancreatic, mammary HER
    Language English
    Publishing date 2022-05-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14102478
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Immune Checkpoint Proteins, Metabolism and Adhesion Molecules: Overlooked Determinants of CAR T-Cell Migration?

    Simula, Luca / Ollivier, Emma / Icard, Philippe / Donnadieu, Emmanuel

    Cells

    2022  Volume 11, Issue 11

    Abstract: Adoptive transfer of T cells genetically engineered to express chimeric antigen receptors (CAR) has demonstrated striking efficacy for the treatment of several hematological malignancies, including B-cell lymphoma, leukemia, and multiple myeloma. However, ...

    Abstract Adoptive transfer of T cells genetically engineered to express chimeric antigen receptors (CAR) has demonstrated striking efficacy for the treatment of several hematological malignancies, including B-cell lymphoma, leukemia, and multiple myeloma. However, many patients still do not respond to this therapy or eventually relapse after an initial remission. In most solid tumors for which CAR T-cell therapy has been tested, efficacy has been very limited. In this context, it is of paramount importance to understand the mechanisms of tumor resistance to CAR T cells. Possible factors contributing to such resistance have been identified, including inherent CAR T-cell dysfunction, the presence of an immunosuppressive tumor microenvironment, and tumor-intrinsic factors. To control tumor growth, CAR T cells have to migrate actively enabling a productive conjugate with their targets. To date, many cells and factors contained within the tumor microenvironment have been reported to negatively control the migration of T cells and their ability to reach cancer cells. Recent evidence suggests that additional determinants, such as immune checkpoint proteins, cellular metabolism, and adhesion molecules, may modulate the motility of CAR T cells in tumors. Here, we review the potential impact of these determinants on CAR T-cell motility, and we discuss possible strategies to restore intratumoral T-cell migration with a special emphasis on approaches targeting these determinants.
    MeSH term(s) Cell Movement ; Humans ; Immune Checkpoint Proteins ; Neoplasms/therapy ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Chimeric Antigen/metabolism ; Tumor Microenvironment
    Chemical Substances Immune Checkpoint Proteins ; Receptors, Antigen, T-Cell ; Receptors, Chimeric Antigen
    Language English
    Publishing date 2022-06-06
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11111854
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: New Therapeutic Strategies for Lung Cancer.

    Icard, Philippe / Damotte, Diane / Alifano, Marco

    Cancers

    2021  Volume 13, Issue 8

    Abstract: Non-small cell lung cancer (NSCLC) accounts for approximately 27% of all cancer-related deaths worldwide, thus representing a major health problem [ ... ]. ...

    Abstract Non-small cell lung cancer (NSCLC) accounts for approximately 27% of all cancer-related deaths worldwide, thus representing a major health problem [...].
    Language English
    Publishing date 2021-04-16
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13081937
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  6. Article ; Online: The dual role of citrate in cancer.

    Icard, Philippe / Simula, Luca / Zahn, Grit / Alifano, Marco / Mycielska, Maria E

    Biochimica et biophysica acta. Reviews on cancer

    2023  Volume 1878, Issue 6, Page(s) 188987

    Abstract: Citrate is a key metabolite of the Krebs cycle that can also be exported in the cytosol, where it performs several functions. In normal cells, citrate sustains protein acetylation, lipid synthesis, gluconeogenesis, insulin secretion, bone tissues ... ...

    Abstract Citrate is a key metabolite of the Krebs cycle that can also be exported in the cytosol, where it performs several functions. In normal cells, citrate sustains protein acetylation, lipid synthesis, gluconeogenesis, insulin secretion, bone tissues formation, spermatozoid mobility, and immune response. Dysregulation of citrate metabolism is implicated in several pathologies, including cancer. Here we discuss how cancer cells use citrate to sustain their proliferation, survival, and metastatic progression. Also, we propose two paradoxically opposite strategies to reduce tumour growth by targeting citrate metabolism in preclinical models. In the first strategy, we propose to administer in the tumor microenvironment a high amount of citrate, which can then act as a glycolysis inhibitor and apoptosis inducer, whereas the other strategy targets citrate transporters to starve cancer cells from citrate. These strategies, effective in several preclinical in vitro and in vivo cancer models, could be exploited in clinics, particularly to increase sensibility to current anti-cancer agents.
    MeSH term(s) Humans ; Citric Acid/metabolism ; Neoplasms/pathology ; Glycolysis/physiology ; Citric Acid Cycle ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Tumor Microenvironment
    Chemical Substances Citric Acid (2968PHW8QP) ; Antineoplastic Agents
    Language English
    Publishing date 2023-09-17
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2918802-7
    ISSN 1879-2561 ; 0304-419X
    ISSN (online) 1879-2561
    ISSN 0304-419X
    DOI 10.1016/j.bbcan.2023.188987
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7162: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  7. Article ; Online: Fructose-1,6-bisphosphate promotes PI3K and glycolysis in T cells?

    Icard, Philippe / Alifano, Marco / Donnadieu, Emmanuel / Simula, Luca

    Trends in endocrinology and metabolism: TEM

    2021  Volume 32, Issue 8, Page(s) 540–543

    Abstract: We propose that fructose-1,6-bisphosphate (F-1,6-BP) promotes a feedback loop between phosphofructokinase-1 (PFK1), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), and PFK2/PFKFB3, which enhances aerobic glycolysis and sustains effector T ( ... ...

    Abstract We propose that fructose-1,6-bisphosphate (F-1,6-BP) promotes a feedback loop between phosphofructokinase-1 (PFK1), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), and PFK2/PFKFB3, which enhances aerobic glycolysis and sustains effector T (T
    MeSH term(s) Adenosine Triphosphate/biosynthesis ; Citric Acid ; Fructosediphosphates/metabolism ; Glycolysis ; Lymphocyte Activation ; Mitochondria ; Neoplasms ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphofructokinase-1/genetics ; Phosphofructokinase-1/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; T-Lymphocytes/metabolism
    Chemical Substances Fructosediphosphates ; Citric Acid (2968PHW8QP) ; Adenosine Triphosphate (8L70Q75FXE) ; Phosphofructokinase-1 (EC 2.7.1.11) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; fructose-1,6-diphosphate (M7522JYX1H)
    Language English
    Publishing date 2021-05-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2021.04.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2999: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Immune Checkpoint Proteins, Metabolism and Adhesion Molecules

    Luca Simula / Emma Ollivier / Philippe Icard / Emmanuel Donnadieu

    Cells, Vol 11, Iss 1854, p

    Overlooked Determinants of CAR T-Cell Migration?

    2022  Volume 1854

    Abstract: Adoptive transfer of T cells genetically engineered to express chimeric antigen receptors (CAR) has demonstrated striking efficacy for the treatment of several hematological malignancies, including B-cell lymphoma, leukemia, and multiple myeloma. However, ...

    Abstract Adoptive transfer of T cells genetically engineered to express chimeric antigen receptors (CAR) has demonstrated striking efficacy for the treatment of several hematological malignancies, including B-cell lymphoma, leukemia, and multiple myeloma. However, many patients still do not respond to this therapy or eventually relapse after an initial remission. In most solid tumors for which CAR T-cell therapy has been tested, efficacy has been very limited. In this context, it is of paramount importance to understand the mechanisms of tumor resistance to CAR T cells. Possible factors contributing to such resistance have been identified, including inherent CAR T-cell dysfunction, the presence of an immunosuppressive tumor microenvironment, and tumor-intrinsic factors. To control tumor growth, CAR T cells have to migrate actively enabling a productive conjugate with their targets. To date, many cells and factors contained within the tumor microenvironment have been reported to negatively control the migration of T cells and their ability to reach cancer cells. Recent evidence suggests that additional determinants, such as immune checkpoint proteins, cellular metabolism, and adhesion molecules, may modulate the motility of CAR T cells in tumors. Here, we review the potential impact of these determinants on CAR T-cell motility, and we discuss possible strategies to restore intratumoral T-cell migration with a special emphasis on approaches targeting these determinants.
    Keywords T cells ; chimeric antigen receptor ; migration ; PD-1 ; metabolism ; adhesion ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: Is there a real need for a remotely actuated magnetic chest drain device?

    Fournel, Ludovic / Alifano, Marco / Icard, Philippe

    Journal of thoracic disease

    2020  Volume 11, Issue 12, Page(s) 5677–5679

    Language English
    Publishing date 2020-01-22
    Publishing country China
    Document type Editorial ; Comment
    ZDB-ID 2573571-8
    ISSN 2077-6624 ; 2072-1439
    ISSN (online) 2077-6624
    ISSN 2072-1439
    DOI 10.21037/jtd.2019.12.60
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Corrigendum to "The reduced concentration of citrate in cancer cells: An indicator of cancer aggressiveness and a possible therapeutic target" [Drug Resistance Updates 29 (2016) 47-53].

    Icard, Philippe / Lincet, Hubert

    Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

    2017  Volume 30, Page(s) 63

    Language English
    Publishing date 2017-01
    Publishing country Scotland
    Document type Published Erratum
    ZDB-ID 1474513-6
    ISSN 1532-2084 ; 1368-7646
    ISSN (online) 1532-2084
    ISSN 1368-7646
    DOI 10.1016/j.drup.2017.01.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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