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Article ; Online: S100 proteins in AML: differentiation and beyond.

Tamburini, Jerome

2017 Volume 129, Issue 14, Page(s) 1893–1894

MeSH term(s)	Cell Differentiation ; S100 Proteins
Chemical Substances	S100 Proteins
Language	English
Publishing date	2017-04-06
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2017-02-767566
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Article ; Online: Ferroptose, métabolisme lipidique, C/EBPα et résistance thérapeutique dans les leucémies aiguës myéloïdes.

Birsen, Rudy / Lauture, Laura / Sarry, Jean-Emmanuel / Tamburini, Jérome

Medecine sciences : M/S

2023 Volume 39, Issue 12, Page(s) 917–920

Title translation	Ferroptosis, lipid metabolism, C/EBPα and therapeutic resistance in acute myeloid leukemia.
MeSH term(s)	Humans ; CCAAT-Enhancer-Binding Protein-alpha ; Drug Resistance, Neoplasm/genetics ; Ferroptosis ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/therapy ; Lipid Metabolism/genetics
Chemical Substances	CCAAT-Enhancer-Binding Protein-alpha
Language	French
Publishing date	2023-12-18
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2023171
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Article ; Online: AMPK activation induces immunogenic cell death in AML.

Mondesir, Johanna / Ghisi, Margherita / Poillet, Laura / Bossong, Robert A / Kepp, Oliver / Kroemer, Guido / Sarry, Jean-Emmanuel / Tamburini, Jérôme / Lane, Andrew A

Blood advances

2023 Volume 7, Issue 24, Page(s) 7585–7596

Abstract: Survival of patients with acute myeloid leukemia (AML) can be improved by allogeneic hematopoietic stem cell transplantation (allo-HSCT) because of the antileukemic activity of T and natural killer cells from the donor. However, the use of allo-HSCT is ... ...

Abstract	Survival of patients with acute myeloid leukemia (AML) can be improved by allogeneic hematopoietic stem cell transplantation (allo-HSCT) because of the antileukemic activity of T and natural killer cells from the donor. However, the use of allo-HSCT is limited by donor availability, recipient age, and potential severe side effects. Similarly, the efficacy of immunotherapies directing autologous T cells against tumor cells, including T-cell recruiting antibodies, chimeric antigen receptor T-cell therapy, and immune checkpoint inhibitors are limited in AML because of multiple mechanisms of leukemia immune escape. This has prompted a search for novel immunostimulatory approaches. Here, we show that activation of adenosine 5'-monophosphate-activated protein kinase (AMPK), a master regulator of cellular energy balance, by the small molecule GSK621 induces calreticulin (CALR) membrane exposure in murine and human AML cells. When CALR is exposed on the cell surface, it serves as a damage-associated molecular pattern that stimulates immune responses. We found that GSK621-treated murine leukemia cells promote the activation and maturation of bone marrow-derived dendritic cells. Moreover, vaccination with GSK621-treated leukemia cells had a protective effect in syngeneic immunocompetent recipients bearing transplanted AMLs. This effect was lost in recipients depleted of CD4/CD8 T cells. Together, these results demonstrate that AMPK activation by GSK621 elicits traits of immunogenic cell death and promotes a robust immune response against leukemia. Pharmacologic AMPK activation thus represents a new potential target for improving the activity of immunotherapy in AML.
MeSH term(s)	Animals ; Humans ; Mice ; AMP-Activated Protein Kinases ; Immunogenic Cell Death ; Immunotherapy/methods ; Immunotherapy, Adoptive ; Leukemia, Myeloid, Acute/drug therapy
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2023-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2022009444
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Article: Co-activation of AMPK and mTORC1 as a new therapeutic option for acute myeloid leukemia.

Sujobert, Pierre / Tamburini, Jerome

Molecular & cellular oncology

2015 Volume 3, Issue 4, Page(s) e1071303

Abstract: We report the therapeutic potential of GSK621, an AMP-activated protein kinase (AMPK) agonist, in acute myeloid leukemia (AML). GSK621-induced cytotoxicity is restricted to AML cells compared to normal hematopoietic progenitors due to a unique synthetic ... ...

Abstract	We report the therapeutic potential of GSK621, an AMP-activated protein kinase (AMPK) agonist, in acute myeloid leukemia (AML). GSK621-induced cytotoxicity is restricted to AML cells compared to normal hematopoietic progenitors due to a unique synthetic lethal interaction of co-activation of AMPK and mammalian target of rapamycin complex 1 (mTORC1) that involves the stress response pathway. AMPK activation thus represents an attractive perspective for cancer therapy.
Language	English
Publishing date	2015-08-27
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2015.1071303
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Article: Rationale for Targeting Deregulated Metabolic Pathways as a Therapeutic Strategy in Acute Myeloid Leukemia.

Chapuis, Nicolas / Poulain, Laury / Birsen, Rudy / Tamburini, Jerome / Bouscary, Didier

Frontiers in oncology

2019 Volume 9, Page(s) 405

Abstract: Metabolic reprogramming is a common cancer cell phenotype as it sustains growth and proliferation. Targeting metabolic activities offers a wide range of therapeutic possibilities which are applicable to acute myeloid leukemia (AML). Indeed, in addition ... ...

Abstract	Metabolic reprogramming is a common cancer cell phenotype as it sustains growth and proliferation. Targeting metabolic activities offers a wide range of therapeutic possibilities which are applicable to acute myeloid leukemia (AML). Indeed, in addition to the IDH1/2-mutated AML model which established the proof-of-concept for specifically targeting metabolic adaptations in AML, several recent reports have expanded the scope of such strategies in these diseases. This review highlights recent findings on metabolic deregulation in AML and summarizes their implications in leukemogenesis.
Language	English
Publishing date	2019-05-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2019.00405
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Article ; Online: Mitochondrial fusion is a therapeutic vulnerability of acute myeloid leukemia.

Larrue, Clement / Mouche, Sarah / Lin, Shan / Simonetta, Federico / Scheidegger, Nastassja K / Poulain, Laury / Birsen, Rudy / Sarry, Jean-Emmanuel / Stegmaier, Kimberly / Tamburini, Jerome

Leukemia

2023 Volume 37, Issue 4, Page(s) 765–775

Abstract: Mitochondrial metabolism recently emerged as a critical dependency in acute myeloid leukemia (AML). The shape of mitochondria is tightly regulated by dynamin GTPase proteins, which drive opposing fusion and fission forces to consistently adapt ... ...

Abstract	Mitochondrial metabolism recently emerged as a critical dependency in acute myeloid leukemia (AML). The shape of mitochondria is tightly regulated by dynamin GTPase proteins, which drive opposing fusion and fission forces to consistently adapt bioenergetics to the cellular context. Here, we showed that targeting mitochondrial fusion was a new vulnerability of AML cells, when assayed in patient-derived xenograft (PDX) models. Genetic depletion of mitofusin 2 (MFN2) or optic atrophy 1 (OPA1) or pharmacological inhibition of OPA1 (MYLS22) blocked mitochondrial fusion and had significant anti-leukemic activity, while having limited impact on normal hematopoietic cells ex vivo and in vivo. Mechanistically, inhibition of mitochondrial fusion disrupted mitochondrial respiration and reactive oxygen species production, leading to cell cycle arrest at the G
MeSH term(s)	Humans ; Mitochondrial Dynamics/genetics ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism ; Energy Metabolism ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Mitochondrial Proteins/metabolism
Chemical Substances	Reactive Oxygen Species ; Mitochondrial Proteins
Language	English
Publishing date	2023-02-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-023-01835-x
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Zs.A 2295: Show issues

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Article ; Online: Urgent Chemotherapy in Sepsis-Like Shock Related to Hematologic Malignancies.

Cherruault, Marlène / Le Goff, Marielle / Tamburini, Jérôme / Pène, Frédéric

Critical care medicine

2018 Volume 46, Issue 5, Page(s) e465–e468

Abstract: Objectives: Hematologic malignancies may result in multiple organ involvement including pulmonary and renal dysfunctions, and the less common acute circulatory failure. We herein addressed the outcome of patients with sepsis-like shock related to ... ...

Abstract	Objectives: Hematologic malignancies may result in multiple organ involvement including pulmonary and renal dysfunctions, and the less common acute circulatory failure. We herein addressed the outcome of patients with sepsis-like shock related to aggressive hematologic malignancies. Design: A 10-year (2007-2016) monocenter retrospective study. Settings: A medical ICU in a tertiary care center. Patients: Patients with circulatory shock requiring vasopressors and who subsequently received chemotherapy. Shock was presumably related to the underlying malignancy after ruling out an ongoing or new-onset infectious process. The extent and time course of organ failures was assessed by a modified Sequential Organ Failure Assessment score devoid of the platelet component. Interventions: None. Measurements and main results: Seventeen patients were included, including 13 with non-Hodgkin lymphoma, two with hyperleukocytic acute myeloid leukemia, and two with "Human Herpes virus 8"-associated multicentric Castleman's disease. The following associated conditions prompted urgent administration of chemotherapy: tumor lysis syndrome (n = 10), hemophagocytic lymphohistiocytosis (n = 3), compressive bulky tumor (n = 3), pulmonary involvement (n = 3), and disseminated intravascular coagulation (n = 1). Following the initiation of chemotherapy, a number of patients died rapidly from untractable multiple organ failure. In contrast, chemotherapy led to a fast and dramatic improvement in organ failures in early survivors, as shown by the decrease in the modified Sequential Organ Failure Assessment score. However, the overall outcome was poor since only four and three patients could be discharged alive from the ICU and the hospital, and three and two patients remained alive at 6 months and 1 year. Conclusions: Multiple organ dysfunction syndrome related to hematologic malignancies is associated with a dismal outcome. A chemotherapy trial may provide a fast prognostic assessment of the reversibility of organ failure.
MeSH term(s)	Female ; Hematologic Neoplasms/complications ; Humans ; Male ; Middle Aged ; Multiple Organ Failure/etiology ; Retrospective Studies ; Shock/diagnosis ; Shock/drug therapy ; Shock/etiology ; Vasoconstrictor Agents/therapeutic use
Chemical Substances	Vasoconstrictor Agents
Language	English
Publishing date	2018-01-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	197890-1
ISSN	1530-0293 ; 0090-3493
ISSN (online)	1530-0293
ISSN	0090-3493
DOI	10.1097/CCM.0000000000002990
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Zs.A 1261: Show issues

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Article: AMP-Activated Protein Kinase Contributes to Apoptosis Induced by the Bcl-2 Inhibitor Venetoclax in Acute Myeloid Leukemia.

Legrand, Noémie / Pradier, Amandine / Poulain, Laury / Mouche, Sarah / Birsen, Rudy / Larrue, Clément / Simonetta, Federico / Tamburini, Jerome

Cancers

2021 Volume 13, Issue 23

Abstract: The treatment of acute myeloid leukemia (AML) remains a challenge especially among the elderly. The Bcl-2 inhibitor venetoclax recently showed significant survival benefits in AML patients when combined to low-dose cytarabine or azacitidine. Bcl-2 ... ...

Abstract	The treatment of acute myeloid leukemia (AML) remains a challenge especially among the elderly. The Bcl-2 inhibitor venetoclax recently showed significant survival benefits in AML patients when combined to low-dose cytarabine or azacitidine. Bcl-2 inhibition initiate mitochondrial apoptosis, but also respiration and cellular ATP production in AML. AMP-Activated Protein Kinase (AMPK) is a central energy sensor activated by increased AMP:ATP ratio to restore the cellular energy balance. Unexpectedly, we observed that venetoclax inhibited AMPK activity through caspase-dependent degradation of AMPK subunits in AML cells. On the other hand, genetic models of AMPK invalidation and re-expression suggested that AMPK participated to the early stages of apoptotic response through a negative regulation of multi-domain anti-apoptotic effectors such as Mcl-1 or Bcl-xL. Together our results suggested a new link between AMPK and Bcl-2-dependent mitochondrial apoptosis that participated to the anti-leukemic activity of venetoclax in AML.
Language	English
Publishing date	2021-11-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13235966
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Article ; Online: AMPK Activation Promotes Tight Junction Assembly in Intestinal Epithelial Caco-2 Cells.

Olivier, Séverine / Leclerc, Jocelyne / Grenier, Adrien / Foretz, Marc / Tamburini, Jérôme / Viollet, Benoit

International journal of molecular sciences

2019 Volume 20, Issue 20

Abstract: The AMP-activated protein kinase (AMPK) is principally known as a major regulator of cellular energy status, but it has been recently shown to play a key structural role in cell-cell junctions. The aim of this study was to evaluate the impact of AMPK ... ...

Abstract	The AMP-activated protein kinase (AMPK) is principally known as a major regulator of cellular energy status, but it has been recently shown to play a key structural role in cell-cell junctions. The aim of this study was to evaluate the impact of AMPK activation on the reassembly of tight junctions in intestinal epithelial Caco-2 cells. We generated Caco-2 cells invalidated for AMPK α1/α2 (AMPK dKO) by CRISPR/Cas9 technology and evaluated the effect of the direct AMPK activator 991 on the reassembly of tight junctions following a calcium switch assay. We analyzed the integrity of the epithelial barrier by measuring the trans-epithelial electrical resistance (TEER), the paracellular permeability, and quantification of zonula occludens 1 (ZO-1) deposit at plasma membrane by immunofluorescence. Here, we demonstrated that AMPK deletion induced a delay in tight junction reassembly and relocalization at the plasma membrane during calcium switch, leading to impairments in the establishment of TEER and paracellular permeability. We also showed that 991-induced AMPK activation accelerated the reassembly and reorganization of tight junctions, improved the development of TEER and paracellular permeability after calcium switch. Thus, our results show that AMPK activation ensures a better recovery of epithelial barrier function following injury.
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Caco-2 Cells ; Calcium/metabolism ; Cell Membrane Permeability ; DNA Mutational Analysis ; Epithelial Cells/metabolism ; Humans ; Intestinal Mucosa/metabolism ; MAP Kinase Signaling System ; Mutation ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Tight Junctions/metabolism
Chemical Substances	Protein Subunits ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-10-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20205171
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Article: Evidence for IL-35 Expression in Diffuse Large B-Cell Lymphoma and Impact on the Patient's Prognosis.

Larousserie, Frédérique / Kebe, Diakho / Huynh, Tony / Audebourg, Anne / Tamburini, Jérôme / Terris, Benoît / Devergne, Odile

Frontiers in oncology

2019 Volume 9, Page(s) 563

Abstract: IL-35 is an immunosuppressive cytokine of the IL-12 family consisting of two subunits, EBV-induced gene 3 (EBI3) and p35. It has been shown to play a pro-tumor role in murine tumor models, and in various types of human cancer such as colorectal, ... ...

Abstract	IL-35 is an immunosuppressive cytokine of the IL-12 family consisting of two subunits, EBV-induced gene 3 (EBI3) and p35. It has been shown to play a pro-tumor role in murine tumor models, and in various types of human cancer such as colorectal, pancreatic, or liver carcinoma, its expression has been associated with a worse clinical outcome. Here, we show by analyzing gene expression data from public databases and by immunohistochemical studies that IL-35 is overexpressed by tumor cells in diffuse-large B-cell lymphoma (DLBCL) compared to another type of mature aggressive B-cell lymphoma, Burkitt lymphoma. However, while high IL-35 expression was significantly associated with a worse overall survival in DLBCL patients treated with chemotherapy only (cyclophosphamide, doxorubicin, vincristine, prednisone, CHOP), no significant correlation between IL-35 expression levels and the patient outcome was observed in DLBCL patients treated with CHOP combined to rituximab (R-CHOP), the current conventional treatment. In addition, we found that an anti-IL-35 antibody, clone 15k8D10, used to assess IL-35 expression by immunohistochemistry in various human tissues including tumors does not recognize IL-35 heterodimer, nor its individual subunits EBI3 and p35, but cross-reacts with human IgG1, indicating that IL-35 expression in human cancers needs to be re-evaluated.
Language	English
Publishing date	2019-06-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2019.00563
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