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Article ; Online: Targeting glycolysis to rescue 2-hydroxyglutarate immunosuppressive effects in dendritic cells and acute myeloid leukemia.

Savino, Angela Maria / Stuani, Lucille

2024

Abstract: Not available. ...

Abstract	Not available.
Language	English
Publishing date	2024-03-14
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.284893
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Article ; Online: Microenvironmental Aspartate Preserves Leukemic Cells from Therapy-Induced Metabolic Collapse.

Stuani, Lucille / Sarry, Jean-Emmanuel

Cell metabolism

2020 Volume 32, Issue 3, Page(s) 321–323

Abstract: Metabolic dialogue between tumors and their microenvironment emerges as a key regulator of chemoresistance, the major barrier for the treatment of several cancers. In this issue of Cell Metabolism, van Gastel et al. decipher the pivotal role of stromal ... ...

Abstract	Metabolic dialogue between tumors and their microenvironment emerges as a key regulator of chemoresistance, the major barrier for the treatment of several cancers. In this issue of Cell Metabolism, van Gastel et al. decipher the pivotal role of stromal glutamine-derived aspartate to sustain pyrimidine biosynthesis in chemoresistant acute myeloid leukemia (AML) and thus state it as a target for anti-cancer therapy.
MeSH term(s)	Aspartic Acid ; Drug Resistance, Neoplasm ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Tumor Microenvironment
Chemical Substances	Aspartic Acid (30KYC7MIAI)
Language	English
Publishing date	2020-09-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2020.08.008
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Zs.A 6169: Show issues

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Article ; Online: Help from outside: cysteine to survive in AML.

Stuani, Lucille / Sarry, Jean-Emmanuel

Blood

2019 Volume 134, Issue 4, Page(s) 336–338

MeSH term(s)	Cysteine ; Electron Transport Complex II ; Humans ; Leukemia, Myeloid, Acute ; Stem Cells
Chemical Substances	Electron Transport Complex II (EC 1.3.5.1) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2019-04-29
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.2019001580
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Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Exploiting metabolic vulnerabilities for personalized therapy in acute myeloid leukemia.

Stuani, Lucille / Sabatier, Marie / Sarry, Jean-Emmanuel

BMC biology

2019 Volume 17, Issue 1, Page(s) 57

Abstract: Changes in cell metabolism and metabolic adaptation are hallmark features of many cancers, including leukemia, that support biological processes involved into tumor initiation, growth, and response to therapeutics. The discovery of mutations in key ... ...

Abstract	Changes in cell metabolism and metabolic adaptation are hallmark features of many cancers, including leukemia, that support biological processes involved into tumor initiation, growth, and response to therapeutics. The discovery of mutations in key metabolic enzymes has highlighted the importance of metabolism in cancer biology and how these changes might constitute an Achilles heel for cancer treatment. In this Review, we discuss the role of metabolic and mitochondrial pathways dysregulated in acute myeloid leukemia, and the potential of therapeutic intervention targeting these metabolic dependencies on the proliferation, differentiation, stem cell function and cell survival to improve patient stratification and outcomes.
MeSH term(s)	Cell Differentiation ; Cell Proliferation ; Cell Survival ; Humans ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/therapy ; Metabolic Networks and Pathways ; Mitochondria/metabolism ; Stem Cells/metabolism
Language	English
Publishing date	2019-07-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2133020-7
ISSN	1741-7007 ; 1741-7007
ISSN (online)	1741-7007
ISSN	1741-7007
DOI	10.1186/s12915-019-0670-4
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Article: Inosine Induces Stemness Features in CAR T cells and Enhances Potency.

Klysz, Dorota D / Fowler, Carley / Malipatlolla, Meena / Stuani, Lucille / Freitas, Katherine A / Meier, Stefanie / Daniel, Bence / Sandor, Katalin / Xu, Peng / Huang, Jing / Labanieh, Louai / Leruste, Amaury / Bashti, Malek / Keerthi, Vimal / Mata-Alcazar, Janette / Gkitsas, Nikolaos / Guerrero, Justin A / Fisher, Chris / Patel, Sunny /

Asano, Kyle / Patel, Shabnum / Davis, Kara L / Satpathy, Ansuman T / Feldman, Steven A / Sotillo, Elena / Mackall, Crystal L

bioRxiv : the preprint server for biology

2023

Abstract: Adenosine (Ado) mediates immune suppression in the tumor microenvironment and exhausted ... ...

Abstract	Adenosine (Ado) mediates immune suppression in the tumor microenvironment and exhausted CD8
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.21.537859
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Article ; Online: Inosine induces stemness features in CAR-T cells and enhances potency.

Klysz, Dorota D / Fowler, Carley / Malipatlolla, Meena / Stuani, Lucille / Freitas, Katherine A / Chen, Yiyun / Meier, Stefanie / Daniel, Bence / Sandor, Katalin / Xu, Peng / Huang, Jing / Labanieh, Louai / Keerthi, Vimal / Leruste, Amaury / Bashti, Malek / Mata-Alcazar, Janette / Gkitsas, Nikolaos / Guerrero, Justin A / Fisher, Chris /

Patel, Sunny / Asano, Kyle / Patel, Shabnum / Davis, Kara L / Satpathy, Ansuman T / Feldman, Steven A / Sotillo, Elena / Mackall, Crystal L

Cancer cell

2024 Volume 42, Issue 2, Page(s) 266–282.e8

Abstract: Adenosine (Ado) mediates immune suppression in the tumor microenvironment and exhausted ... ...

Abstract	Adenosine (Ado) mediates immune suppression in the tumor microenvironment and exhausted CD8
MeSH term(s)	Humans ; T-Lymphocytes/metabolism ; Inosine
Chemical Substances	Inosine (5A614L51CT)
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2024.01.002
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: De novo structure determination of 3-((3-aminopropyl)amino)-4-hydroxybenzoic acid, a novel and abundant metabolite in Acinetobacter baylyi ADP1.

Thomas, Marion / Stuani, Lucille / Darii, Ekaterina / Lechaplais, Christophe / Pateau, Emilie / Tabet, Jean-Claude / Salanoubat, Marcel / Saaidi, Pierre-Loïc / Perret, Alain

Metabolomics : Official journal of the Metabolomic Society

2019 Volume 15, Issue 3, Page(s) 45

Abstract: Introduction: Metabolite identification remains a major bottleneck in the understanding of metabolism. Many metabolomics studies end up with unknown compounds, leaving a landscape of metabolites and metabolic pathways to be unraveled. Therefore, ... ...

Abstract	Introduction: Metabolite identification remains a major bottleneck in the understanding of metabolism. Many metabolomics studies end up with unknown compounds, leaving a landscape of metabolites and metabolic pathways to be unraveled. Therefore, identifying novel compounds within a metabolome is an entry point into the 'dark side' of metabolism. Objectives: This work aimed at elucidating the structure of a novel metabolite that was first detected in the soil bacterium Acinetobacter baylyi ADP1 (ADP1). Methods: We used high resolution multi-stage tandem mass spectrometry for characterizing the metabolite within the metabolome. We purified the molecule for 1D- and 2D-NMR ( Results: We determined the de novo structure of a previously unreported metabolite: 3-((3-aminopropyl)amino)-4-hydroxybenzoic acid. The proposed structure was validated by comparison to a synthetic standard. With a concentration in the millimolar range, this compound appears as a major metabolite in ADP1, which we anticipate to participate to an unsuspected metabolic pathway. This novel metabolite was also detected in another γ-proteobacterium. Conclusion: Structure elucidation of this abundant and novel metabolite in ADP1 urges to decipher its biosynthetic pathway and cellular function.
MeSH term(s)	Acinetobacter/chemistry ; Acinetobacter/metabolism ; Magnetic Resonance Spectroscopy/methods ; Metabolome ; Metabolomics/methods ; Parabens/chemistry ; Parabens/metabolism ; Tandem Mass Spectrometry/methods
Chemical Substances	Parabens
Language	English
Publishing date	2019-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2250617-2
ISSN	1573-3890 ; 1573-3882
ISSN (online)	1573-3890
ISSN	1573-3882
DOI	10.1007/s11306-019-1508-3
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Article ; Online: AMPK-PERK axis represses oxidative metabolism and enhances apoptotic priming of mitochondria in acute myeloid leukemia.

Cell reports

2022 Volume 38, Issue 1, Page(s) 110197

Abstract: AMP-activated protein kinase (AMPK) regulates the balance between cellular anabolism and catabolism dependent on energy resources to maintain proliferation and survival. Small-compound AMPK activators show anti-cancer activity in preclinical models. ... ...

Abstract	AMP-activated protein kinase (AMPK) regulates the balance between cellular anabolism and catabolism dependent on energy resources to maintain proliferation and survival. Small-compound AMPK activators show anti-cancer activity in preclinical models. Using the direct AMPK activator GSK621, we show that the unfolded protein response (UPR) is activated by AMPK in acute myeloid leukemia (AML) cells. Mechanistically, the UPR effector protein kinase RNA-like ER kinase (PERK) represses oxidative phosphorylation, tricarboxylic acid (TCA) cycle, and pyrimidine biosynthesis and primes the mitochondrial membrane to apoptotic signals in an AMPK-dependent manner. Accordingly, in vitro and in vivo studies reveal synergy between the direct AMPK activator GSK621 and the Bcl-2 inhibitor venetoclax. Thus, selective AMPK-activating compounds kill AML cells by rewiring mitochondrial metabolism that primes mitochondria to apoptosis by BH3 mimetics, holding therapeutic promise in AML.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/physiology ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Line, Tumor ; Citric Acid Cycle/drug effects ; Drug Evaluation, Preclinical ; Female ; HEK293 Cells ; HL-60 Cells ; Humans ; Imidazoles/pharmacology ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Male ; Mice ; Middle Aged ; Mitochondria/metabolism ; Oxidative Phosphorylation/drug effects ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Pyrimidinones/pharmacology ; Sulfonamides/pharmacology ; THP-1 Cells ; U937 Cells ; Unfolded Protein Response/physiology ; Young Adult ; eIF-2 Kinase/metabolism
Chemical Substances	Antineoplastic Agents ; Bridged Bicyclo Compounds, Heterocyclic ; GSK621 ; Imidazoles ; Proto-Oncogene Proteins c-bcl-2 ; Pyrimidinones ; Sulfonamides ; EIF2AK3 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; venetoclax (N54AIC43PW)
Language	English
Publishing date	2022-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110197
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Article ; Online: CD36 Drives Metastasis and Relapse in Acute Myeloid Leukemia.

Farge, Thomas / Nakhle, Jean / Lagarde, Damien / Cognet, Guillaume / Polley, Nathaniel / Castellano, Rémy / Nicolau, Marie-Laure / Bosc, Claudie / Sabatier, Marie / Sahal, Ambrine / Saland, Estelle / Jeanson, Yannick / Guiraud, Nathan / Boet, Emeline / Bergoglio, Camille / Gotanègre, Mathilde / Mouchel, Pierre-Luc / Stuani, Lucille / Larrue, Clément /

Sallese, Marie / De Mas, Véronique / Moro, Cedric / Dray, Cédric / Collette, Yves / Raymond-Letron, Isabelle / Ader, Isabelle / Récher, Christian / Sarry, Jean-Emmanuel / Cabon, Florence / Vergez, François / Carrière, Audrey

Cancer research

2023 Volume 83, Issue 17, Page(s) 2824–2838

Abstract: Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and ... ...

Abstract	Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and relapse in acute myeloid leukemia (AML). In a cohort of 1,273 AML patients, we uncovered that the multifunctional scavenger receptor CD36 was positively associated with extramedullary dissemination of leukemic blasts, increased risk of relapse after intensive chemotherapy, and reduced event-free and overall survival. CD36 was dispensable for lipid uptake but fostered blast migration through its binding with thrombospondin-1. CD36-expressing blasts, which were largely enriched after chemotherapy, exhibited a senescent-like phenotype while maintaining their migratory ability. In xenograft mouse models, CD36 inhibition reduced metastasis of blasts and prolonged survival of chemotherapy-treated mice. These results pave the way for the development of CD36 as an independent marker of poor prognosis in AML patients and a promising actionable target to improve the outcome of patients. Significance: CD36 promotes blast migration and extramedullary disease in acute myeloid leukemia and represents a critical target that can be exploited for clinical prognosis and patient treatment.
MeSH term(s)	Humans ; Animals ; Mice ; Leukemia, Myeloid, Acute/pathology ; Treatment Outcome ; Prognosis ; Recurrence ; Blast Crisis/pathology ; Chronic Disease
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-3682
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Article ; Online: Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells.

Larrue, Clément / Guiraud, Nathan / Mouchel, Pierre-Luc / Dubois, Marine / Farge, Thomas / Gotanègre, Mathilde / Bosc, Claudie / Saland, Estelle / Nicolau-Travers, Marie-Laure / Sabatier, Marie / Serhan, Nizar / Sahal, Ambrine / Boet, Emeline / Mouche, Sarah / Heydt, Quentin / Aroua, Nesrine / Stuani, Lucille / Kaoma, Tony / Angenendt, Linus /

Mikesch, Jan-Henrik / Schliemann, Christoph / Vergez, François / Tamburini, Jérôme / Récher, Christian / Sarry, Jean-Emmanuel

Nature communications

2021 Volume 12, Issue 1, Page(s) 422

Abstract: Drug tolerant/resistant leukemic stem cell (LSC) subpopulations may explain frequent relapses in acute myeloid leukemia (AML), suggesting that these relapse-initiating cells (RICs) persistent after chemotherapy represent bona fide targets to prevent drug ...

Abstract	Drug tolerant/resistant leukemic stem cell (LSC) subpopulations may explain frequent relapses in acute myeloid leukemia (AML), suggesting that these relapse-initiating cells (RICs) persistent after chemotherapy represent bona fide targets to prevent drug resistance and relapse. We uncover that calcitonin receptor-like receptor (CALCRL) is expressed in RICs, and that the overexpression of CALCRL and/or of its ligand adrenomedullin (ADM), and not CGRP, correlates to adverse outcome in AML. CALCRL knockdown impairs leukemic growth, decreases LSC frequency, and sensitizes to cytarabine in patient-derived xenograft models. Mechanistically, the ADM-CALCRL axis drives cell cycle, DNA repair, and mitochondrial OxPHOS function of AML blasts dependent on E2F1 and BCL2. Finally, CALCRL depletion reduces LSC frequency of RICs post-chemotherapy in vivo. In summary, our data highlight a critical role of ADM-CALCRL in post-chemotherapy persistence of these cells, and disclose a promising therapeutic target to prevent relapse in AML.
MeSH term(s)	Adrenomedullin/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Calcitonin Gene-Related Peptide/metabolism ; Calcitonin Receptor-Like Protein/genetics ; Calcitonin Receptor-Like Protein/metabolism ; Cell Cycle/drug effects ; Cell Cycle/genetics ; Cell Line, Tumor ; DNA Repair/drug effects ; DNA Repair/genetics ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/mortality ; Leukemia, Myeloid, Acute/pathology ; Male ; Mice ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Neoplasm Recurrence, Local/prevention & control ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/pathology ; Oxidative Phosphorylation/drug effects ; Primary Cell Culture ; Prognosis ; Xenograft Model Antitumor Assays
Chemical Substances	ADM protein, human ; Antineoplastic Agents ; CALCRL protein, human ; Calcitonin Receptor-Like Protein ; Adrenomedullin (148498-78-6) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2021-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-20717-9
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