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  1. Artikel ; Online: Corrigendum to "Post-translational regulation of metabolism in fumarate hydratase deficient cancer cells" [Metabol. Eng. 45 (2018) 149-157].

    Gonçalves, Emanuel / Sciacovelli, Marco / Costa, Ana S H / Tran, Maxine Gia Binh / Johnson, Timothy Isaac / Machado, Daniel / Frezza, Christian / Saez-Rodriguez, Julio

    Metabolic engineering

    2024  Band 82, Seite(n) 297–298

    Sprache Englisch
    Erscheinungsdatum 2024-01-19
    Erscheinungsland Belgium
    Dokumenttyp Published Erratum
    ZDB-ID 1470383-x
    ISSN 1096-7184 ; 1096-7176
    ISSN (online) 1096-7184
    ISSN 1096-7176
    DOI 10.1016/j.ymben.2024.01.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: The context-specific roles of urea cycle enzymes in tumorigenesis.

    Hajaj, Emma / Sciacovelli, Marco / Frezza, Christian / Erez, Ayelet

    Molecular cell

    2021  Band 81, Heft 18, Seite(n) 3749–3759

    Abstract: The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in ... ...

    Abstract The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in different cancers at various stages and suggest that these changes are dynamic and should hence be viewed in a context-specific manner. Understanding the evolvability in the activity of the UC pathway in cancer has implications for cancer-immune cell interactions and for cancer diagnosis and therapy.
    Mesh-Begriff(e) Ammonia/metabolism ; Carcinogenesis/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/metabolism ; Gene Expression/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Urea/metabolism ; Urea Cycle Disorders, Inborn/metabolism ; Urea Cycle Disorders, Inborn/physiopathology
    Chemische Substanzen Ammonia (7664-41-7) ; Urea (8W8T17847W)
    Sprache Englisch
    Erscheinungsdatum 2021-08-31
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2021.08.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Metabolic reprogramming and epithelial-to-mesenchymal transition in cancer.

    Sciacovelli, Marco / Frezza, Christian

    The FEBS journal

    2017  Band 284, Heft 19, Seite(n) 3132–3144

    Abstract: Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial-to-mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory ...

    Abstract Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial-to-mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory capacity, enabling tumour dissemination and metastasis. EMT is associated with a complex metabolic reprogramming, orchestrated by EMT transcription factors, which support the energy requirements of increased motility and growth in harsh environmental conditions. The discovery that mutations in metabolic genes such as FH, SDH and IDH activate EMT provided further evidence that EMT and metabolism are intertwined. In this review, we discuss the role of EMT in cancer and the underpinning metabolic reprogramming. We also put forward the hypothesis that, by altering chromatin structure and function, metabolic pathways engaged by EMT are necessary for its full activation.
    Mesh-Begriff(e) Cell Movement ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cellular Reprogramming/genetics ; Chromatin/chemistry ; Chromatin/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Fumarate Hydratase/genetics ; Fumarate Hydratase/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Isocitrate Dehydrogenase/genetics ; Isocitrate Dehydrogenase/metabolism ; Metabolic Networks and Pathways/genetics ; Mutation ; Neoplasm Invasiveness ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Succinate Dehydrogenase/genetics ; Succinate Dehydrogenase/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemische Substanzen Chromatin ; Transcription Factors ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; Succinate Dehydrogenase (EC 1.3.99.1) ; Fumarate Hydratase (EC 4.2.1.2)
    Sprache Englisch
    Erscheinungsdatum 2017-05-21
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14090
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: The context-specific roles of urea cycle enzymes in tumorigenesis

    Hajaj, Emma / Sciacovelli, Marco / Frezza, Christian / Erez, Ayelet

    Molecular cell. 2021 Sept. 16, v. 81, no. 18

    2021  

    Abstract: The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in ... ...

    Abstract The expression of the urea cycle (UC) proteins is dysregulated in multiple cancers, providing metabolic benefits to tumor survival, proliferation, and growth. Here, we review the main changes described in the expression of UC enzymes and metabolites in different cancers at various stages and suggest that these changes are dynamic and should hence be viewed in a context-specific manner. Understanding the evolvability in the activity of the UC pathway in cancer has implications for cancer-immune cell interactions and for cancer diagnosis and therapy.
    Schlagwörter carcinogenesis ; metabolites ; neoplasms ; therapeutics ; urea cycle
    Sprache Englisch
    Erscheinungsverlauf 2021-0916
    Umfang p. 3749-3759.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2021.08.005
    Datenquelle NAL Katalog (AGRICOLA)

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  5. Artikel: Metabolic reprogramming and epithelial‐to‐mesenchymal transition in cancer

    Sciacovelli, Marco / Christian Frezza

    FEBS journal. 2017 Oct., v. 284, no. 19

    2017  

    Abstract: Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial‐to‐mesenchymal transition (EMT). This process endows cancer cells with increased invasive and ... ...

    Abstract Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial‐to‐mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory capacity, enabling tumour dissemination and metastasis. EMT is associated with a complex metabolic reprogramming, orchestrated by EMT transcription factors, which support the energy requirements of increased motility and growth in harsh environmental conditions. The discovery that mutations in metabolic genes such as FH, SDH and IDH activate EMT provided further evidence that EMT and metabolism are intertwined. In this review, we discuss the role of EMT in cancer and the underpinning metabolic reprogramming. We also put forward the hypothesis that, by altering chromatin structure and function, metabolic pathways engaged by EMT are necessary for its full activation.
    Schlagwörter biochemical pathways ; chromatin ; energy requirements ; environmental factors ; epithelium ; genes ; metabolism ; metastasis ; migratory behavior ; mutation ; neoplasm cells ; neoplasms ; transcription factors
    Sprache Englisch
    Erscheinungsverlauf 2017-10
    Umfang p. 3132-3144.
    Erscheinungsort John Wiley & Sons, Ltd
    Dokumenttyp Artikel
    Anmerkung REVIEW
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14090
    Datenquelle NAL Katalog (AGRICOLA)

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  6. Artikel ; Online: Fumarate hydratase in cancer: A multifaceted tumour suppressor.

    Schmidt, Christina / Sciacovelli, Marco / Frezza, Christian

    Seminars in cell & developmental biology

    2019  Band 98, Seite(n) 15–25

    Abstract: Cancer is now considered a multifactorial disorder with different aetiologies and outcomes. Yet, all cancers share some common molecular features. Among these, the reprogramming of cellular metabolism has emerged as a key player in tumour initiation and ... ...

    Abstract Cancer is now considered a multifactorial disorder with different aetiologies and outcomes. Yet, all cancers share some common molecular features. Among these, the reprogramming of cellular metabolism has emerged as a key player in tumour initiation and progression. The finding that metabolic enzymes such as fumarate hydratase (FH), succinate dehydrogenase (SDH) and isocitrate dehydrogenase (IDH), when mutated, cause cancer suggested that metabolic dysregulation is not only a consequence of oncogenic transformation but that it can act as cancer driver. However, the mechanisms underpinning the link between metabolic dysregulation and cancer remain only partially understood. In this review we discuss the role of FH loss in tumorigenesis, focusing on the role of fumarate as a key activator of a variety of oncogenic cascades. We also discuss how these alterations are integrated and converge towards common biological processes. This review highlights the complexity of the signals elicited by FH loss, describes that fumarate can act as a bona fide oncogenic event, and provides a compelling hypothesis of the stepwise neoplastic progression after FH loss.
    Mesh-Begriff(e) Fumarate Hydratase/genetics ; Fumarate Hydratase/metabolism ; Humans ; Mutation ; Neoplasms/enzymology ; Neoplasms/metabolism ; Neoplasms/pathology
    Chemische Substanzen Fumarate Hydratase (EC 4.2.1.2)
    Sprache Englisch
    Erscheinungsdatum 2019-05-22
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2019.05.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Fumarate drives EMT in renal cancer.

    Sciacovelli, Marco / Frezza, Christian

    Cell death and differentiation

    2016  Band 24, Heft 1, Seite(n) 1–2

    Mesh-Begriff(e) Animals ; Epithelial-Mesenchymal Transition ; Fumarate Hydratase/metabolism ; Fumarates/metabolism ; Humans ; Kidney Neoplasms/pathology ; Mice ; Models, Biological
    Chemische Substanzen Fumarates ; Fumarate Hydratase (EC 4.2.1.2)
    Sprache Englisch
    Erscheinungsdatum 2016-11-25
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/cdd.2016.137
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Oncometabolites: Unconventional triggers of oncogenic signalling cascades.

    Sciacovelli, Marco / Frezza, Christian

    Free radical biology & medicine

    2016  Band 100, Seite(n) 175–181

    Abstract: Cancer is a complex and heterogeneous disease thought to be caused by multiple genetic lesions. The recent finding that enzymes of the tricarboxylic acid (TCA) cycle are mutated in cancer rekindled the hypothesis that altered metabolism might also have a ...

    Abstract Cancer is a complex and heterogeneous disease thought to be caused by multiple genetic lesions. The recent finding that enzymes of the tricarboxylic acid (TCA) cycle are mutated in cancer rekindled the hypothesis that altered metabolism might also have a role in cellular transformation. Attempts to link mitochondrial dysfunction to cancer uncovered the unexpected role of small molecule metabolites, now known as oncometabolites, in tumorigenesis. In this review, we describe how oncometabolites can contribute to tumorigenesis. We propose that lesions of oncogenes and tumour suppressors are only one of the possible routes to tumorigenesis, which include accumulation of oncometabolites triggered by environmental cues.
    Mesh-Begriff(e) Animals ; Carcinogenesis ; Citric Acid Cycle ; Humans ; Neoplasms/metabolism ; Signal Transduction
    Sprache Englisch
    Erscheinungsdatum 2016-04-23
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2016.04.025
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Evaluation of the cardiovascular risk in patients undergoing major non-cardiac surgery: role of cardiac-specific biomarkers.

    Clerico, Aldo / Zaninotto, Martina / Aimo, Alberto / Musetti, Veronica / Perrone, Marco / Padoan, Andrea / Dittadi, Ruggero / Sandri, Maria Teresa / Bernardini, Sergio / Sciacovelli, Laura / Trenti, Tommaso / Malloggi, Lucia / Moretti, Marco / Burgio, Maria Aurora / Manno, Massimiliano Luca / Migliardi, Marco / Fortunato, Antonio / Plebani, Mario

    Clinical chemistry and laboratory medicine

    2022  Band 60, Heft 10, Seite(n) 1525–1542

    Abstract: Major adverse cardiovascular events are frequently observed in patients undergoing major non-cardiac surgery during the peri-operative period. At this time, the possibility to predict cardiovascular events remains limited, despite the introduction of ... ...

    Abstract Major adverse cardiovascular events are frequently observed in patients undergoing major non-cardiac surgery during the peri-operative period. At this time, the possibility to predict cardiovascular events remains limited, despite the introduction of several algorithms to calculate the risk of adverse events, mainly death and major adverse cardiovascular events (MACE) based on the clinical history, risk factors (sex, age, lipid profile, serum creatinine) and non-invasive cardiac exams (electrocardiogram, echocardiogram, stress tests). The cardiac-specific biomarkers natriuretic peptides (NPs) and cardiac troponins (cTn) have been proposed as additional tools for risk prediction in the peri-operative period, particularly for the identification of myocardial injury in patients undergoing major non-cardiac surgery. The prognostic information from the measurement of BNP/NT-proBNP and hs-cTn is independent and complementary to other important indicators of risk, also including ECG and imaging techniques. Elevated levels of cardiac-specific biomarkers before surgery are associated with a markedly higher risk of MACE during the peri-operative period. BNP/NT-proBNP and hs-cTn should be measured in all patients during the clinical evaluation before surgery, particularly during intermediate- or high-risk surgery, in patients aged >65 years and/or with comorbidities. Several questions remain to be assessed in dedicated clinical studies, such as how to optimize the management of patients with raised cardiac specific biomarkers before surgery, and whether a strategy based on biomarker measurement improves patient outcomes and is cost-effective.
    Mesh-Begriff(e) Biomarkers ; Cardiovascular Diseases ; Heart Disease Risk Factors ; Humans ; Natriuretic Peptide, Brain ; Peptide Fragments ; Prognosis ; Risk Assessment ; Risk Factors
    Chemische Substanzen Biomarkers ; Peptide Fragments ; Natriuretic Peptide, Brain (114471-18-0)
    Sprache Englisch
    Erscheinungsdatum 2022-07-20
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 1418007-8
    ISSN 1437-4331 ; 1434-6621 ; 1437-8523
    ISSN (online) 1437-4331
    ISSN 1434-6621 ; 1437-8523
    DOI 10.1515/cclm-2022-0481
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: FOXA2 controls the anti-oxidant response in FH-deficient cells.

    Rogerson, Connor / Sciacovelli, Marco / Maddalena, Lucas A / Pouikli, Andromachi / Segarra-Mondejar, Marc / Valcarcel-Jimenez, Lorea / Schmidt, Christina / Yang, Ming / Ivanova, Elena / Kent, Joshua / Mora, Ariane / Cheeseman, Danya / Carroll, Jason S / Kelsey, Gavin / Frezza, Christian

    Cell reports

    2023  Band 42, Heft 7, Seite(n) 112751

    Abstract: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a cancer syndrome caused by inactivating germline mutations in fumarate hydratase (FH) and subsequent accumulation of fumarate. Fumarate accumulation leads to profound epigenetic changes and the ... ...

    Abstract Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a cancer syndrome caused by inactivating germline mutations in fumarate hydratase (FH) and subsequent accumulation of fumarate. Fumarate accumulation leads to profound epigenetic changes and the activation of an anti-oxidant response via nuclear translocation of the transcription factor NRF2. The extent to which chromatin remodeling shapes this anti-oxidant response is currently unknown. Here, we explored the effects of FH loss on the chromatin landscape to identify transcription factor networks involved in the remodeled chromatin landscape of FH-deficient cells. We identify FOXA2 as a key transcription factor that regulates anti-oxidant response genes and subsequent metabolic rewiring cooperating without direct interaction with the anti-oxidant regulator NRF2. The identification of FOXA2 as an anti-oxidant regulator provides additional insights into the molecular mechanisms behind cell responses to fumarate accumulation and potentially provides further avenues for therapeutic intervention for HLRCC.
    Mesh-Begriff(e) Female ; Humans ; Fumarate Hydratase/genetics ; Antioxidants ; NF-E2-Related Factor 2/genetics ; Leiomyomatosis/genetics ; Uterine Neoplasms/genetics ; Skin Neoplasms/genetics ; Neoplastic Syndromes, Hereditary/genetics ; Chromatin ; Kidney Neoplasms/genetics ; Carcinoma, Renal Cell/genetics ; Hepatocyte Nuclear Factor 3-beta/genetics
    Chemische Substanzen Fumarate Hydratase (EC 4.2.1.2) ; Antioxidants ; NF-E2-Related Factor 2 ; Chromatin ; FOXA2 protein, human ; Hepatocyte Nuclear Factor 3-beta (135845-92-0)
    Sprache Englisch
    Erscheinungsdatum 2023-07-04
    Erscheinungsland United States
    Dokumenttyp 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.2023.112751
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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