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Article ; 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 Volume 82, Page(s) 297–298

Language	English
Publishing date	2024-01-19
Publishing country	Belgium
Document type	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
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Zs.A 6288: Show issues

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

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

Molecular cell

2021 Volume 81, Issue 18, Page(s) 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 term(s)	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
Chemical Substances	Ammonia (7664-41-7) ; Urea (8W8T17847W)
Language	English
Publishing date	2021-08-31
Publishing country	United States
Document type	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
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Zs.A 5055: Show issues

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

Sciacovelli, Marco / Frezza, Christian

The FEBS journal

2017 Volume 284, Issue 19, Page(s) 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 term(s)	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
Chemical Substances	Chromatin ; Transcription Factors ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; Succinate Dehydrogenase (EC 1.3.99.1) ; Fumarate Hydratase (EC 4.2.1.2)
Language	English
Publishing date	2017-05-21
Publishing country	England
Document type	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
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Zs.A 260: Show issues

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

Schmidt, Christina / Sciacovelli, Marco / Frezza, Christian

Seminars in cell & developmental biology

2019 Volume 98, Page(s) 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 term(s)	Fumarate Hydratase/genetics ; Fumarate Hydratase/metabolism ; Humans ; Mutation ; Neoplasms/enzymology ; Neoplasms/metabolism ; Neoplasms/pathology
Chemical Substances	Fumarate Hydratase (EC 4.2.1.2)
Language	English
Publishing date	2019-05-22
Publishing country	England
Document type	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
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Zs.A 2918: Show issues

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Article ; Online: Fumarate drives EMT in renal cancer.

Sciacovelli, Marco / Frezza, Christian

Cell death and differentiation

2016 Volume 24, Issue 1, Page(s) 1–2

MeSH term(s)	Animals ; Epithelial-Mesenchymal Transition ; Fumarate Hydratase/metabolism ; Fumarates/metabolism ; Humans ; Kidney Neoplasms/pathology ; Mice ; Models, Biological
Chemical Substances	Fumarates ; Fumarate Hydratase (EC 4.2.1.2)
Language	English
Publishing date	2016-11-25
Publishing country	England
Document type	Journal Article
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2016.137
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Zs.A 4230: 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)
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Article: 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 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.
Keywords	carcinogenesis ; metabolites ; neoplasms ; therapeutics ; urea cycle
Language	English
Dates of publication	2021-0916
Size	p. 3749-3759.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2021.08.005
Database	NAL-Catalogue (AGRICOLA)

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Article: Metabolic reprogramming and epithelialâtoâmesenchymal 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 epithelialâtoâmesenchymal 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 epithelialâtoâmesenchymal 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.
Keywords	biochemical pathways ; chromatin ; energy requirements ; environmental factors ; epithelium ; genes ; metabolism ; metastasis ; migratory behavior ; mutation ; neoplasm cells ; neoplasms ; transcription factors
Language	English
Dates of publication	2017-10
Size	p. 3132-3144.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.14090
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Oncometabolites: Unconventional triggers of oncogenic signalling cascades.

Sciacovelli, Marco / Frezza, Christian

Free radical biology & medicine

2016 Volume 100, Page(s) 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 term(s)	Animals ; Carcinogenesis ; Citric Acid Cycle ; Humans ; Neoplasms/metabolism ; Signal Transduction
Language	English
Publishing date	2016-04-23
Publishing country	United States
Document type	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
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Zs.A 2109: Show issues

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Article ; 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 Volume 60, Issue 10, Page(s) 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 term(s)	Biomarkers ; Cardiovascular Diseases ; Heart Disease Risk Factors ; Humans ; Natriuretic Peptide, Brain ; Peptide Fragments ; Prognosis ; Risk Assessment ; Risk Factors
Chemical Substances	Biomarkers ; Peptide Fragments ; Natriuretic Peptide, Brain (114471-18-0)
Language	English
Publishing date	2022-07-20
Publishing country	Germany
Document type	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
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Zs.A 121: Show issues

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Article ; 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 Volume 42, Issue 7, Page(s) 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 term(s)	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
Chemical Substances	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)
Language	English
Publishing date	2023-07-04
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.2023.112751
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