Doriane Lorendeau
Katholieke Universiteit Leuven
5 Papers
102 Citations
Doriane Lorendeau is an academic researcher from Katholieke Universiteit Leuven. The author has contributed to research in topics: Pyruvate carboxylase & Metabolic network. The author has an hindex of 5, co-authored 5 publications.
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Papers
Breast Cancer-Derived Lung Metastases Show Increased Pyruvate Carboxylase-Dependent Anaplerosis
Stefan Christen,Doriane Lorendeau,Roberta Schmieder,Dorien Broekaert,Kristine Metzger,Koen Veys,Ilaria Elia,Joerg Martin Buescher,Martin F. Orth,Shawn M. Davidson,Thomas G. P. Grunewald,Katrien De Bock,Sarah-Maria Fendt +12 more
TL;DR: In this paper, the authors measured PC-dependent anaplerosis in breast-cancer-derived lung metastases compared to their primary cancers using in-vivo 13C tracer analysis.
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Breast Cancer-Derived Lung Metastases Show Increased Pyruvate Carboxylase-Dependent Anaplerosis
Stefan Christen,Doriane Lorendeau,Roberta Schmieder,Dorien Broekaert,Kristine Metzger,Koen Veys,Ilaria Elia,Joerg Martin Buescher,Martin F. Orth,Shawn M. Davidson,Thomas G. P. Grunewald,Katrien De Bock,Sarah-Maria Fendt +12 more
- 01 Oct 2016
TL;DR: It is shown that breast cancer cells proliferating as lung metastases activate PC-dependent anaplerosis in response to the lung microenvironment, and it is found that mitochondrial pyruvate concentrations can promote PC- dependent anaplosis via enzyme kinetics.
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Dual loss of succinate dehydrogenase (SDH) and complex I activity is necessary to recapitulate the metabolic phenotype of SDH mutant tumors.
Doriane Lorendeau,Gianmarco Rinaldi,Ruben Boon,Pieter Spincemaille,Kristine Metzger,Christian Jäger,Stefan Christen,Xiangyi Dong,Sabine Kuenen,Karin Voordeckers,Patrik Verstreken,David Cassiman,Pieter Vermeersch,Catherine M. Verfaillie,Karsten Hiller,Sarah-Maria Fendt +15 more
TL;DR: It is shown that complex I function defines the metabolic differences between SDH mutation associated tumors and neurodegenerative diseases, which could open novel therapeutic options against both diseases.
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HIF1α Suppresses Tumor Cell Proliferation through Inhibition of Aspartate Biosynthesis
Florinda Meléndez-Rodríguez,Florinda Meléndez-Rodríguez,Andres A. Urrutia,Doriane Lorendeau,Gianmarco Rinaldi,Olga Roche,Olga Roche,Nuray Böğürcü-Seidel,Marta Ortega Muelas,Claudia Mesa-Ciller,Guillermo Turiel,Antonio Bouthelier,Pablo Hernansanz-Agustín,Ainara Elorza,Elia Escasany,Qilong Oscar Yang Li,Mar Torres-Capelli,Daniel Tello,Esther Fuertes,Enrique Fraga,Antonio Martínez-Ruiz,Antonio Martínez-Ruiz,Belén Pérez,José M. Giménez-Bachs,Antonio S. Salinas-Sánchez,Till Acker,Ricardo Sánchez Prieto,Ricardo Sánchez Prieto,Sarah-Maria Fendt,Katrien De Bock,Julián Aragonés,Julián Aragonés +31 more
TL;DR: It is shown that Hif1α inhibits cytosolic and mitochondrial aspartate biosynthesis and that this mechanism is the molecular basis for HIF1α tumor suppressor activity.
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Metabolic control of signalling pathways and metabolic auto-regulation.
TL;DR: In the context of mammalian target of rapamycin, AMP‐activated protein kinase and p53, the orchestrated interplay between metabolism and cellular signalling as well as transcriptional regulation is reviewed.
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