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1. Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer

Author

Li, Carman Man-Chung, Cordes, Alyssa, Oliphant, Michael U. J., Quinn, S. Aidan, Thomas, Mayura, Selfors, Laura M., Silvestri, Francesca, Girnius, Nomeda, Rinaldi, Gianmarco, Zoeller, Jason J., Shapiro, Hana, Tsiobikas, Christina, Gupta, Kushali P., Pathania, Shailja, Regev, Aviv, Kadoch, Cigall, Muthuswamy, Senthil K., and Brugge, Joan S.

Published
2024
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2. Author Correction: Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer

Author

Li, Carman Man-Chung, Cordes, Alyssa, Oliphant, Michael U. J., Quinn, S. Aidan, Thomas, Mayura, Selfors, Laura M., Silvestri, Francesca, Girnius, Nomeda, Rinaldi, Gianmarco, Zoeller, Jason J., Shapiro, Hana, Tsiobikas, Christina, Gupta, Kushali P., Pathania, Shailja, Regev, Aviv, Kadoch, Cigall, Muthuswamy, Senthil K., and Brugge, Joan S.

Published
2024
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3. miR-449a/miR-340 reprogram cell identity and metabolism in fusion-negative rhabdomyosarcoma

Author

Pozzo, Enrico, Yedigaryan, Laura, Giarratana, Nefele, Wang, Chao-chi, Garrido, Gabriel Miró, Degreef, Ewoud, Marini, Vittoria, Rinaldi, Gianmarco, van der Veer, Bernard K., Sassi, Gabriele, Eelen, Guy, Planque, Mélanie, Fanzani, Alessandro, Koh, Kian Peng, Carmeliet, Peter, Yustein, Jason T., Fendt, Sarah-Maria, Uyttebroeck, Anne, and Sampaolesi, Maurilio

Published
2025
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6. PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Author

Rossi, Matteo, Altea-Manzano, Patricia, Demicco, Margherita, Doglioni, Ginevra, Bornes, Laura, Fukano, Marina, Vandekeere, Anke, Cuadros, Alejandro M., Fernández-García, Juan, Riera-Domingo, Carla, Jauset, Cristina, Planque, Mélanie, Alkan, H. Furkan, Nittner, David, Zuo, Dongmei, Broadfield, Lindsay A., Parik, Sweta, Pane, Antonino Alejandro, Rizzollo, Francesca, Rinaldi, Gianmarco, Zhang, Tao, Teoh, Shao Thing, Aurora, Arin B., Karras, Panagiotis, Vermeire, Ines, Broekaert, Dorien, Elsen, Joke Van, Knott, Maximilian M. L., Orth, Martin F., Demeyer, Sofie, Eelen, Guy, Dobrolecki, Lacey E., Bassez, Ayse, Brussel, Thomas Van, Sotlar, Karl, Lewis, Michael T., Bartsch, Harald, Wuhrer, Manfred, Veelen, Peter van, Carmeliet, Peter, Cools, Jan, Morrison, Sean J., Marine, Jean-Christophe, Lambrechts, Diether, Mazzone, Massimiliano, Hannon, Gregory J., Lunt, Sophia Y., Grünewald, Thomas G. P., Park, Morag, Rheenen, Jacco van, and Fendt, Sarah-Maria

Published
2022
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7. Macrophages are metabolically heterogeneous within the tumor microenvironment

Author

Geeraerts, Xenia, Fernández-Garcia, Juan, Hartmann, Felix J., de Goede, Kyra E., Martens, Liesbet, Elkrim, Yvon, Debraekeleer, Ayla, Stijlemans, Benoit, Vandekeere, Anke, Rinaldi, Gianmarco, De Rycke, Riet, Planque, Mélanie, Broekaert, Dorien, Meinster, Elisa, Clappaert, Emile, Bardet, Pauline, Murgaski, Aleksandar, Gysemans, Conny, Nana, Frank Aboubakar, Saeys, Yvan, Bendall, Sean C., Laoui, Damya, Van den Bossche, Jan, Fendt, Sarah-Maria, and Van Ginderachter, Jo A.

Published
2021
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10. Author Correction: PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Author

Rossi, Matteo, Altea-Manzano, Patricia, Demicco, Margherita, Doglioni, Ginevra, Bornes, Laura, Fukano, Marina, Vandekeere, Anke, Cuadros, Alejandro M., Fernández-García, Juan, Riera-Domingo, Carla, Jauset, Cristina, Planque, Mélanie, Alkan, H. Furkan, Nittner, David, Zuo, Dongmei, Broadfield, Lindsay A., Parik, Sweta, Pane, Antonino Alejandro, Rizzollo, Francesca, Rinaldi, Gianmarco, Zhang, Tao, Teoh, Shao Thing, Aurora, Arin B., Karras, Panagiotis, Vermeire, Ines, Broekaert, Dorien, Elsen, Joke Van, Knott, Maximilian M. L., Orth, Martin F., Demeyer, Sofie, Eelen, Guy, Dobrolecki, Lacey E., Bassez, Ayse, Brussel, Thomas Van, Sotlar, Karl, Lewis, Michael T., Bartsch, Harald, Wuhrer, Manfred, Veelen, Peter van, Carmeliet, Peter, Cools, Jan, Morrison, Sean J., Marine, Jean-Christophe, Lambrechts, Diether, Mazzone, Massimiliano, Hannon, Gregory J., Lunt, Sophia Y., Grünewald, Thomas G. P., Park, Morag, Rheenen, Jacco van, and Fendt, Sarah-Maria

Published
2022
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12. Correction: The ribosomal RPL10 R98S mutation drives IRES-dependent BCL-2 translation in T-ALL

Author

Kampen, Kim R., Sulima, Sergey O., Verbelen, Benno, Girardi, Tiziana, Vereecke, Stijn, Fancello, Laura, Rinaldi, Gianmarco, Verbeeck, Jelle, Op de Beeck, Joyce, Uyttebroeck, Anne, Meijerink, Jules P. P., Moorman, Anthony V., Harrison, Christine J., Spincemaille, Pieter, Cools, Jan, Cassiman, David, Fendt, Sarah-Maria, Vermeersch, Pieter, and De Keersmaecker, Kim

Published
2019
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14. HIF-1[alpha] metabolically controls collagen synthesis and modification in chondrocytes

Author

Stegen, Steve, Laperre, Kjell, Eelen, Guy, Rinaldi, Gianmarco, Fraisl, Peter, Torrekens, Sophie, and Van Looveren, Riet

Subjects
Physiological aspects, Risk factors, Genetic aspects, Cartilage cells -- Physiological aspects, Osteochondrodysplasias -- Risk factors -- Genetic aspects, Glutamine metabolism -- Physiological aspects, Transcription factors -- Physiological aspects, Bone development -- Genetic aspects, Physiological research, Glutamine, Dysplasia, Hydroxylation, Oxidation-reduction reactions, Proline, Proteases, Post-translational modifications, Collagen, Lysine, Fibrosis, Glucose
Abstract

Author(s): Steve Stegen [sup.1] , Kjell Laperre [sup.1] , Guy Eelen [sup.2] [sup.3] , Gianmarco Rinaldi [sup.4] [sup.5] , Peter Fraisl [sup.2] [sup.3] , Sophie Torrekens [sup.1] , Riet Van [...], Endochondral ossification, an important process in vertebrate bone formation, is highly dependent on correct functioning of growth plate chondrocytes.sup.1. Proliferation of these cells determines longitudinal bone growth and the matrix deposited provides a scaffold for future bone formation. However, these two energy-dependent anabolic processes occur in an avascular environment.sup.1,2. In addition, the centre of the expanding growth plate becomes hypoxic, and local activation of the hypoxia-inducible transcription factor HIF-1[alpha] is necessary for chondrocyte survival by unidentified cell-intrinsic mechanisms.sup.3-6. It is unknown whether there is a requirement for restriction of HIF-1[alpha] signalling in the other regions of the growth plate and whether chondrocyte metabolism controls cell function. Here we show that prolonged HIF-1[alpha] signalling in chondrocytes leads to skeletal dysplasia by interfering with cellular bioenergetics and biosynthesis. Decreased glucose oxidation results in an energy deficit, which limits proliferation, activates the unfolded protein response and reduces collagen synthesis. However, enhanced glutamine flux increases [alpha]-ketoglutarate levels, which in turn increases proline and lysine hydroxylation on collagen. This metabolically regulated collagen modification renders the cartilaginous matrix more resistant to protease-mediated degradation and thereby increases bone mass. Thus, inappropriate HIF-1[alpha] signalling results in skeletal dysplasia caused by collagen overmodification, an effect that may also contribute to other diseases involving the extracellular matrix such as cancer and fibrosis.Increased glutamine metabolism caused by unregulated HIF-1[alpha] signalling in mouse chondrocytes results in increased post-translational modification of collagen and skeletal dysplasia, demonstrating that strict regulation of HIF-1[alpha] signalling in chondrocytes is essential for normal bone growth.

Published
2019
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15. Evidence for an alternative fatty acid desaturation pathway increasing cancer plasticity

Author

Vriens, Kim, Christen, Stefan, Parik, Sweta, Broekaert, Dorien, Yoshinaga, Kazuaki, Talebi, Ali, Dehairs, Jonas, Escalona-Noguero, Carmen, Schmieder, Roberta, Cornfield, Thomas, Charlton, Catriona, Romero-Pérez, Laura, Rossi, Matteo, Rinaldi, Gianmarco, Orth, Martin F., Boon, Ruben, Kerstens, Axelle, Kwan, Suet Ying, Faubert, Brandon, Méndez-Lucas, Andrés, Kopitz, Charlotte C., Chen, Ting, Fernandez-Garcia, Juan, Duarte, João A. G., Schmitz, Arndt A., Steigemann, Patrick, Najimi, Mustapha, Hägebarth, Andrea, Van Ginderachter, Jo A., Sokal, Etienne, Gotoh, Naohiro, Wong, Kwok-Kin, Verfaillie, Catherine, Derua, Rita, Munck, Sebastian, Yuneva, Mariia, Beretta, Laura, DeBerardinis, Ralph J., Swinnen, Johannes V., Hodson, Leanne, Cassiman, David, Verslype, Chris, Christian, Sven, Grünewald, Sylvia, Grünewald, Thomas G. P., and Fendt, Sarah-Maria

Published
2019
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17. Translatome analysis reveals altered serine and glycine metabolism in T-cell acute lymphoblastic leukemia cells

Author

Kampen, Kim R., Fancello, Laura, Girardi, Tiziana, Rinaldi, Gianmarco, Planque, Mélanie, Sulima, Sergey O., Loayza-Puch, Fabricio, Verbelen, Benno, Vereecke, Stijn, Verbeeck, Jelle, Op de Beeck, Joyce, Royaert, Jonathan, Vermeersch, Pieter, Cassiman, David, Cools, Jan, Agami, Reuven, Fiers, Mark, Fendt, Sarah-Maria, and De Keersmaecker, Kim

Published
2019
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18. Data from Repurposing the Antidepressant Sertraline as SHMT Inhibitor to Suppress Serine/Glycine Synthesis–Addicted Breast Tumor Growth

Author

Geeraerts, Shauni Lien, primary, Kampen, Kim Rosalie, primary, Rinaldi, Gianmarco, primary, Gupta, Purvi, primary, Planque, Mélanie, primary, Louros, Nikolaos, primary, Heylen, Elien, primary, De Cremer, Kaat, primary, De Brucker, Katrijn, primary, Vereecke, Stijn, primary, Verbelen, Benno, primary, Vermeersch, Pieter, primary, Schymkowitz, Joost, primary, Rousseau, Frederic, primary, Cassiman, David, primary, Fendt, Sarah-Maria, primary, Voet, Arnout, primary, Cammue, Bruno P.A., primary, Thevissen, Karin, primary, and De Keersmaecker, Kim, primary

Published
2023
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19. Supplementary Information from Repurposing the Antidepressant Sertraline as SHMT Inhibitor to Suppress Serine/Glycine Synthesis–Addicted Breast Tumor Growth

Author

Geeraerts, Shauni Lien, primary, Kampen, Kim Rosalie, primary, Rinaldi, Gianmarco, primary, Gupta, Purvi, primary, Planque, Mélanie, primary, Louros, Nikolaos, primary, Heylen, Elien, primary, De Cremer, Kaat, primary, De Brucker, Katrijn, primary, Vereecke, Stijn, primary, Verbelen, Benno, primary, Vermeersch, Pieter, primary, Schymkowitz, Joost, primary, Rousseau, Frederic, primary, Cassiman, David, primary, Fendt, Sarah-Maria, primary, Voet, Arnout, primary, Cammue, Bruno P.A., primary, Thevissen, Karin, primary, and De Keersmaecker, Kim, primary

Published
2023
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20. Brca1haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer

Author

Li, Carman Man-Chung, Cordes, Alyssa, Oliphant, Michael U. J., Quinn, S. Aidan, Thomas, Mayura, Selfors, Laura M., Silvestri, Francesca, Girnius, Nomeda, Rinaldi, Gianmarco, Zoeller, Jason J., Shapiro, Hana, Tsiobikas, Christina, Gupta, Kushali P., Pathania, Shailja, Regev, Aviv, Kadoch, S. Cigall, Muthuswamy, Senthil K., and Brugge, Joan S.

Abstract

Germline BRCA1mutation carriers face a high breast cancer risk; however, the underlying mechanisms for this risk are not completely understood. Using a new genetically engineered mouse model of germline Brca1heterozygosity, we demonstrate that early tumor onset in a Brca1heterozygous background cannot be fully explained by the conventional ‘two-hit’ hypothesis, suggesting the existence of inherent tumor-promoting alterations in the Brca1heterozygous state. Single-cell RNA sequencing and assay for transposase-accessible chromatin with sequencing analyses uncover a unique set of differentially accessible chromatin regions in ostensibly normal Brca1heterozygous mammary epithelial cells, distinct from wild-type cells and partially mimicking the chromatin and RNA-level changes in tumor cells. Transcription factor analyses identify loss of ELF5 and gain of AP-1 sites in these epigenetically primed regions; in vivo experiments further implicate AP-1 and Wnt10aas strong promoters of Brca1-related breast cancer. These findings reveal a previously unappreciated epigenetic effect of Brca1haploinsufficiency in accelerating tumorigenesis, advancing our mechanistic understanding and informing potential therapeutic strategies.

Published
2024
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22. Skeletal progenitors preserve proliferation and self-renewal upon inhibition of mitochondrial respiration by rerouting the TCA cycle.

Author

KU Leuven - Laboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism, KU Leuven - Prometheus, Division of Skeletal Tissue Engineerin, KU Leuven - Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology and Leuven Cancer Institute, VIB Center for Cancer Biology - Laboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer Biology - Laboratory of Angiogenesis and Vascular Metabolism, KU Leuven - Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology and Leuven Cancer Institute, KU Leuven - Metabolomics Expertise Center, Department of Oncology, VIB Center for Cancer Biology - Metabolomics Expertise Center, KU Leuven - Laboratory of Functional Epigenetics, Department of Human Genetics, UCL - SSS/DDUV - Institut de Duve, Tournaire, Guillaume, Loopmans, Shauni, Stegen, Steve, Rinaldi, Gianmarco, Eelen, Guy, Torrekens, Sophie, Moermans, Karen, Carmeliet, Peter, Ghesquière, Bart, Thienpont, Bernard, Fendt, Sarah-Maria, Van Gastel, Nick, Carmeliet, Geert, KU Leuven - Laboratory of Clinical and Experimental Endocrinology, Department of Chronic Diseases and Metabolism, KU Leuven - Prometheus, Division of Skeletal Tissue Engineerin, KU Leuven - Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology and Leuven Cancer Institute, VIB Center for Cancer Biology - Laboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer Biology - Laboratory of Angiogenesis and Vascular Metabolism, KU Leuven - Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology and Leuven Cancer Institute, KU Leuven - Metabolomics Expertise Center, Department of Oncology, VIB Center for Cancer Biology - Metabolomics Expertise Center, KU Leuven - Laboratory of Functional Epigenetics, Department of Human Genetics, UCL - SSS/DDUV - Institut de Duve, Tournaire, Guillaume, Loopmans, Shauni, Stegen, Steve, Rinaldi, Gianmarco, Eelen, Guy, Torrekens, Sophie, Moermans, Karen, Carmeliet, Peter, Ghesquière, Bart, Thienpont, Bernard, Fendt, Sarah-Maria, Van Gastel, Nick, and Carmeliet, Geert

Abstract

A functional electron transport chain (ETC) is crucial for supporting bioenergetics and biosynthesis. Accordingly, ETC inhibition decreases proliferation in cancer cells but does not seem to impair stem cell proliferation. However, it remains unclear how stem cells metabolically adapt. In this study, we show that pharmacological inhibition of complex III of the ETC in skeletal stem and progenitor cells induces glycolysis side pathways and reroutes the tricarboxylic acid (TCA) cycle to regenerate NAD and preserve cell proliferation. These metabolic changes also culminate in increased succinate and 2-hydroxyglutarate levels that inhibit Ten-eleven translocation (TET) DNA demethylase activity, thereby preserving self-renewal and multilineage potential. Mechanistically, mitochondrial malate dehydrogenase and reverse succinate dehydrogenase activity proved to be essential for the metabolic rewiring in response to ETC inhibition. Together, these data show that the metabolic plasticity of skeletal stem and progenitor cells allows them to bypass ETC blockade and preserve their self-renewal.

Published
2022

24. Macrophages are metabolically heterogeneous within the tumor microenvironment.

Author

UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Service de pneumologie, Geeraerts, Xenia, Fernández-Garcia, Juan, Hartmann, Felix J, de Goede, Kyra E, Martens, Liesbet, Elkrim, Yvon, Debraekeleer, Ayla, Stijlemans, Benoit, Vandekeere, Anke, Rinaldi, Gianmarco, De Rycke, Riet, Planque, Mélanie, Broekaert, Dorien, Meinster, Elisa, Clappaert, Emile, Bardet, Pauline, Murgaski, Aleksandar, Gysemans, Conny, Aboubakar Nana, Frank, Saeys, Yvan, Bendall, Sean C, Laoui, Damya, Van den Bossche, Jan, Fendt, Sarah-Maria, Van Ginderachter, Jo A, UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - (SLuc) Service de pneumologie, Geeraerts, Xenia, Fernández-Garcia, Juan, Hartmann, Felix J, de Goede, Kyra E, Martens, Liesbet, Elkrim, Yvon, Debraekeleer, Ayla, Stijlemans, Benoit, Vandekeere, Anke, Rinaldi, Gianmarco, De Rycke, Riet, Planque, Mélanie, Broekaert, Dorien, Meinster, Elisa, Clappaert, Emile, Bardet, Pauline, Murgaski, Aleksandar, Gysemans, Conny, Aboubakar Nana, Frank, Saeys, Yvan, Bendall, Sean C, Laoui, Damya, Van den Bossche, Jan, Fendt, Sarah-Maria, and Van Ginderachter, Jo A

Abstract

Macrophages are often prominently present in the tumor microenvironment, where distinct macrophage populations can differentially affect tumor progression. Although metabolism influences macrophage function, studies on the metabolic characteristics of ex vivo tumor-associated macrophage (TAM) subsets are rather limited. Using transcriptomic and metabolic analyses, we now reveal that pro-inflammatory major histocompatibility complex (MHC)-II TAMs display a hampered tricarboxylic acid (TCA) cycle, while reparative MHC-II TAMs show higher oxidative and glycolytic metabolism. Although both TAM subsets rapidly exchange lactate in high-lactate conditions, only MHC-II TAMs use lactate as an additional carbon source. Accordingly, lactate supports the oxidative metabolism in MHC-II TAMs, while it decreases the metabolic activity of MHC-II TAMs. Lactate subtly affects the transcriptome of MHC-II TAMs, increases L-arginine metabolism, and enhances the T cell suppressive capacity of these TAMs. Overall, our data uncover the metabolic intricacies of distinct TAM subsets and identify lactate as a carbon source and metabolic and functional regulator of TAMs.

Published
2021

25. Heterogeneity in PHGDH protein expression potentiates cancer cell dissemination and metastasis

Author

Rossi, Matteo, primary, Doglioni, Ginevra, additional, Bornes, Laura, additional, Broekaert, Dorien, additional, Planque, Mélanie, additional, Fernández-García, Juan, additional, Rinaldi, Gianmarco, additional, Van Elsen, Joke, additional, Nittner, David, additional, Jauset, Cristina, additional, Rizzollo, Francesca, additional, Domingo, Carla Riera, additional, Orth, Martin F, additional, Dobrolecki, Lacey E, additional, Van Brussel, Thomas, additional, Teoh, Shao Thing, additional, Aurora, Arin B, additional, Eelen, Guy, additional, Karras, Panagiotis, additional, Sotlar, Karl, additional, Bartsch, Harald, additional, Marine, Jean-Christophe, additional, Carmeliet, Peter, additional, Morrison, Sean J, additional, Lewis, Michael T, additional, Hannon, Gregory J, additional, Mazzone, Massimiliano, additional, Lambrechts, Diether, additional, van Rheenen, Jacco, additional, Grünewald, Thomas G P, additional, Lunt, Sophia Y, additional, and Fendt, Sarah-Maria, additional

Published
2021
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26. Repurposing the Antidepressant Sertraline as SHMT Inhibitor to Suppress Serine/Glycine Synthesis–Addicted Breast Tumor Growth

Author

Geeraerts, Shauni Lien, primary, Kampen, Kim Rosalie, additional, Rinaldi, Gianmarco, additional, Gupta, Purvi, additional, Planque, Mélanie, additional, Louros, Nikolaos, additional, Heylen, Elien, additional, De Cremer, Kaat, additional, De Brucker, Katrijn, additional, Vereecke, Stijn, additional, Verbelen, Benno, additional, Vermeersch, Pieter, additional, Schymkowitz, Joost, additional, Rousseau, Frederic, additional, Cassiman, David, additional, Fendt, Sarah-Maria, additional, Voet, Arnout, additional, Cammue, Bruno P.A., additional, Thevissen, Karin, additional, and De Keersmaecker, Kim, additional

Published
2021
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27. Abstract 1789: Repurposing the anti-depressant sertraline to target serine/glycine synthesis addicted cancer

Author

Geeraerts, Shauni L., primary, Kampen, Kim R., additional, Rinaldi, Gianmarco, additional, Gupta, Purvi, additional, Planque, Mélanie, additional, De Cremer, Kaat, additional, De Brucker, Katrijn, additional, Vereecke, Stijn, additional, Verbelen, Benno, additional, Vermeersch, Pieter, additional, Cassiman, David, additional, Fendt, Sarah-Maria, additional, Voet, Arnout, additional, Cammue, Bruno P.A., additional, Thevissen, Karin, additional, and De Keersmaecker, Kim, additional

Published
2020
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28. Repurposing the antidepressant sertraline as SHMT inhibitor to suppress serine/glycine synthesis addicted breast tumor growth

Author

Geeraerts, Shauni L., primary, Kampen, Kim R., additional, Rinaldi, Gianmarco, additional, Gupta, Purvi, additional, Planque, Mélanie, additional, De Cremer, Kaat, additional, De Brucker, Katrijn, additional, Vereecke, Stijn, additional, Verbelen, Benno, additional, Vermeersch, Pieter, additional, Cassiman, David, additional, Fendt, Sarah-Maria, additional, Voet, Arnout, additional, Cammue, Bruno P.A., additional, Thevissen, Karin, additional, and De Keersmaecker, Kim, additional

Published
2020
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29. HIF1α Suppresses Tumor Cell Proliferation through Inhibition of Aspartate Biosynthesis

Author

Meléndez-Rodríguez, Florinda, Urrutia, Andrés A., Lorendeau, Doriane, Rinaldi, Gianmarco, Roche, Olga, Böğürcü-Seidel, Nuray, Ortega Muelas, Marta, Mesa-Ciller, Claudia, Turiel, Guillermo, Bouthelier, Antonio, Hernansanz-Agustín, Pablo, Elorza, Ainara, Escasany, Elia, Li, Qilong Oscar Yang, Torres-Capelli, Mar, Tello, Daniel, Fuertes, Esther, Fraga, Enrique, Martínez-Ruiz, Antonio, Pérez, Belen, Giménez-Bachs, Jose Miguel, Salinas-Sánchez, Antonio S., Acker, Till, Sánchez Prieto, Ricardo, Fendt, Sarah-Maria, De Bock, Katrien, and Aragonés, Julián

Published
2019
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30. Evidence for an alternative fatty acid desaturation pathway increasing cancer plasticity

Author

UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique, UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, Vriens, Kim, Christen, Stefan, Parik, Sweta, Broekaert, Dorien, Yoshinaga, Kazuaki, Talebi, Ali, Dehairs, Jonas, Escalona-Noguero, Carmen, Schmieder, Roberta, Cornfield, Thomas, Charlton, Catriona, Romero-Pérez, Laura, Rossi, Matteo, Rinaldi, Gianmarco, Orth, Martin F., Boon, Ruben, Kerstens, Axelle, Kwan, Suet Ying, Faubert, Brandon, Méndez-Lucas, Andrés, Kopitz, Charlotte C., Chen, Ting, Fernandez-Garcia, Juan, Duarte, João A. G., Schmitz, Arndt A., Steigemann, Patrick, Najimi, Mustapha, Hägebarth, Andrea, Van Ginderachter, Jo A., Sokal, Etienne, Gotoh, Naohiro, Wong, Kwok-Kin, Verfaillie, Catherine, Derua, Rita, Munck, Sebastian, Yuneva, Mariia, Beretta, Laura, DeBerardinis, Ralph J., Swinnen, Johannes V., Hodson, Leanne, Cassiman, David, Verslype, Chris, Christian, Sven, Grünewald, Sylvia, Grünewald, Thomas G. P., Fendt, Sarah-Maria, UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique, UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, Vriens, Kim, Christen, Stefan, Parik, Sweta, Broekaert, Dorien, Yoshinaga, Kazuaki, Talebi, Ali, Dehairs, Jonas, Escalona-Noguero, Carmen, Schmieder, Roberta, Cornfield, Thomas, Charlton, Catriona, Romero-Pérez, Laura, Rossi, Matteo, Rinaldi, Gianmarco, Orth, Martin F., Boon, Ruben, Kerstens, Axelle, Kwan, Suet Ying, Faubert, Brandon, Méndez-Lucas, Andrés, Kopitz, Charlotte C., Chen, Ting, Fernandez-Garcia, Juan, Duarte, João A. G., Schmitz, Arndt A., Steigemann, Patrick, Najimi, Mustapha, Hägebarth, Andrea, Van Ginderachter, Jo A., Sokal, Etienne, Gotoh, Naohiro, Wong, Kwok-Kin, Verfaillie, Catherine, Derua, Rita, Munck, Sebastian, Yuneva, Mariia, Beretta, Laura, DeBerardinis, Ralph J., Swinnen, Johannes V., Hodson, Leanne, Cassiman, David, Verslype, Chris, Christian, Sven, Grünewald, Sylvia, Grünewald, Thomas G. P., and Fendt, Sarah-Maria

Abstract

Most tumours have an aberrantly activated lipid metabolism1,2 that enables them to synthesize, elongate and desaturate fatty acids to support proliferation. However, only particular subsets of cancer cells are sensitive to approaches that target fatty acid metabolism and, in particular, fatty acid desaturation3. This suggests that many cancer cells contain an unexplored plasticity in their fatty acid metabolism. Here we show that some cancer cells can exploit an alternative fatty acid desaturation pathway. We identify various cancer cell lines, mouse hepatocellular carcinomas, and primary human liver and lung carcinomas that desaturate palmitate to the unusual fatty acid sapienate to support membrane biosynthesis during proliferation. Accordingly, we found that sapienate biosynthesis enables cancer cells to bypass the known fatty acid desaturation pathway that is dependent on stearoyl-CoA desaturase. Thus, only by targeting both desaturation pathways is the in vitro and in vivo proliferation of cancer cells that synthesize sapienate impaired. Our discovery explains metabolic plasticity in fatty acid desaturation and constitutes an unexplored metabolic rewiring in cancers.

Published
2019

31. The ribosomal RPL10 R98S mutation drives IRES-dependent BCL-2 translation in T-ALL

Author

Kampen, Kim R., primary, Sulima, Sergey O., additional, Verbelen, Benno, additional, Girardi, Tiziana, additional, Vereecke, Stijn, additional, Rinaldi, Gianmarco, additional, Verbeeck, Jelle, additional, Op de Beeck, Joyce, additional, Uyttebroeck, Anne, additional, Meijerink, Jules P. P., additional, Moorman, Anthony V., additional, Harrison, Christine J., additional, Spincemaille, Pieter, additional, Cools, Jan, additional, Cassiman, David, additional, Fendt, Sarah-Maria, additional, Vermeersch, Pieter, additional, and De Keersmaecker, Kim, additional

Published
2018
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34. Dual loss of succinate dehydrogenase (SDH) and complex I activity is necessary to recapitulate the metabolic phenotype of SDH mutant tumors

Author

Lorendeau, Doriane, Rinaldi, Gianmarco, Boon, Ruben, Spincemaille, Pieter, Metzger, Kristine, Jäger, Christian, Christen, Stefan, Dong, Xiangyi, Kuenen, Sabine, Voordeckers, Karin, Verstreken, Patrik, Cassiman, David, Vermeersch, Pieter, Verfaillie, Catherine, Hiller, Karsten, Fendt, Sarah-Maria, Lorendeau, Doriane, Rinaldi, Gianmarco, Boon, Ruben, Spincemaille, Pieter, Metzger, Kristine, Jäger, Christian, Christen, Stefan, Dong, Xiangyi, Kuenen, Sabine, Voordeckers, Karin, Verstreken, Patrik, Cassiman, David, Vermeersch, Pieter, Verfaillie, Catherine, Hiller, Karsten, and Fendt, Sarah-Maria

Published
2016

37. Metabolic interactions in cancer: cellular metabolism at the interface between the microenvironment, the cancer cell phenotype and the epigenetic landscape.

Author

Rinaldi, Gianmarco, Rossi, Matteo, and Fendt, Sarah‐Maria

Subjects
METABOLISM, BIOMASS, CANCER cells, CANCER research, CELL communication
Abstract

Metabolism is tied into complex interactions with cell intrinsic and extrinsic processes that go beyond the conversion of nutrients into energy and biomass. Indeed, metabolism is a central cellular hub that interconnects and influences the microenvironment, the cellular phenotype, cell signaling, and the (epi)genetic landscape. While these interactions evolved to support survival and function of normal cells, they are hijacked by cancer cells to enable cancer maintenance and progression. Thus, a mechanistic and functional understanding of complex metabolic interactions provides a basis for the discovery of novel metabolic vulnerabilities in cancer. In this review, we will summarize and provide context for the to-date discovered complex metabolic interactions by discussing how the microenvironment as well as the cellular phenotype define cancer metabolism, and how metabolism shapes the epigenetic state of cancer cells. Many of the studies investigating the crosstalk of metabolism with cell intrinsic and extrinsic processes have used integrative data analysis approaches at the interface between computational and experimental cancer research, and we will highlight those throughout the review. In conclusion, identifying and understanding complex metabolic interactions is a basis for deciphering novel metabolic vulnerabilities of cancer cells. WIREs Syst Biol Med 2018, 10:e1397. doi: 10.1002/wsbm.1397 This article is categorized under: Biological Mechanisms > Metabolism, Physiology > Mammalian Physiology in Health and Disease [ABSTRACT FROM AUTHOR]

Published
2018
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38. Cover Image, Volume 10, Issue 1.

Author

Rinaldi, Gianmarco, Rossi, Matteo, and Fendt, Sarah‐Maria

Abstract

The cover image, by Gianmarco Rinaldi et al., is based on Advanced Review Metabolic interactions in cancer: cellular metabolism at the interface between the microenvironment, the cancer cell phenotype and the epigenetic landscape, DOI: . [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
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39. Metabolic interactions in cancer: cellular metabolism at the interface between the microenvironment, the cancer cell phenotype and the epigenetic landscape.

Author

Rinaldi G, Rossi M, and Fendt SM

Subjects
Animals, Citric Acid Cycle physiology, DNA metabolism, Epigenomics, Histones metabolism, Humans, Metabolic Networks and Pathways, Neoplasms metabolism, Neoplasms pathology, Tumor Microenvironment physiology
Abstract

Metabolism is tied into complex interactions with cell intrinsic and extrinsic processes that go beyond the conversion of nutrients into energy and biomass. Indeed, metabolism is a central cellular hub that interconnects and influences the microenvironment, the cellular phenotype, cell signaling, and the (epi)genetic landscape. While these interactions evolved to support survival and function of normal cells, they are hijacked by cancer cells to enable cancer maintenance and progression. Thus, a mechanistic and functional understanding of complex metabolic interactions provides a basis for the discovery of novel metabolic vulnerabilities in cancer. In this review, we will summarize and provide context for the to-date discovered complex metabolic interactions by discussing how the microenvironment as well as the cellular phenotype define cancer metabolism, and how metabolism shapes the epigenetic state of cancer cells. Many of the studies investigating the crosstalk of metabolism with cell intrinsic and extrinsic processes have used integrative data analysis approaches at the interface between computational and experimental cancer research, and we will highlight those throughout the review. In conclusion, identifying and understanding complex metabolic interactions is a basis for deciphering novel metabolic vulnerabilities of cancer cells. WIREs Syst Biol Med 2018, 10:e1397. doi: 10.1002/wsbm.1397 This article is categorized under: Biological Mechanisms > Metabolism Physiology > Mammalian Physiology in Health and Disease., (© 2017 Wiley Periodicals, Inc.)

Published
2018
Full Text
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