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1. Aging-accumulated methylmalonic acid serum levels at breast cancer diagnosis are not associated with distant metastases

Author

Wu, Qi, Hatse, Sigrid, Kenis, Cindy, Fernández-García, Juan, Altea-Manzano, Patricia, Billen, Jaak, Planque, Mélanie, Vandekeere, Anke, Lambrechts, Yentl, Richard, François, Punie, Kevin, Neven, Patrick, Smeets, Ann, Nevelsteen, Ines, Floris, Giuseppe, Desmedt, Christine, Gomes, Ana P., Fendt, Sarah-Maria, and Wildiers, Hans

Published
2024
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3. A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling

Author

Altea-Manzano, Patricia, Doglioni, Ginevra, Liu, Yawen, Cuadros, Alejandro M., Nolan, Emma, Fernández-García, Juan, Wu, Qi, Planque, Mélanie, Laue, Kathrin Julia, Cidre-Aranaz, Florencia, Liu, Xiao-Zheng, Marin-Bejar, Oskar, Van Elsen, Joke, Vermeire, Ines, Broekaert, Dorien, Demeyer, Sofie, Spotbeen, Xander, Idkowiak, Jakub, Montagne, Aurélie, Demicco, Margherita, Alkan, H. Furkan, Rabas, Nick, Riera-Domingo, Carla, Richard, François, Geukens, Tatjana, De Schepper, Maxim, Leduc, Sophia, Hatse, Sigrid, Lambrechts, Yentl, Kay, Emily Jane, Lilla, Sergio, Alekseenko, Alisa, Geldhof, Vincent, Boeckx, Bram, de la Calle Arregui, Celia, Floris, Giuseppe, Swinnen, Johannes V., Marine, Jean-Christophe, Lambrechts, Diether, Pelechano, Vicent, Mazzone, Massimiliano, Zanivan, Sara, Cools, Jan, Wildiers, Hans, Baud, Véronique, Grünewald, Thomas G. P., Ben-David, Uri, Desmedt, Christine, Malanchi, Ilaria, and Fendt, Sarah-Maria

Published
2023
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4. 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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5. 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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8. Abstract P2-11-18: Serum methylmalonic acid concentrations at breast cancer diagnosis are not associated with distant metastases

Author

Wu, Qi, primary, Hatse, Sigrid, additional, García, Juan F., additional, Altea-Manzano, Patricia, additional, Billen, Jaak, additional, Planque, Mélanie, additional, Vandekeere, Anke, additional, Lambrechts, Yentl, additional, Richard, François, additional, Laenen, Annouschka, additional, Punie, Kevin, additional, Neven, Patrick, additional, Nevelsteen, Ines, additional, Floris, Giuseppe, additional, Desmedt, Christine, additional, Gomes, Ana, additional, Fendt, Sarah-Maria, additional, and Wildiers, Hans, additional

Published
2023
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9. Reversal of mitochondrial malate dehydrogenase 2 enables anaplerosis via redox rescue in respiration-deficient cells

Author

Altea-Manzano, Patricia, primary, Vandekeere, Anke, additional, Edwards-Hicks, Joy, additional, Roldan, Mar, additional, Abraham, Emily, additional, Lleshi, Xhordi, additional, Guerrieri, Ania Naila, additional, Berardi, Domenica, additional, Wills, Jimi, additional, Junior, Jair Marques, additional, Pantazi, Asimina, additional, Acosta, Juan Carlos, additional, Sanchez-Martin, Rosario M., additional, Fendt, Sarah-Maria, additional, Martin-Hernandez, Miguel, additional, and Finch, Andrew J., additional

Published
2022
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10. CD8+ T cell metabolic rewiring defined by scRNA-seq identifies a critical role of ASNS expression dynamics in T cell differentiation

Author

Fernández-García, Juan, primary, Franco, Fabien, additional, Parik, Sweta, additional, Altea-Manzano, Patricia, additional, Pane, Antonino Alejandro, additional, Broekaert, Dorien, additional, van Elsen, Joke, additional, Di Conza, Giusy, additional, Vermeire, Ines, additional, Schalley, Tessa, additional, Planque, Mélanie, additional, van Brussel, Thomas, additional, Schepers, Rogier, additional, Modave, Elodie, additional, Karakach, Tobias K., additional, Carmeliet, Peter, additional, Lambrechts, Diether, additional, Ho, Ping-Chih, additional, and Fendt, Sarah-Maria, additional

Published
2022
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11. A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation

Author

Altea-Manzano, Patricia, primary, Doglioni, Ginevra, additional, Cuadros, Alejandro M., additional, Nolan, Emma, additional, Fernandez-Garcia, Juan, additional, Wu, Qi, additional, Cidre-Aranaz, Florencia, additional, Montagne, Aurelie, additional, Planque, Mélanie, additional, Marin-Bejar, Oskar, additional, Van Elsen, Joke, additional, Vermeire, Ines, additional, Broekaert, Dorien, additional, Riera-Domingo, Carla, additional, Richard, François, additional, Geukens, Tatjana, additional, De Schepper, Maxim, additional, Leduc, Sophia, additional, Hatse, Sigrid, additional, Lambrechts, Yentl, additional, Kay, Emily Jane, additional, Lilla, Sergio, additional, Demeyer, Sofie, additional, Geldhof, Vincent, additional, Boeckx, Bram, additional, Alekseenko, Alisa, additional, de la Calle Arregui, Celia, additional, Floris, Giuseppe, additional, Marine, Jean-Christophe, additional, Lambrechts, Diether, additional, Pelechano, Vicent, additional, Mazzone, Massimiliano, additional, Zanivan, Sara, additional, Cools, Jan, additional, Wildiers, Hans, additional, Baud, Véronique, additional, Grünewald, Thomas G.P., additional, Desmedt, Christine, additional, Malanchi, Ilaria, additional, and Fendt, Sarah-Maria, additional

Published
2022
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13. In vivoCRISPR screen definesSlc25a37as an organ-specific regulator of antioxidant metabolism in metastasis

Author

Cuadros, Alejandro M., primary, Fernández-Garcia, Juan, additional, Planque, Mélanie, additional, Altea-Manzano, Patricia, additional, Schalley, Tessa, additional, Vermeire, Ines, additional, Broekaert, Dorien, additional, Wu, Qi, additional, Van Brussel, Thomas, additional, Leduc, Sophia, additional, Maetens, Marion, additional, Nguyen, Ha-Linh, additional, Van Baelen, Karen, additional, Darzi, Naama, additional, Floris, Giuseppe, additional, Wildiers, Hans, additional, Desmedt, Christine, additional, Lambrechts, Diether, additional, and Fendt, Sarah-Maria, additional

Published
2022
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14. Reversal of mitochondrial malate dehydrogenase 2 enables anaplerosis via redox rescue in respiration-deficient cells

Author

Stichting ter Bevordering van Natuurwetenschappelijk Onderzoek (The Netherlands), Cancer Research UK, European Research Council, European Commission, Barts Charity, National Cancer Institute (US), Altea-Manzano, Patricia, Vandekeere, Anke, Edwards-Hicks, Joy, Roldan, Mar, Abraham, Emily, Lleshi, Xhordi, Guerrieri, Ania Naila, Berardi, Domenica, Wills, Jimi, Marques Junior, Jair, Pantazi, Asimina, Acosta, Juan C., Sanchez-Martin, Rosario M., Fendt, Sarah-Maria, Martín-Hernández, Miguel, Finch, Andrew J., Stichting ter Bevordering van Natuurwetenschappelijk Onderzoek (The Netherlands), Cancer Research UK, European Research Council, European Commission, Barts Charity, National Cancer Institute (US), Altea-Manzano, Patricia, Vandekeere, Anke, Edwards-Hicks, Joy, Roldan, Mar, Abraham, Emily, Lleshi, Xhordi, Guerrieri, Ania Naila, Berardi, Domenica, Wills, Jimi, Marques Junior, Jair, Pantazi, Asimina, Acosta, Juan C., Sanchez-Martin, Rosario M., Fendt, Sarah-Maria, Martín-Hernández, Miguel, and Finch, Andrew J.

Abstract

Inhibition of the electron transport chain (ETC) prevents the regeneration of mitochondrial NAD+, resulting in cessation of the oxidative tricarboxylic acid (TCA) cycle and a consequent dependence upon reductive carboxylation for aspartate synthesis. NAD+ regeneration alone in the cytosol can rescue the viability of ETC-deficient cells. Yet, how this occurs and whether transfer of oxidative equivalents to the mitochondrion is required remain unknown. Here, we show that inhibition of the ETC drives reversal of the mitochondrial aspartate transaminase (GOT2) as well as malate and succinate dehydrogenases (MDH2 and SDH) to transfer oxidative NAD+ equivalents into the mitochondrion. This supports the NAD+-dependent activity of the mitochondrial glutamate dehydrogenase (GDH) and thereby enables anaplerosis—the entry of glutamine-derived carbon into the TCA cycle and connected biosynthetic pathways. Thus, under impaired ETC function, the cytosolic redox state is communicated into the mitochondrion and acts as a rheostat to support GDH activity and cell viability.

Published
2022

16. Metabolite-derived protein modifications modulating oncogenic signaling.

Author

Yawen Liu, Vandekeere, Anke, Min Xu, Fendt, Sarah-Maria, and Altea-Manzano, Patricia

Subjects
TUMOR microenvironment, ONCOGENES, TUMOR suppressor genes, PROTEINS
Abstract

Malignant growth is defined by multiple aberrant cellular features, including metabolic rewiring, inactivation of tumor suppressors and the activation of oncogenes. Even though these features have been described as separate hallmarks, many studies have shown an extensive mutual regulatory relationship amongst them. On one hand, the change in expression or activity of tumor suppressors and oncogenes has extensive direct and indirect effects on cellular metabolism, activating metabolic pathways required for malignant growth. On the other hand, the tumor microenvironment and tumor intrinsic metabolic alterations result in changes in intracellular metabolite levels, which directly modulate the protein modification of oncogenes and tumor suppressors at both epigenetic and post-translational levels. In this mini-review, we summarize the crosstalk between tumor suppressors/oncogenes and metabolism-induced protein modifications at both levels and explore the impact of metabolic (micro) environments in shaping these. [ABSTRACT FROM AUTHOR]

Published
2022
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17. Microstructural and strength changes in trabecular bone in elderly patients with type 2 diabetes mellitus

Author

Universidad de Sevilla. Departamento de Citología e Histología Normal y Patológica, Universidad de Sevilla. Departamento de Medicina, Giner García, Mercedes, Miranda Díaz, Cristina, Vázquez Gámez, María de los Ángeles, Altea-Manzano, Patricia, Miranda, M.J., Casado-Díaz, Antonio, Pérez Cano, Ramón, Montoya García, María José, Universidad de Sevilla. Departamento de Citología e Histología Normal y Patológica, Universidad de Sevilla. Departamento de Medicina, Giner García, Mercedes, Miranda Díaz, Cristina, Vázquez Gámez, María de los Ángeles, Altea-Manzano, Patricia, Miranda, M.J., Casado-Díaz, Antonio, Pérez Cano, Ramón, and Montoya García, María José

Abstract

Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases worldwide and it is associated with an increased risk of osteoporosis and fragility fractures. Our aim is to analyze the effect of T2DM on bone quality. This is a case-control study. The studied population consisted of 140 patients: 54 subjects with hip fracture (OP) without T2DM, 36 patients with hip fracture and T2DM (OP-T2DM), 28 patients with osteoarthritis (OA) without T2DM, and 22 patients with OA and T2DM (OA-T2DM). Bone markers, bone mineral density, FRAX score, microstructural, and bone material strength from femoral heads were assessed. The group with hip fracture presented lower BMD values than OA (p < 0.05). The OP, OP-T2DM, and OA-T2DM groups showed a decrease in bone volume fraction (BV/TV), in trabecular number (Tb.N), and in trabecular thickness (Tb.Th), while an increase was presented in the structural model index (SMI) and trabecular bone pattern factor (Tb.Pf), The groups OP, OP-T2DM, and OA-T2DM also presented lower values than those in group OA regarding the biomechanical parameters in the form of Young’s modulus or elastic modulus, toughness, ultimate stress, ultimate load, extrinsic stiffness, and work to failure (p < 0.05). Our results show the negative effect of type 2 diabetes mellitus on trabecular bone structure and mechanical properties.

Published
2021

20. In Vivo Evidence for Serine Biosynthesis-Defined Sensitivity of Lung Metastasis, but Not of Primary Breast Tumors, to mTORC1 Inhibition

Author

Rinaldi, Gianmarco, primary, Pranzini, Erica, additional, Van Elsen, Joke, additional, Broekaert, Dorien, additional, Funk, Cornelius M., additional, Planque, Mélanie, additional, Doglioni, Ginevra, additional, Altea-Manzano, Patricia, additional, Rossi, Matteo, additional, Geldhof, Vincent, additional, Teoh, Shao Thing, additional, Ross, Christina, additional, Hunter, Kent W., additional, Lunt, Sophia Y., additional, Grünewald, Thomas G.P., additional, and Fendt, Sarah-Maria, additional

Published
2021
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23. Cellular models with extreme metabophenotypes to study tumor metabolic reprogramming: Development of antitumor nanodevices focused on metabolic targets

Author

Altea-Manzano, Patricia, Sánchez Martín, Rosario María, Martín Hernández, Miguel, Universidad de Granada. Departamento de Química Farmacéutica y Orgánica, and Sánchez-Martín, Rosario M.

Subjects
Metabolismo, Nanotecnología, Células cancerosas, Marcadores tumorales, 616-006, Terapéutica, Nanomedicina, Quimioterapia, Cáncer, Fenotipos
Abstract

Tumor cells need to adapt and evolve efficiently in a hostile cellular niche, frequently subjected to a hypoxic microenvironment and with fluctuations in availability of nutrients. These metabolic adaptations of cancer cells have not arisen as a consequence of an accidental adaptation, but due to a very precise regulated process for cell transformation and oncogenesis. Therefore, we intend to study many of the metabolic targets that are still to be deciphered, particularly in some cancer-specific subtypes such as respiratory deficient tumoral cells that can play a key role in tumor evolution. In addition, the discovery of these key metabolic targets can improve the development and optimization of new therapeutic strategies through the use of nanotechnology based approaches. The main aims of this project are: (a) to elucidate the most important adaptations and metabolic targets in tumor cells, mainly in models of carcinogenic cells deficient in respiration, such as the extreme metabolic phenotype proposed in this work; (b) to take advantage of the metabolic knowledge to identify therapeutic targets susceptible of nanotechnological applications, that allow a selective and specific impact in the cancerous cells using our cellular models to develop a new approach for the study of cell proliferation through the use of nanoparticles.; (c) To develop an efficient nanotechnology fluorescence based method to track cell proliferation as the uncontrolled cell proliferation is a hallmark of cancer cells, being crucial cell proliferation assays to study the influence of metabolic changes in cancer progression. A deep study of the map of metabolic status in tumor cell models according to the following study parameters to corroborate the proposed metabofotypes has been carried out (Aim 1). Results has been achieved that include (i) analysis of the degree of tumor "addiction" to certain metabolites that play a central role in cellular bioenergetics, (ii) study of the dependence of these metabolites establishing profiles of resistance / susceptibility to inhibitors of key enzymes of their metabolism. (iii) study the expression and activity profiles of certain oncogenes to determine their relevance in the metabolic reprogramming process of the cellular models. Additionally in this section a metabolomic approximation by mass spectrometry to identify the most important metabolic routes and targets is described. To implement these nanotechnology approaches based on tumor metabolism (Aim 2), the results achieved are: (i) evaluation of nanodevices efficiency in cancer cell model based on respiration deficient cells with an extreme metabolic phenotype, (ii) development and evaluation of a controlled drug delivery system for combined metabolic-based therapy and (iii) development and validation of multifunctionalized nanodevices for targeted drug delivery system to tumor cells with selective metabolic profiles. To develop a novel tracking method based on nanoparticles (Aim 3), the method has been validated in several adherent cells and also in suspension cells including hard-to-transfect cells. Even more interesting is the fact that monitoring of cell proliferation of lymphocytes has been successfully achieved (so far the only efficient method to do this lymphocytes monitoring is CFSE staining). The method was also validated in a cell-based assay which determined the induced cellular arrest through MMC effect, showing the power of the method for long-term cellular assays. Furthermore, this new method does not alter the cell cycle hence presenting no cytotoxic effects., Tesis Univ. Granada. Programa Oficial de Doctorado en Biomedicina

Published
2017

26. CD8+T cell metabolic rewiring defined by scRNA-seq identifies a critical role of ASNS expression dynamics in T cell differentiation

Author

Fernández-García, Juan, Franco, Fabien, Parik, Sweta, Altea-Manzano, Patricia, Pane, Antonino Alejandro, Broekaert, Dorien, van Elsen, Joke, Di Conza, Giusy, Vermeire, Ines, Schalley, Tessa, Planque, Mélanie, van Brussel, Thomas, Schepers, Rogier, Modave, Elodie, Karakach, Tobias K., Carmeliet, Peter, Lambrechts, Diether, Ho, Ping-Chih, and Fendt, Sarah-Maria

Abstract

T cells dynamically rewire their metabolism during an immune response. We applied single-cell RNA sequencing to CD8+T cells activated and differentiated in vitroin physiological medium to resolve these metabolic dynamics. We identify a differential time-dependent reliance of activating T cells on the synthesis versus uptake of various non-essential amino acids, which we corroborate with functional assays. We also identify metabolic genes that potentially dictate the outcome of T cell differentiation, by ranking them based on their expression dynamics. Among them, we find asparagine synthetase (Asns), whose expression peaks for effector T cells and decays toward memory formation. Disrupting these expression dynamics by ASNS overexpression promotes an effector phenotype, enhancing the anti-tumor response of adoptively transferred CD8+T cells in a mouse melanoma model. We thus provide a resource of dynamic expression changes during CD8+T cell activation and differentiation, and identify ASNS expression dynamics as a modulator of CD8+T cell differentiation.

Published
2022
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27. 13 C Tracer Analysis and Metabolomics in Dormant Cancer Cells.

Author

Altea-Manzano P, Fendt SM, and Vera-Ramirez L

Subjects
Humans, Cell Line, Tumor, Breast Neoplasms metabolism, Breast Neoplasms pathology, Cell Culture Techniques methods, Female, Tumor Microenvironment, Metabolome, Metabolomics methods, Carbon Isotopes
Abstract

Over the last two decades, major advances in the field of tumor dormancy have been made. Yet, it is not completely understood how dormant disseminated tumor cells survive and transition to a proliferative state to generate a metastatic lesion. On the other hand, metabolic rewiring has been shown to influence metastasis development through the modulation of both intracellular signaling and the crosstalk between metastatic cells and their microenvironment. Thus, studying the metabolic features of dormant disseminated tumor cells has gained importance in understanding the dormancy process. Here, we describe a method to perform metabolomics and 13 C tracer analysis in 3D cultures of dormant breast cancer cells., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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28. CD8 + T cell metabolic rewiring defined by scRNA-seq identifies a critical role of ASNS expression dynamics in T cell differentiation.

Author

Fernández-García J, Franco F, Parik S, Altea-Manzano P, Pane AA, Broekaert D, van Elsen J, Di Conza G, Vermeire I, Schalley T, Planque M, van Brussel T, Schepers R, Modave E, Karakach TK, Carmeliet P, Lambrechts D, Ho PC, and Fendt SM

Subjects
Mice, Animals, Single-Cell Analysis, Lymphocyte Activation, Cell Differentiation, Disease Models, Animal, CD8-Positive T-Lymphocytes, Melanoma metabolism
Abstract

T cells dynamically rewire their metabolism during an immune response. We applied single-cell RNA sequencing to CD8 + T cells activated and differentiated in vitro in physiological medium to resolve these metabolic dynamics. We identify a differential time-dependent reliance of activating T cells on the synthesis versus uptake of various non-essential amino acids, which we corroborate with functional assays. We also identify metabolic genes that potentially dictate the outcome of T cell differentiation, by ranking them based on their expression dynamics. Among them, we find asparagine synthetase (Asns), whose expression peaks for effector T cells and decays toward memory formation. Disrupting these expression dynamics by ASNS overexpression promotes an effector phenotype, enhancing the anti-tumor response of adoptively transferred CD8 + T cells in a mouse melanoma model. We thus provide a resource of dynamic expression changes during CD8 + T cell activation and differentiation, and identify ASNS expression dynamics as a modulator of CD8 + T cell differentiation., Competing Interests: Declaration of interests P.-C.H. is on the scientific advisory board for Elixiron Immunotherapeutics, Acepodia, and Novartis; has received funding from Elixiron Immunotherapeutics; and is the founder of Pilatus Biosciences. S.-M.F. has received funding from Bayer, Merck, Black Belt Therapeutics, and Alesta Therapeutics; has consulted for Fund+; and is on the scientific advisory board for Alesta Therapeutics and the editorial board of Cell Reports., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2022
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29. Analyzing the Metabolism of Metastases in Mice.

Author

Altea-Manzano P, Broekaert D, Duarte JAG, Fernández-García J, Planque M, and Fendt SM

Subjects
Animals, Carbon Isotopes metabolism, Cell Line, Tumor, Disease Models, Animal, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Rats, Rats, Sprague-Dawley, Metabolomics methods, Neoplasm Metastasis pathology, Neoplasms metabolism
Abstract

Metastasis formation is the leading cause of death in cancer patients. It has recently emerged that cancer cells adapt their metabolism to successfully transition through the metastatic cascade. Consequently, measuring and analyzing the in vivo metabolism of metastases has the potential to reveal novel treatment strategies to prevent metastasis formation. Here, we describe two different metastasis mouse models and how their metabolism can be analyzed with metabolomics and 13 C tracer analysis.

Published
2020
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