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272 results on '"Puisieux, Alain"'

1. A druggable copper-signalling pathway that drives inflammation

Author

Solier, Stéphanie, Müller, Sebastian, Cañeque, Tatiana, Versini, Antoine, Mansart, Arnaud, Sindikubwabo, Fabien, Baron, Leeroy, Emam, Laila, Gestraud, Pierre, Pantoș, G. Dan, Gandon, Vincent, Gaillet, Christine, Wu, Ting-Di, Dingli, Florent, Loew, Damarys, Baulande, Sylvain, Durand, Sylvère, Sencio, Valentin, Robil, Cyril, Trottein, François, Péricat, David, Näser, Emmanuelle, Cougoule, Céline, Meunier, Etienne, Bègue, Anne-Laure, Salmon, Hélène, Manel, Nicolas, Puisieux, Alain, Watson, Sarah, Dawson, Mark A., Servant, Nicolas, Kroemer, Guido, Annane, Djillali, and Rodriguez, Raphaël

Published
2023
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3. Guidelines and definitions for research on epithelial–mesenchymal transition

Author

Yang, Jing, Antin, Parker, Berx, Geert, Blanpain, Cédric, Brabletz, Thomas, Bronner, Marianne, Campbell, Kyra, Cano, Amparo, Casanova, Jordi, Christofori, Gerhard, Dedhar, Shoukat, Derynck, Rik, Ford, Heide L, Fuxe, Jonas, García de Herreros, Antonio, Goodall, Gregory J, Hadjantonakis, Anna-Katerina, Huang, Ruby YJ, Kalcheim, Chaya, Kalluri, Raghu, Kang, Yibin, Khew-Goodall, Yeesim, Levine, Herbert, Liu, Jinsong, Longmore, Gregory D, Mani, Sendurai A, Massagué, Joan, Mayor, Roberto, McClay, David, Mostov, Keith E, Newgreen, Donald F, Nieto, M Angela, Puisieux, Alain, Runyan, Raymond, Savagner, Pierre, Stanger, Ben, Stemmler, Marc P, Takahashi, Yoshiko, Takeichi, Masatoshi, Theveneau, Eric, Thiery, Jean Paul, Thompson, Erik W, Weinberg, Robert A, Williams, Elizabeth D, Xing, Jianhua, Zhou, Binhua P, and Sheng, Guojun

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Aetiology, 2.1 Biological and endogenous factors, Generic health relevance, Animals, Biomedical Research, Cell Movement, Cell Plasticity, Consensus, Developmental Biology, Epithelial-Mesenchymal Transition, Humans, Neoplasms, Terminology as Topic, EMT International Association, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organization from epithelial to mesenchymal phenotypes, which leads to functional changes in cell migration and invasion. EMT occurs in a diverse range of physiological and pathological conditions and is driven by a conserved set of inducing signals, transcriptional regulators and downstream effectors. With over 5,700 publications indexed by Web of Science in 2019 alone, research on EMT is expanding rapidly. This growing interest warrants the need for a consensus among researchers when referring to and undertaking research on EMT. This Consensus Statement, mediated by 'the EMT International Association' (TEMTIA), is the outcome of a 2-year-long discussion among EMT researchers and aims to both clarify the nomenclature and provide definitions and guidelines for EMT research in future publications. We trust that these guidelines will help to reduce misunderstanding and misinterpretation of research data generated in various experimental models and to promote cross-disciplinary collaboration to identify and address key open questions in this research field. While recognizing the importance of maintaining diversity in experimental approaches and conceptual frameworks, we emphasize that lasting contributions of EMT research to increasing our understanding of developmental processes and combatting cancer and other diseases depend on the adoption of a unified terminology to describe EMT.

Published
2020

4. Low level of Fibrillarin, a ribosome biogenesis factor, is a new independent marker of poor outcome in breast cancer

Author

Nguyen Van Long, Flora, Lardy-Cleaud, Audrey, Carène, Dimitri, Rossoni, Caroline, Catez, Frédéric, Rollet, Paul, Pion, Nathalie, Monchiet, Déborah, Dolbeau, Agathe, Martin, Marjorie, Simioni, Valentin, Bray, Susan, Le Beherec, Doris, Mosele, Fernanda, Bouakka, Ibrahim, Colombe-Vermorel, Amélie, Odeyer, Laetitia, Diot, Alexandra, Jordan, Lee B., Thompson, Alastair M., Jamen, Françoise, Dubois, Thierry, Chabaud, Sylvie, Michiels, Stefan, Treilleux, Isabelle, Bourdon, Jean-Christophe, Pérol, David, Puisieux, Alain, André, Fabrice, Diaz, Jean-Jacques, and Marcel, Virginie

Published
2022
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5. EU-LIFE charter of independent life science research institutes

Author

Superti-Furga, Giulio, Agostinho, Marta, Bury, Jo, Cook, Simon, Durinx, Christine, Ender, Anita, van Luenen, Henri, Lund, Anders H, Medema, René H, Miączyńska, Marta, Nickel, Dorthe, Pelicci, Pier Giuseppe, Puisieux, Alain, Ripatti, Samuli, Sander, Maike, Schubeler, Dirk, Serrano, Luis, Sommer, Thomas, Sonne-Hansen, Katrine, Tomančák, Pavel, Vives, Joan, Vontas, John, Bettencourt-Dias, Mónica, Superti-Furga, Giulio, Agostinho, Marta, Bury, Jo, Cook, Simon, Durinx, Christine, Ender, Anita, van Luenen, Henri, Lund, Anders H, Medema, René H, Miączyńska, Marta, Nickel, Dorthe, Pelicci, Pier Giuseppe, Puisieux, Alain, Ripatti, Samuli, Sander, Maike, Schubeler, Dirk, Serrano, Luis, Sommer, Thomas, Sonne-Hansen, Katrine, Tomančák, Pavel, Vives, Joan, Vontas, John, and Bettencourt-Dias, Mónica

Abstract

The diverse range of organizations contributing to the global research ecosystem is believed to enhance the overall quality and resilience of its output. Mid-sized autonomous research institutes, distinct from universities, play a crucial role in this landscape. They often lead the way in new research fields and experimental methods, including those in social and organizational domains, which are vital for driving innovation. The EU-LIFE alliance was established with the goal of fostering excellence by developing and disseminating best practices among European biomedical research institutes. As directors of the 15 EU-LIFE institutes, we have spent a decade comparing and refining our processes. Now, we are eager to share the insights we've gained. To this end, we have crafted this Charter, outlining 10 principles we deem essential for research institutes to flourish and achieve ground-breaking discoveries. These principles, detailed in the Charter, encompass excellence, independence, training, internationality and inclusivity, mission focus, technological advancement, administrative innovation, cooperation, societal impact, and public engagement. Our aim is to inspire the establishment of new institutes that adhere to these principles and to raise awareness about their significance. We are convinced that they should be viewed a crucial component of any national and international innovation strategies.

Published
2024

8. Cooperative pro-tumorigenic adaptation to oncogenic RAS through epithelial-to-mesenchymal plasticity

Author

De Blander, Hadrien, primary, Tonon, Laurie, additional, Fauvet, Frédérique, additional, Pommier, Roxane M., additional, Lamblot, Christelle, additional, Benhassoun, Rahma, additional, Angileri, Francesca, additional, Gibert, Benjamin, additional, Rodriguez, Raphaël, additional, Ouzounova, Maria, additional, Morel, Anne-Pierre, additional, and Puisieux, Alain, additional

Published
2024
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11. Dissecting the origin of heterogeneity in uterine and ovarian carcinosarcomas

Author

Sertier, Anne-Sophie, primary, Ferrari, Anthony, additional, Pommier, Roxane M., additional, Treilleux, Isabelle, additional, Boyault, Sandrine, additional, Devouassoux-Shisheboran, Mojgan, additional, Kielbassa, Janice, additional, Thomas, Emilie, additional, Tonon, Laurie, additional, Le Texier, Vincent, additional, Charreton, Amandine, additional, Morel, Anne-Pierre, additional, Floquet, Anne, additional, Joly, Florence, additional, Berton-Rigaud, Dominique, additional, Ferron, Gwenaël, additional, Arnould, Laurent, additional, Croce, Sabrina, additional, Bataillon, Guillaume, additional, Saintigny, Pierre, additional, Mery-Lamarche, Eliane, additional, Sagan, Christine, additional, Senaratne, Aruni P., additional, Gut, Ivo G., additional, Calvo, Fabien, additional, Viari, Alain, additional, Ouzounova, Maria, additional, Ray-Coquard, Isabelle, additional, and Puisieux, Alain, additional

Published
2023
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14. In Vivo Characterization of the Toxicological Properties of DPhP, One of the Main Degradation Products of Aryl Phosphate Esters

Author

Selmi-Ruby, Samia, Marin-Saez, Jesus, Fildier, Aurelie, Bulete, Audrey, Abdallah, Myriam, Garcia, Jessica, Deverchere, Julie, Spinner, Loic, Giroud, Barbara, Ibanez, Sebastien, Granjon, Thierry, Bardel, Claire, Puisieux, Alain, Fervers, Beatrice, Vulliet, Emmanuelle, Payen, Lea, and Vigneron, Arnaud M.

Subjects
Medical research, Medicine, Experimental, Toxicological chemistry -- Research, Plasticizers -- Chemical properties -- Health aspects, Phosphates -- Health aspects -- Chemical properties, Aromatic amines -- Chemical properties, Environmental issues, Health
Abstract

Background: Aryl phosphate esters (APEs) are widely used and commonly present in the environment. Health hazards associated with these compounds remain largely unknown and the effects of diphenyl phosphate (DPhP), one of their most frequent derivatives, are poorly characterized. Objective: Our aim was to investigate whether DPhP per se may represent a more relevant marker of exposure to APEs than direct assessment of their concentration and determine its potential deleterious biological effects in chronically exposed mice. Methods: Conventional animals (FVB mice) were acutely or chronically exposed to relevant doses of DPhP or to triphenyl phosphate (TPhP), one of its main precursors. Both molecules were measured in blood and other tissues by liquid chromatography-mass spectrometry (LC-MS). Effects of chronic DPhP exposure were addressed through liver multi-omics analysis to determine the corresponding metabolic profile. Deep statistical exploration was performed to extract correlated information, guiding further physiological analyses. Results: Multi-omics analysis confirmed the existence of biological effects of DPhP, even at a very low dose of 0.1mg/mL in drinking water. Chemical structural homology and pathway mapping demonstrated a clear reduction of the fatty acid catabolic processes centered on acylcarnitine and mitochondrial [beta]-oxidation in mice exposed to DPhP in comparison with those treated with vehicle. An interesting finding was that in mice exposed to DPhP, mRNA, expression of genes involved in lipid catabolic processes and regulated by peroxisome proliferator-activated receptor alpha (PPAR[alpha]) was lower than that in vehicle-treated mice. Immunohistochemistry analysis showed a specific down- regulation of HMGCS2, a kernel target gene of PPAR[alpha]. Overall, DPhP absorption disrupted body weight-gain processes. Conclusions: Our results suggest that in mice, the effects of chronic exposure to DPhP, even at a low dose, are not negligible. Fatty acid metabolism in the liver is essential for controlling fast and feast periods, with adverse consequences on the overall physiology. Therefore, the impact of DPhP on circulating fat, cardiovascular pathologies and metabolic disease incidence deserves, in light of our results, further investigations. https://doi.org/10.1289/EHP6826, Introduction Diphenyl phosphate (DPhP) has been used as a main biomarker for assessing exposure to aryl phosphate esters (APEs), especially triphenyl phosphate (TPhP), a molecule suspected of presenting human health [...]

Published
2020
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15. ZEB1‐mediated melanoma cell plasticity enhances resistance to MAPK inhibitors

Author

Richard, Geoffrey, Dalle, Stéphane, Monet, Marie‐Ambre, Ligier, Maud, Boespflug, Amélie, Pommier, Roxane M, de la Fouchardière, Arnaud, Perier‐Muzet, Marie, Depaepe, Lauriane, Barnault, Romain, Tondeur, Garance, Ansieau, Stéphane, Thomas, Emilie, Bertolotto, Corine, Ballotti, Robert, Mourah, Samia, Battistella, Maxime, Lebbé, Céleste, Thomas, Luc, Puisieux, Alain, and Caramel, Julie

Published
2016
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18. ZEB1 transcription factor promotes immune escape in melanoma

Author

Plaschka, Maud, primary, Benboubker, Valentin, additional, Grimont, Maxime, additional, Berthet, Justine, additional, Tonon, Laurie, additional, Lopez, Jonathan, additional, Le-Bouar, Myrtille, additional, Balme, Brigitte, additional, Tondeur, Garance, additional, de la Fouchardière, Arnaud, additional, Larue, Lionel, additional, Puisieux, Alain, additional, Grinberg-Bleyer, Yenkel, additional, Bendriss-Vermare, Nathalie, additional, Dubois, Bertrand, additional, Caux, Christophe, additional, Dalle, Stéphane, additional, and Caramel, Julie, additional

Published
2022
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24. Author Correction: Guidelines and definitions for research on epithelial–mesenchymal transition (Nature Reviews Molecular Cell Biology, (2020), 21, 6, (341-352), 10.1038/s41580-020-0237-9)

Author

Yang, Jing, Antin, Parker, Berx, Geert, Blanpain, Cédric, Brabletz, Thomas, Bronner, Marianne, Campbell, Kyra, Cano, Amparo, Casanova, Jordi, Christofori, Gerhard, Dedhar, Shoukat, Derynck, Rik, Ford, Heide L., Fuxe, Jonas, García de Herreros, Antonio, Goodall, Gregory J., Hadjantonakis, Anna Katerina, Huang, Ruby Y.J., Kalcheim, Chaya, Kalluri, Raghu, Kang, Yibin, Khew-Goodall, Yeesim, Levine, Herbert, Liu, Jinsong, Longmore, Gregory D., Mani, Sendurai A., Massagué, Joan, Mayor, Roberto, McClay, David, Mostov, Keith E., Newgreen, Donald F., Nieto, M. Angela, Puisieux, Alain, Runyan, Raymond, Savagner, Pierre, Stanger, Ben, Stemmler, Marc P., Takahashi, Yoshiko, Takeichi, Masatoshi, Theveneau, Eric, Thiery, Jean Paul, Thompson, Erik W., Weinberg, Robert A., Williams, Elizabeth D., Xing, Jianhua, Zhou, Binhua P., Sheng, Guojun, other, and, Yang, Jing, Antin, Parker, Berx, Geert, Blanpain, Cédric, Brabletz, Thomas, Bronner, Marianne, Campbell, Kyra, Cano, Amparo, Casanova, Jordi, Christofori, Gerhard, Dedhar, Shoukat, Derynck, Rik, Ford, Heide L., Fuxe, Jonas, García de Herreros, Antonio, Goodall, Gregory J., Hadjantonakis, Anna Katerina, Huang, Ruby Y.J., Kalcheim, Chaya, Kalluri, Raghu, Kang, Yibin, Khew-Goodall, Yeesim, Levine, Herbert, Liu, Jinsong, Longmore, Gregory D., Mani, Sendurai A., Massagué, Joan, Mayor, Roberto, McClay, David, Mostov, Keith E., Newgreen, Donald F., Nieto, M. Angela, Puisieux, Alain, Runyan, Raymond, Savagner, Pierre, Stanger, Ben, Stemmler, Marc P., Takahashi, Yoshiko, Takeichi, Masatoshi, Theveneau, Eric, Thiery, Jean Paul, Thompson, Erik W., Weinberg, Robert A., Williams, Elizabeth D., Xing, Jianhua, Zhou, Binhua P., Sheng, Guojun, and other, and

Abstract

In the supplementary information, the reference to Contreras et al. 2016 was removed (as it relates to a gene different from E2-2/TCF4), and ‘(TCF7L2)’ was deleted from the table. Misspellings in the author name Ruby Y. J. Huang and in the PyMT glossary definition were also corrected. These changes have been made to the HTML and PDF versions of the article.

Published
2021

27. Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma

Author

Janoueix-Lerosey, Isabelle, Lequin, Delphine, Brugieres, Laurence, Ribeiro, Agnes, de Pontual, Loic, Combaret, Valerie, Raynal, Virginie, Puisieux, Alain, Schleiermacher, Gudrun, Pierron, Gaelle, Valteau-Couanet, Dominique, Frebourg, Thierry, Michon, Jean, Lyonnet, Stanislas, Amiel, Jeanne, and Delattre, Olivier

Subjects
Gene mutations -- Identification and classification -- Research -- Genetic aspects, Phosphotransferases -- Research -- Genetic aspects, Neuroblastoma -- Genetic aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation, Identification and classification, Research, Genetic aspects
Abstract

Neuroblastoma, a tumour derived from the peripheral sympathetic nervous system, is one of the most frequent solid tumours in childhood (1,2). It usually occurs sporadically but familial cases are observed, [...]

Published
2008

28. Ribosomal RNA 2′O-methylation as a novel layer of inter-tumour heterogeneity in breast cancer

Author

Marcel, Virginie, Kielbassa, Janice, Marchand, Virginie, Natchiar, Kundhavai S, Paraqindes, Hermes, Nguyen Van Long, Flora, Ayadi, Lilia, Bourguignon-Igel, Valérie, Lo Monaco, Piero, Monchiet, Déborah, Scott, Véronique, Tonon, Laurie, Bray, Susan E, Diot, Alexandra, Jordan, Lee B, Thompson, Alastair M, Bourdon, Jean-Christophe, Dubois, Thierry, André, Fabrice, Catez, Frédéric, Puisieux, Alain, Motorin, Yuri, Klaholz, Bruno P, Viari, Alain, Diaz, Jean-Jacques, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Synergie Lyon Cancer-Platform of Bioinformatics-Gilles Thomas, Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Ingénierie, Biologie et Santé en Lorraine (IBSLor), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Ingénierie Moléculaire et Physiopathologie Articulaire (IMoPA), Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Prédicteurs moléculaires et nouvelles cibles en oncologie (PMNCO), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Ninewells Hospital and Medical School [Dundee], Baylor College of Medicine (BCM), Baylor University, Institut Curie [Paris], Inria Grenoble - Rhône-Alpes, Institut National de Recherche en Informatique et en Automatique (Inria), Klaholz, Bruno, Université de Lorraine (UL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and ANR-17-CE11-0002,HumanRibosome,Structure et fonction de complexes du ribosome humain(2017)

Subjects
AcademicSubjects/SCI01140, 0303 health sciences, AcademicSubjects/SCI01060, [SDV]Life Sciences [q-bio], AcademicSubjects/SCI00030, Standard Article, AcademicSubjects/SCI01180, 3. Good health, [SDV] Life Sciences [q-bio], 03 medical and health sciences, 0302 clinical medicine, 030220 oncology & carcinogenesis, AcademicSubjects/SCI00980, Corrigendum, 030304 developmental biology
Abstract

International audience; Recent epitranscriptomics studies unravelled that ribosomal RNA (rRNA) 2′O-methylation is an additional layer of gene expression regulation highlighting the ribosome as a novel actor of translation control. However, this major finding lies on evidences coming mainly, if not exclusively, from cellular models. Using the innovative next-generation RiboMeth-seq technology, we established the first rRNA 2′O-methylation landscape in 195 primary human breast tumours. We uncovered the existence of compulsory/stable sites, which show limited inter-patient variability in their 2′O-methylation level, which map on functionally important sites of the human ribosome structure and which are surrounded by variable sites found from the second nucleotide layers. Our data demonstrate that some positions within the rRNA molecules can tolerate absence of 2′O-methylation in tumoral and healthy tissues. We also reveal that rRNA 2′O-methylation exhibits intra- and inter-patient variability in breast tumours. Its level is indeed differentially associated with breast cancer subtype and tumour grade. Altogether, our rRNA 2′O-methylation profiling of a large-scale human sample collection provides the first compelling evidence that ribosome variability occurs in humans and suggests that rRNA 2′O-methylation might represent a relevant element of tumour biology useful in clinic. This novel variability at molecular level offers an additional layer to capture the cancer heterogeneity and associates with specific features of tumour biology thus offering a novel targetable molecular signature in cancer.

Published
2020
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29. Zeb1 expression by tumor or stromal cells is associated with spatial distribution patterns of CD8+ tumor-infiltrating lymphocytes: a hypothesis-generating study on 113 triple negative breast cancers

Author

Ouled Dhaou, Mona, kossai, Myriam, Morel, Anne-Pierre, Devouassoux-Shisheboran, Mojgan, Puisieux, Alain, Penault-Llorca, Frédérique, Radosevic-Robin, Nina, Imagerie Moléculaire et Stratégies Théranostiques (IMoST), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020]), Centre Jean Perrin [Clermont-Ferrand] (UNICANCER/CJP), UNICANCER, Département cancer environnement (Centre Léon Bérard - Lyon), Centre Léon Bérard [Lyon], Service d'Anatomo-Pathologie [Hôpital de la Croix-Rousse - HCL], Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Institut Curie [Paris], and COLO, Mouniati

Subjects
[SDV] Life Sciences [q-bio], lymphocytes, spatial, triple negative breast cancer, [SDV]Life Sciences [q-bio], chemical and pharmacologic phenomena, Original Article, immunotherapy, Zeb1
Abstract

International audience; Spatial organization of tumor microenvironment (TME) may influence tumor response to immunomodulatory therapies. Zeb1 is a driver of epithelial-mesenchymal transition, with several roles in immune cell development, however its role in shaping of the immune TME is not fully explored. We conducted a pre-multiplex spatial analysis study to verify whether Zeb1 influences spatial distribution of tumor-infiltrating lymphocytes (TILs) in triple negative breast cancer (TNBC). We applied single and double immunohistochemistry to analyze spatial relationships between CD8+, FoxP3+ and CD20+ tumor-infiltrating lymphocytes (TILs) and the cells expressing Zeb1 in formalin-fixed, paraffin-embedded surgical specimens of 113 TNBCs. 15.5% of cases had Zeb1+ tumor cells and 72.8% of cases had stroma rich in Zeb1+ cells. Low density of intratumoral CD8+ TILs was observed in almost all TNBCs with high or moderate Zeb1+ expression in tumor cells (22/23 cases, 95.6%), and in 90.4% of TNBCs (75/83 cases) with stroma rich in Zeb1+ cells. On the other side, a majority of TNBCs with stroma rich in Zeb1+ cells had high density of stromal CD8+ TILs (55/83 cases, 66.3%). These associations were not observed between Zeb1-expressing cells and FoxP3+ or CD20+ TILs. This in situ analysis showed specific spatial relationship between tumor or stromal Zeb1+ cells and CD8+ TILs, which need to be validated in other cohorts. Zeb1 was highlighted both as a marker of tumor cell EMT and of tumor stroma richness in mesenchymal cells. Several hypotheses about causes of the observed relationship between Zeb1 and TILs are generated and the approaches to verify them discussed. Zeb1 is worth further investigation as a potential biomarker of intratumor immunosuppression of TNBC and of its response to immunotherapies.

Published
2020

30. Ribosomal RNA 2′ O-methylation as a novel layer of inter-tumour heterogeneity in breast cancer

Author

Marcel, Virginie, primary, Kielbassa, Janice, additional, Marchand, Virginie, additional, Natchiar, Kundhavai S, additional, Paraqindes, Hermes, additional, Van Long, Flora Nguyen, additional, Ayadi, Lilia, additional, Bourguignon-Igel, Valérie, additional, Monaco, Piero Lo, additional, Monchiet, Déborah, additional, Scott, Véronique, additional, Tonon, Laurie, additional, Bray, Susan E, additional, Diot, Alexandra, additional, Jordan, Lee B, additional, Thompson, Alastair M, additional, Bourdon, Jean-Christophe, additional, Dubois, Thierry, additional, André, Fabrice, additional, Catez, Frédéric, additional, Puisieux, Alain, additional, Motorin, Yuri, additional, Klaholz, Bruno P, additional, Viari, Alain, additional, and Diaz, Jean-Jacques, additional

Published
2021
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37. EMT Transcription Factor ZEB1 Represses the Mutagenic POLθ-Mediated End-Joining Pathway in Breast Cancers

Author

Prodhomme, Mélanie K., primary, Pommier, Roxane M., additional, Franchet, Camille, additional, Fauvet, Frédérique, additional, Bergoglio, Valérie, additional, Brousset, Pierre, additional, Morel, Anne-Pierre, additional, Brunac, Anne-Cécile, additional, Devouassoux-Shisheboran, Mojgan, additional, Petrilli, Virginie, additional, Moyret-Lalle, Caroline, additional, Hoffmann, Jean-Sébastien, additional, Puisieux, Alain, additional, and Tissier, Agnès, additional

Published
2020
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40. Publisher Correction: LifeTime and improving European healthcare through cell-based interceptive medicine

Author

Rajewsky, Nikolaus, Almouzni, Geneviève, Clevers, Hans, Heutink, Peter, Heymans, Stephane R B, Heyn, Holger, Huch, Meritxell, Huitinga, Inge, Jackowiak, Paulina, Jongsma, Karin R, Journot, Laurent, Junker, Jan Philipp, Katz, Shauna, De Strooper, Bart, Kehren, Jeanne, Kempa, Stefan, Kirchhof, Paulus, Klein, Christine, Koralewska, Natalia, Korbel, Jan O, Kühnemund, Malte, Lamond, Angus I, Lauwers, Elsa, Le Ber, Isabelle, Eggert, Angelika, Leinonen, Ville, López-Tobón, Alejandro, Lundberg, Emma, Lunkes, Astrid, Maatz, Henrike, Mann, Matthias, Marelli, Luca, Matser, Vera, Matthews, Paul M, Mechta-Grigoriou, Fatima, Ellenberg, Jan, Menon, Radhika, Nielsen, Anne F, Pagani, Massimiliano, Pasterkamp, R Jeroen, Pitkänen, Asla, Popescu, Valentin, Pottier, Cyril, Puisieux, Alain, Rademakers, Rosa, Reiling, Dory, Fernández, Xosé M, Reiner, Orly, Remondini, Daniel, Ritchie, Craig, Rohrer, Jonathan D, Saliba, Antoine-Emmanuel, Sanchez-Valle, Raquel, Santosuosso, Amedeo, Sauter, Arnold, Scheltema, Richard A, Scheltens, Philip, Figlerowicz, Marek, Schiller, Herbert B, Schneider, Anja, Seibler, Philip, Sheehan-Rooney, Kelly, Shields, David J, Sleegers, Kristel, Smit, August B, Smith, Kenneth G C, Smolders, Ilse, Synofzik, Matthis, Gasser, Susan M, Tam, Wai Long, Teichmann, Sarah A, Thom, Maria, Turco, Margherita Y, van Beusekom, Heleen M M, Vandenberghe, Rik, Van den Hoecke, Silvie, van de Poel, Ibo, van der Ven, Andre, van der Zee, Julie, Hubner, Norbert, van Lunzen, Jan, van Minnebruggen, Geert, van Oudenaarden, Alexander, Van Paesschen, Wim, van Swieten, John C, van Vught, Remko, Verhage, Matthijs, Verstreken, Patrik, Villa, Carlo Emanuele, Vogel, Jörg, Kjems, Jørgen, von Kalle, Christof, Walter, Jörn, Weckhuysen, Sarah, Weichert, Wilko, Wood, Louisa, Ziegler, Anette-Gabriele, Zipp, Frauke, Knoblich, Jürgen A, Gorski, Stanislaw A, Krabbe, Grietje, Lichter, Peter, Linnarsson, Sten, Marine, Jean-Christophe, Marioni, John C, Marti-Renom, Marc A, Netea, Mihai G, Nickel, Dörthe, Nollmann, Marcelo, Novak, Halina R, Aerts, Stein, Parkinson, Helen, Piccolo, Stefano, Pinheiro, Inês, Pombo, Ana, Popp, Christian, Reik, Wolf, Roman-Roman, Sergio, Rosenstiel, Philip, Schultze, Joachim L, Stegle, Oliver, Amit, Ido, Tanay, Amos, Testa, Giuseppe, Thanos, Dimitris, Theis, Fabian J, Torres-Padilla, Maria-Elena, Valencia, Alfonso, Vallot, Céline, Vidal, Marie, Voet, Thierry, Bertero, Michela G, Groups, LifeTime Community Working, Alberi, Lavinia, Alexander, Stephanie, Alexandrov, Theodore, Arenas, Ernest, Bagni, Claudia, Balderas, Robert, Bandelli, Andrea, Becher, Burkhard, Becker, Matthias, Bock, Christoph, Beerenwinkel, Niko, Benkirane, Monsef, Beyer, Marc, Bickmore, Wendy A, Biessen, Erik E A L, Blomberg, Niklas, Blumcke, Ingmar, Bodenmiller, Bernd, Borroni, Barbara, Boumpas, Dimitrios T, Bredenoord, Annelien L, Bourgeron, Thomas, Bowers, Sarion, Braeken, Dries, Brooksbank, Catherine, Brose, Nils, Bruining, Hilgo, Bury, Jo, Caporale, Nicolo, Cattoretti, Giorgio, Chabane, Nadia, Cavalli, Giacomo, Chneiweiss, Hervé, Cook, Stuart A, Curatolo, Paolo, de Jonge, Marien I, Deplancke, Bart, de Witte, Peter, Dimmeler, Stefanie, Draganski, Bogdan, Drews, Anna, Chiocca, Susanna, Dumbrava, Costica, Engelhardt, Stefan, Gasser, Thomas, Giamarellos-Bourboulis, Evangelos J, Graff, Caroline, Grün, Dominic, Gut, Ivo G, Hansson, Oskar, Henshall, David C, and Herland, Anna

Subjects
Male, medicine.medical_specialty, Legislation, Medical, Cell- and Tissue-Based Therapy, MEDLINE, Diseases, Artificial Intelligence, Health care, Pathology, medicine, Humans, Medical physics, Multidisciplinary, Education, Medical, business.industry, Published Erratum, Publisher Correction, Europe, Early Diagnosis, Health, Medicine, Female, ddc:500, Single-Cell Analysis, Systems biology, business, Delivery of Health Care, Biomarkers, Cell based
Abstract

Here we describe the LifeTime Initiative, which aims to track, understand and target human cells during the onset and progression of complex diseases, and to analyse their response to therapy at single-cell resolution. This mission will be implemented through the development, integration and application of single-cell multi-omics and imaging, artificial intelligence and patient-derived experimental disease models during the progression from health to disease. The analysis of large molecular and clinical datasets will identify molecular mechanisms, create predictive computational models of disease progression, and reveal new drug targets and therapies. The timely detection and interception of disease embedded in an ethical and patient-centred vision will be achieved through interactions across academia, hospitals, patient associations, health data management systems and industry. The application of this strategy to key medical challenges in cancer, neurological and neuropsychiatric disorders, and infectious, chronic inflammatory and cardiovascular diseases at the single-cell level will usher in cell-based interceptive medicine in Europe over the next decade.

Published
2021
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42. Integrated analysis highlights APC11 protein expression as a likely new independent predictive marker for colorectal cancer

Author

Drouet, Youenn, Treilleux, Isabelle, Viari, Alain, Léon, Sophie, Devouassoux-Shisheboran, Mojgan, Voirin, Nicolas, de la Fouchardiere, Christelle, Manship, Brigitte, Puisieux, Alain, Lasset, Christine, Moyret-Lalle, Caroline, Biostatistiques santé, Département biostatistiques et modélisation pour la santé et l'environnement [LBBE], Laboratoire de Biométrie et Biologie Evolutive - UMR 5558 (LBBE), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS)-Laboratoire de Biométrie et Biologie Evolutive - UMR 5558 (LBBE), Université de Lyon-Université de Lyon-Institut National de Recherche en Informatique et en Automatique (Inria)-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Centre National de la Recherche Scientifique (CNRS), Centre Léon Bérard, Lyon, France, parent, Equipe de recherche européenne en algorithmique et biologie formelle et expérimentale (ERABLE), Inria Grenoble - Rhône-Alpes, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria), Baobab, Département PEGASE [LBBE] (PEGASE), Hôpital de la Croix-Rousse [CHU - HCL], Hospices Civils de Lyon (HCL), Université de Lyon, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Sagot, Marie-France

Subjects
Adult, Aged, 80 and over, Male, Science, [SDV]Life Sciences [q-bio], Middle Aged, Prognosis, digestive system diseases, Article, Disease-Free Survival, [SDV] Life Sciences [q-bio], Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Chromosomal Instability, Biomarkers, Tumor, Medicine, Humans, Female, Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome, Neoplasm Metastasis, Colorectal Neoplasms, Aged
Abstract

International audience; After a diagnosis of colorectal cancer (CRC), approximately 50% of patients will present distant metastasis. Although significant progress has been made in treatments, most of them will die from the disease. We investigated the predictive and prognostic potential of APC11, the catalytic subunit of APC/C, which has never been examined in the context of CRC. The expression of APC11 was assessed in CRC cell lines, in tissue microarrays (TMAs) and in public datasets. Overexpression of APC11 mRNA was associated with chromosomal instability, lymphovascular invasion and residual tumor. Regression models accounting for the effects of well-known protein markers highlighted association of APC11 protein expression with residual tumor (odds ratio: OR = 6.51; 95% confidence intervals: CI = 1.54-27.59; P = 0.012) and metastasis at diagnosis (OR = 3.87; 95% CI = 1.20-2.45; P = 0.024). Overexpression of APC11 protein was also associated with worse distant relapse-free survival (hazard ratio: HR = 2.60; 95% CI = 1.26-5.37; P = 0.01) and worse overall survival (HR = 2.69; 95% CI = 1.31-5.51; P = 0.007). APC11 overexpression in primary CRC thus represents a potentially novel theranostic marker of metastatic CRC. Colorectal cancer (CRC) is the third most frequent cancer and the fourth cause of cancer-related mortality worldwide 1. Patient survival is highly dependent on the stage of CRC at the time of diagnosis but approximately 50% of the patients will be concerned by distant metastasis development, either present at diagnosis (20%) or occurring after the curative-intent surgery of the primary tumor. The most frequent sites affected by metastatic CRC (mCRC) are the liver and lung 1. The current first-line standard-of-care for mCRC relies on the combination of cytotoxic chemotherapy (5FU/FA, oxaliplatin, irinotecan) and biologic agents (anti VEGF(R) or anti-EGFR mon-oclonal antibodies) guided by the molecular profile of the tumor. Surgery or local tumor ablation may also play a role in the treatment of mCRC patients, especially those with oligometastatic disease. Several biomarkers, mostly predictive, are routinely used for mCRC 2,3. Activating RAS mutations (KRAS and NRAS), present in nearly 50% of mCRC cases, are negative predictive markers of anti-EGFR inhibitor efficacy (cetuximab, panitumumab) and RAS testing is now mandatory in all mCRC patients, from the first-line meta-static setting. V600E-BRAF mutation is a significant negative poor-prognostic marker for patients with mCRC and may be a negative predictive factor for anti-EGFR therapies.

Published
2018
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45. Upstream ORF affects MYCN translation depending on exon 1b alternative splicing

Author

Tutrone Giovani, Bertrand Christophe, Furhman Lydie, Delloye-Bourgeois Céline, Locher Clara, Valsesia-Wittmann Sandrine, Besançon Roger, Jallas Anne-Catherine, Garin Elisabeth, and Puisieux Alain

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The MYCN gene is transcribed into two major mRNAs: one full-length (MYCN) and one exon 1b-spliced (MYCNΔ1b) mRNA. But nothing is known about their respective ability to translate the MYCN protein. Methods Plasmids were prepared to enable translation from the upstream (uORF) and major ORF of the two MYCN transcripts. Translation was studied after transfection in neuroblastoma SH-EP cell line. Impact of the upstream AUG on translation was evaluated after directed mutagenesis. Functional study with the two MYCN mRNAs was conducted by a cell viability assay. Existence of a new protein encoded by the MYCNΔ1b uORF was explored by designing a rabbit polyclonal antibody against a specific epitope of this protein. Results Both are translated, but higher levels of protein were seen with MYCNΔ1b mRNA. An upstream ORF was shown to have positive cis-regulatory activity on translation from MYCN but not from MYCNΔ1b mRNA. In transfected SH-EP neuroblastoma cells, high MYCN dosage obtained with MYCNΔ1b mRNA translation induces an antiapoptotic effect after serum deprivation that was not observed with low MYCN expression obtained with MYCN mRNA. Here, we showed that MYCNOT: MYCN Overlap Transcript, a new protein of unknown function is translated from the upstream AUG of MYCNΔ1b mRNA. Conclusions Existence of upstream ORF in MYCN transcripts leads to a new level of MYCN regulation. The resulting MYCN dosage has a weak but significant anti-apoptotic activity after intrinsic apoptosis induction.

Published
2009
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46. Effect of bortezomib on human neuroblastoma: analysis of molecular mechanisms involved in cytotoxicity

Author

Rousseau Raphaël, Brejon Stéphanie, Iacono Isabelle, Boyault Sandrine, Combaret Valérie, and Puisieux Alain

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Bortezomib, a specific and selective inhibitor of the 26S proteasome with antitumor activity against a wide range of malignancies, has been approved for the treatment of relapsed or refractory multiple myeloma and other cancers. Recently, bortezomib has been identified as an effective inhibitor of neuroblastoma cell growth and angiogenesis. Results In the present study, we demonstrate that some neuroblastoma cell lines are actually resistant to bortezomib. We have sought to characterize the main pathway by which proteasome inhibition leads to apoptosis, and to define the mechanism responsible for resistance to bortezomib in neuroblastoma cells. Our results show that SB202190, an inhibitor of mitogen-activated protein kinase (MAPK) p38, enhances the ability of bortezomib to induce apoptosis by preventing the phosphorylation of the heat shock protein (HSP) 27. Conclusion This study opens the way to further clinical investigations and suggests a potential benefit of using a combination of bortezomib with an inhibitor of p38 MAPK for the treatment of neuroblastoma relapse.

Published
2008
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47. Prognostic significance of urokinase plasminogen activator and plasminogen activator inhibitor-1 mRNA expression in lymph node- and hormone receptor-positive breast cancer

Author

Krause Alexander, Paye Malick, Bachelot Thomas, Verjat Thibault, Leissner Philippe, Puisieux Alain, and Mougin Bruno

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background One of the most thoroughly studied systems in relation to its prognostic relevance in patients with breast cancer, is the plasminogen activation system that comprises of, among others, the urokinase Plasminogen Activator (uPA) and its main inhibitor, the Plasminogen Activator Inhibitor-1 (PAI-1). In this study, we investigated the prognostic value of uPA and PAI-1 at the mRNA level in lymph node- and hormone receptor-positive breast cancer. Methods The study included a retrospective series of 87 patients with hormone-receptor positive and axillary lymph node-positive breast cancer. All patients received radiotherapy, adjuvant anthracycline-based chemotherapy and five years of tamoxifen treatment. The median patient age was 54 and the median follow-up time was 79 months. Distant relapse occurred in 30 patients and 22 patients died from breast cancer during follow-up. We investigated the prognostic value of uPA and PAI-1 at the mRNA level as measured by real-time quantitative RT-PCR. Results uPA and PAI-1 gene expression was not found to be correlated with any of the established clinical and pathological factors. Metastasis-free Survival (MFS) and Breast Cancer specific Survival (BCS) were significantly shorter in patients expressing high levels of PAI-1 mRNA (p < 0.0001; p < 0.0001; respectively). In Cox multivariate analysis, the level of PAI-1 mRNA appeared to be the strongest prognostic factor for MFS (Hazard Ratio (HR) = 10.12; p = 0.0002) and for BCS (HR = 13.17; p = 0.0003). Furthermore, uPA gene expression was not significantly associated neither with MFS (p = 0.41) nor with BCS (p = 0.19). In a Cox-multivariate regression analysis, uPA expression did not demonstrate significant independent prognostic value. Conclusion These findings indicate that high PAI-1 mRNA expression represents a strong and independent unfavorable prognostic factor for the development of metastases and for breast cancer specific survival in a population of hormone receptor- and lymph node-positive breast cancer patients.

Published
2006
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48. Additional file 2: Table S2. of A 13-gene expression-based radioresistance score highlights the heterogeneity in the response to radiation therapy across HPV-negative HNSCC molecular subtypes

Author

Jean-Philippe Foy, Bazire, Louis, Ortiz-Cuaran, Sandra, Deneuve, Sophie, Kielbassa, Janice, Thomas, Emilie, Viari, Alain, Puisieux, Alain, Goudot, Patrick, ChloĂŠ Bertolus, Foray, Nicolas, Kirova, Youlia, Verrelle, Pierre, and Saintigny, Pierre

Subjects
stomatognathic diseases
Abstract

Clinical and pathological parameters of the cohort from TCGA for selection of genes associated with disease-free survival. This cohort includes 128 patients suffering from human papillomavirus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) and who were treated by surgery and adjuvant radiotherapy. (DOCX 16 kb)

Published
2017
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49. Additional file 7: Figure S3. of A 13-gene expression-based radioresistance score highlights the heterogeneity in the response to radiation therapy across HPV-negative HNSCC molecular subtypes

Author

Jean-Philippe Foy, Bazire, Louis, Ortiz-Cuaran, Sandra, Deneuve, Sophie, Kielbassa, Janice, Thomas, Emilie, Viari, Alain, Puisieux, Alain, Goudot, Patrick, ChloĂŠ Bertolus, Foray, Nicolas, Kirova, Youlia, Verrelle, Pierre, and Saintigny, Pierre

Abstract

RadR score and in vitro sensitivity to Elesclomol, TW37, Cisplatine andPLX4720 in >700 cancer cell lines from the Genomics of Drug Sensitivity in Cancer database. TheRadR score was compared between sensitive and resistant cell lines to Cisplatin, TW47, PLX4720 andelesclomol. Number of tested samples is shown for each drug. (PPTX 494 kb)

Published
2017
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50. Additional file 1: Figure S1. of Destabilization of the TWIST1/E12 complex dimerization following the R154P point-mutation of TWIST1: an in silico approach

Author

Bouard, Charlotte, Terreux, Raphael, Tissier, Agnès, Jacqueroud, Laurent, Vigneron, Arnaud, Ansieau, Stéphane, Puisieux, Alain, and Payen, Léa

Abstract

Consequence of impaired TWIST1/E12 (TE) dimerization on DNA binding. a-c: Dictionary of secondary structure of proteins (DSSP) parameters were calculated for the TE and TE R154P models, to obtain information on secondary structure and solvent accessibility of TWIST1 and E12 residues. (a) Bar chart presenting the variation in solvent accessibility of TWIST1 residues. (b) 3D representation of the conserved TWIST1 (grey ribbon)/E12 (green ribbon) complex displaying residue 154 represented in cartoon and residues impacted by DSSP calculations represented in CPK. (c) Bar chart presenting the variation in solvent accessibility of E12 residues. (PDF 196 kb)

Published
2017
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