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48 results on '"Draskovic, Irena"'

1. An Online Health Community for Aneurysmal Subarachnoid Hemorrhage Patients: A Pilot Study

Author

Boogaarts, Hieronymus, van Nuenen-Platvoet, Willemijn, van den Abbeele, Leonie, Petersen, Harriette, Draskovic, Irena, de Vries, Joost, Westert, Gert, Grotenhuis, J Andre, and Bartels, Ronald

Subjects
Medicine, Computer applications to medicine. Medical informatics, R858-859.7
Abstract

BackgroundAneurysmal subarachnoid hemorrhage (aSAH) is a condition affecting relatively young patients and has high rates of morbidity and mortality. Online health communities have emerged to fill the void for patient advocacy and information, allowing individuals with shared experiences and chronic disorders to connect. ObjectiveWe have developed an online health community for aSAH patients, and this pilot study was conducted to evaluate it from a patient’s perspective. MethodsWe implemented an online, members-only, health community (MijnSAB, translation: MySAH) in addition to the usual aSAH care at Radboudumc, Nijmegen, the Netherlands. A questionnaire that was sent to consecutive aSAH patients was used to evaluate the usability and utility of MySAH. Answers were provided using a 5-point Likert scale. There was also one open-ended question asking about what was missing from the MySAH tool. ResultsIn total, 66 consecutive patients with aneurysmal subarachnoid hemorrhage were informed about the online health community. Of 64 potential MySAH users, 26 patients gained access to MySAH, 20 of whom were willing to participate in the evaluation. Those who used the community were younger (P=.03) and in a better condition at discharge (P=.03). The patients were positive about MySAH’s contribution to the quality of their care, but not to their quality of life. Most patients (18/20, 90%) reported that they would recommend the community to others in their position. Open suggestions on how to improve the tool included more frequent blogs, including by a rehabilitation specialist. ConclusionsThis pilot study showed that the online health community, MySAH, has a beneficial effect on the aftercare of patients suffering from aSAH because it gives easy access to relevant information provided by peers or caregivers. Due to the variable clinical outcomes after aSAH, the tool will mainly be useful for a select group of patients (with a better clinical outcome).

Published
2014
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2. Data from Telomerase Activation and ATRX Mutations Are Independent Risk Factors for Metastatic Pheochromocytoma and Paraganglioma

Author

Job, Sylvie, primary, Draskovic, Irena, primary, Burnichon, Nelly, primary, Buffet, Alexandre, primary, Cros, Jérôme, primary, Lépine, Charles, primary, Venisse, Annabelle, primary, Robidel, Estelle, primary, Verkarre, Virginie, primary, Meatchi, Tchao, primary, Sibony, Mathilde, primary, Amar, Laurence, primary, Bertherat, Jérôme, primary, de Reyniès, Aurélien, primary, Londoño-Vallejo, Arturo, primary, Favier, Judith, primary, Castro-Vega, Luis Jaime, primary, and Gimenez-Roqueplo, Anne-Paule, primary

Published
2023
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3. Supplementary Data from Telomerase Activation and ATRX Mutations Are Independent Risk Factors for Metastatic Pheochromocytoma and Paraganglioma

Author

Job, Sylvie, primary, Draskovic, Irena, primary, Burnichon, Nelly, primary, Buffet, Alexandre, primary, Cros, Jérôme, primary, Lépine, Charles, primary, Venisse, Annabelle, primary, Robidel, Estelle, primary, Verkarre, Virginie, primary, Meatchi, Tchao, primary, Sibony, Mathilde, primary, Amar, Laurence, primary, Bertherat, Jérôme, primary, de Reyniès, Aurélien, primary, Londoño-Vallejo, Arturo, primary, Favier, Judith, primary, Castro-Vega, Luis Jaime, primary, and Gimenez-Roqueplo, Anne-Paule, primary

Published
2023
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6. FISH-in-CHIPS: A Microfluidic Platform for Molecular Typing of Cancer Cells

Author

Perez-Toralla, Karla, primary, Mottet, Guillaume, additional, Tulukcuoglu-Guneri, Ezgi, additional, Champ, Jérôme, additional, Bidard, François-Clément, additional, Pierga, Jean-Yves, additional, Klijanienko, Jerzy, additional, Draskovic, Irena, additional, Malaquin, Laurent, additional, Viovy, Jean-Louis, additional, and Descroix, Stéphanie, additional

Published
2017
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13. A mosaic genetic screen reveals distinct roles for trithorax and Polycomb group genes in Drosophila eye development

Author

Janody, Florence, Lee, Jeffrey D., Jahren, Neal, Hazelett, Dennis J., Benlali, Aude, Miura, Grant I., Draskovic, Irena, and Treisman, Jessica E.

Subjects
Biological sciences
Abstract

The wave of differentiation that traverses the Drosophila eye disc requires rapid transitions in gene expression that are controlled by a number of signaling molecules also required in other developmental processes. We have used a mosaic genetic screen to systematically identify autosomal genes required for the normal pattern of photoreceptor differentiation, independent of their requirements for viability. In addition to genes known to be important for eye development and to known and novel components of the Hedgehog, Decapentaplegic, Wingless, Epidermal growth factor receptor, and Notch signaling pathways, we identified several members of the Polycomb and trithorax classes of genes encoding general transcriptional regulators. Mutations in these genes disrupt the transitions between zones along the anterior-posterior axis of the eye disc that express different combinations of transcription factors. Different trithorax group genes have very different mutant phenotypes, indicating that target genes differ in their requirements for chromatin remodeling, histone modification, and coactivation factors.

Published
2004

16. Germline mutation of MDM4 , a major p53 regulator, in a familial syndrome of defective telomere maintenance

Author

Toufektchan, Eléonore, primary, Lejour, Vincent, additional, Durand, Romane, additional, Giri, Neelam, additional, Draskovic, Irena, additional, Bardot, Boris, additional, Laplante, Pierre, additional, Jaber, Sara, additional, Alter, Blanche P., additional, Londono-Vallejo, José-Arturo, additional, Savage, Sharon A., additional, and Toledo, Franck, additional

Published
2020
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18. Modulation of the ATM/autophagy pathway by a G-quadruplex ligand tips the balance between senescence and apoptosis in cancer cells

Author

Beauvarlet, Jennifer, Bensadoun, Paul, Darbo, Elodie, Labrunie, Gaelle, Rousseau, Benoît, Richard, Elodie, Draskovic, Irena, Londono-Vallejo, Arturo, Dupuy, Jean-William, Nath Das, Rabindra, Guédin, Aurore, Robert, Guillaume, Orange, Francois, Croce, Sabrina, Valesco, Valerie, Soubeyran, Pierre, Ryan, Kevin M, Mergny, Jean-Louis, Djavaheri-Mergny, Mojgan, Institut Bergonié [Bordeaux], UNICANCER, Actions for OnCogenesis understanding and Target Identification in ONcology (ACTION), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bordeaux Segalen - Bordeaux 2-Institut Bergonié [Bordeaux], UNICANCER-UNICANCER, Acides Nucléiques : Régulations Naturelle et Artificielle (ARNA), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Institut Européen de Chimie et Biologie (IECB), Centre National de la Recherche Scientifique (CNRS)-Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Bordeaux (UB), Dynamique de l'information génétique : bases fondamentales et cancer (DIG CANCER), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Sorbonne Université (SU), Sorbonne Université (SU), Institut Curie [Paris], Centre Génomique Fonctionnelle Bordeaux [Bordeaux] (CGFB), Institut Polytechnique de Bordeaux-Université de Bordeaux Ségalen [Bordeaux 2], Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), University of Glasgow, Czech Academy of Sciences [Prague] (CAS), Institut Bergonié - Département de médecine, Université Bordeaux Segalen - Bordeaux 2-Centre régional de lutte contre le cancer [CRLCC], Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Conditions Extrêmes et Matériaux : Haute Température et Irradiation (CEMHTI), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Centre Commun de Mesures Imagerie Cellulaire, Université de Lille, Sciences et Technologies, Telomeres and Cancer Laboratory, Institut Curie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Curie-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'Anatomie Pathologique Générale, CHU Strasbourg-Hôpital de Hautepierre [Strasbourg], Plateforme de génétique moléculaire des cancers d'Aquitaine, Institut Bergonié - CRLCC Bordeaux, Régulation et dynamique des génomes, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Gestionnaire, Hal Sorbonne Université, UNICANCER-UNICANCER-Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), and Université Nice Sophia Antipolis (1965 - 2019) (UNS)

Subjects
Male, [SDV]Life Sciences [q-bio], Apoptosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, Ataxia Telangiectasia Mutated Proteins, Mice, SCID, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Ligands, Mice, Chemical Biology and Nucleic Acid Chemistry, [SDV.CAN] Life Sciences [q-bio]/Cancer, Mice, Inbred NOD, Cell Line, Tumor, Neoplasms, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Autophagy, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Animals, Humans, Cellular Senescence, ComputingMilieux_MISCELLANEOUS, Mice, Knockout, Xenograft Model Antitumor Assays, G-Quadruplexes, A549 Cells, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], DNA Damage, HeLa Cells, Signal Transduction
Abstract

International audience; G-quadruplex ligands exert their antiproliferative effects through telomere-dependent and telomere-independent mechanisms, but the inter-relationships among autophagy, cell growth arrest and cell death induced by these ligands remain largely unexplored. Here, we demonstrate that the G-quadruplex ligand 20A causes growth arrest of cancer cells in culture and in a HeLa cell xenografted mouse model. This response is associated with the induction of senescence and apoptosis. Transcriptomic analysis of 20A treated cells reveals a significant functional enrichment of biological pathways related to growth arrest, DNA damage response and the lysosomal pathway. 20A elicits global DNA damage but not telomeric damage and activates the ATM and autophagy pathways. Loss of ATM following 20A treatment inhibits both autophagy and senescence and sensitizes cells to death. Moreover, disruption of autophagy by deletion of two essential autophagy genes ATG5 and ATG7 leads to failure of CHK1 activation by 20A and subsequently increased cell death. Our results, therefore, identify the activation of ATM by 20A as a critical player in the balance between senescence and apoptosis and autophagy as one of the key mediators of such regulation. Thus, targeting the ATM/autophagy pathway might be a promising strategy to achieve the maximal anticancer effect of this compound.

Published
2019

21. Improving person-centred care in nursing homes through dementia-care mapping: design of a cluster-randomised controlled trial

Author

van de Ven Geertje, Draskovic Irena, Adang Eddy MM, Donders Rogier ART, Post Aukje, Zuidema Sytse U, Koopmans Raymond TCM, and Vernooij-Dassen Myrra JFJ

Subjects
Geriatrics, RC952-954.6
Abstract

Abstract Background The effectiveness and efficiency of nursing-home dementia care are suboptimal: there are high rates of neuropsychiatric symptoms among the residents and work-related stress among the staff. Dementia-care mapping is a person-centred care method that may alleviate both the resident and the staff problems. The main objective of this study is to evaluate the effectiveness and cost-effectiveness of dementia-care mapping in nursing-home dementia care. Methods/Design The study is a cluster-randomised controlled trial, with nursing homes grouped in clusters. Studywise minimisation is the allocation method. Nursing homes in the intervention group will receive a dementia-care-mapping intervention, while the control group will receive usual care. The primary outcome measure is resident agitation, to be assessed with the Cohen-Mansfield Agitation Inventory. The secondary outcomes are resident neuropsychiatric symptoms, assessed with the Neuropsychiatric Inventory - Nursing Homes and quality of life, assessed with Qualidem and the EQ-5D. The staff outcomes are stress reactions, job satisfaction and job-stress-related absenteeism, and staff turnover rate, assessed with the Questionnaire about Experience and Assessment of Work, the General Health Questionnaire-12, and the Maastricht Job Satisfaction Scale for Health Care, respectively. We will collect the data from the questionnaires and electronic registration systems. We will employ linear mixed-effect models and cost-effectiveness analyses to evaluate the outcomes. We will use structural equation modelling in the secondary analysis to evaluate the plausibility of a theoretical model regarding the effectiveness of the dementia-care mapping intervention. We will set up process analyses, including focus groups with staff, to determine the relevant facilitators of and barriers to implementing dementia-care mapping broadly. Discussion A novelty of dementia-care mapping is that it offers an integral person-centred approach to dementia care in nursing homes. The major strengths of the study design are the large sample size, the cluster-randomisation, and the one-year follow-up. The generalisability of the implementation strategies may be questionable because the motivation for person-centred care in both the intervention and control nursing homes is above average. The results of this study may be useful in improving the quality of care and are relevant for policymakers. Trial registration The trial is registered in the Netherlands National Trial Register: NTR2314.

Published
2012
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22. Human RTEL1 stabilizes long G-overhangs allowing telomerase-dependent over-extension

Author

Porreca, Rosa M, Glousker, Galina, Awad, Aya, Matilla Fernandez, Maria I, Gibaud, Anne, Naucke, Christian, Cohen, Scott B, Bryan, Tracy M, Tzfati, Yehuda, Draskovic, Irena, Londoño-Vallejo, Arturo, Dynamique de l'information génétique : bases fondamentales et cancer (DIG CANCER), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Université Pierre et Marie Curie - Paris 6 (UPMC), and Université Pierre et Marie Curie - Paris 6 (UPMC)

Subjects
Guanine, [SDV]Life Sciences [q-bio], Telomere-Binding Proteins, DNA Helicases, Humans, Telomere Homeostasis, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Genome Integrity, Repair and Replication, Telomere, Telomerase, Shelterin Complex, ComputingMilieux_MISCELLANEOUS, Cell Line
Abstract

Telomere maintenance protects the cell against genome instability and senescence. Accelerated telomere attrition is a characteristic of premature aging syndromes including Dyskeratosis congenita (DC). Mutations in hRTEL1 are associated with a severe form of DC called Hoyeraal-Hreidarsson syndrome (HHS). HHS patients carry short telomeres and HHS cells display telomere damage. Here we investigated how hRTEL1 contributes to telomere maintenance in human primary as well as tumor cells. Transient depletion of hRTEL1 resulted in rapid telomere shortening only in the context of telomerase-positive cells with very long telomeres and high levels of telomerase. The effect of hRTEL1 on telomere length is telomerase dependent without impacting telomerase biogenesis or targeting of the enzyme to telomeres. Instead, RTEL1 depletion led to a decrease in both G-overhang content and POT1 association with telomeres with limited telomere uncapping. Strikingly, overexpression of POT1 restored telomere length but not the overhang, demonstrating that G-overhang loss is the primary defect caused by RTEL1 depletion. We propose that hRTEL1 contributes to the maintenance of long telomeres by preserving long G-overhangs, thereby facilitating POT1 binding and elongation by telomerase.

Published
2018

23. Telomerase Activation and ATRX Mutations Are Independent Risk Factors for Metastatic Pheochromocytoma and Paraganglioma

Author

Job, Sylvie, primary, Draskovic, Irena, additional, Burnichon, Nelly, additional, Buffet, Alexandre, additional, Cros, Jérôme, additional, Lépine, Charles, additional, Venisse, Annabelle, additional, Robidel, Estelle, additional, Verkarre, Virginie, additional, Meatchi, Tchao, additional, Sibony, Mathilde, additional, Amar, Laurence, additional, Bertherat, Jérôme, additional, de Reyniès, Aurélien, additional, Londoño-Vallejo, Arturo, additional, Favier, Judith, additional, Castro-Vega, Luis Jaime, additional, and Gimenez-Roqueplo, Anne-Paule, additional

Published
2019
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24. FISH-in-CHIPS: A Microfluidic Platform for Molecular Typing of Cancer Cells

Author

Perez-Toralla, Karla, Mottet, Guillaume, Tulukcuoglu-Guneri, Ezgi, Champ, Jérôme, Bidard, François-Clément, Pierga, Jean-Yves, Klijanienko, Jerzy, Draskovic, Irena, Malaquin, Laurent, Viovy, Jean-Louis, Descroix, Stéphanie, Venzac, B., Diakité, L., Herthnek, D., Cissé, I., Bockelmann, U., Université Pierre et Marie Curie - Paris 6 - UFR de Médecine Pierre et Marie Curie (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC), Physico-Chimie-Curie (PCC), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC), and Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Curie [Paris]-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio], dissemin
Abstract

International audience; Microfluidics offer powerful tools for the control, manipulation, and analysis of cells, in particular for theassessment of cell malignancy or the study of cell subpopulations. However, implementing complex biologicalprotocols on chip remains a challenge. Sample preparation is often performed off chip using multiplemanually performed steps, and protocols usually include different dehydration and drying steps thatare not always compatible with a microfluidic format.Here, we report the implementation of a Fluorescence in situ Hybridization (FISH) protocol forthe molecular typing of cancer cells in a simple and low-cost device. The geometry of the chip allowsintegrating the sample preparation steps to efficiently assess the genomic content of individual cellsusing a minute amount of sample. The FISH protocol can be fully automated, thus enabling its use inroutine clinical practice.

Published
2017

25. The N-Terminal Domain of cGAS Determines Preferential Association with Centromeric DNA and Innate Immune Activation in the Nucleus

Author

Gentili, Matteo, Lahaye, Xavier, Nadalin, Francesca, Nader, Guilherme P.F., Puig Lombardi, Emilia, Herve, Solène, De Silva, Nilushi, Rookhuizen, Derek, Zueva, Elina, Goudot, Christel, Maurin, Mathieu, Bochnakian, Aurore, Amigorena, Sebastian, Piel, Matthieu, Fachinetti, Daniele, Manel, Nicolas, Beauvarlet, Jennifer, Bensadoun, Paul, Darbo, Elodie, Labrunie, Gaelle, Rousseau, Benoit, Richard, Elodie, Draskovic, Irena, Dupuy, Jean-William, Nath Das, Rabindra, Guédin, Aurore, Robert, Guillaume, Orange, François, Croce, Sabrina, Valesco, Valerie, Soubeyran, Pierre, Ryan, Kevin, Mergny, Jean-Louis, Mergny, Mojgan, Borie, Raphael, Bouvry, Diane, Cottin, Vincent, Gauvain, Clement, Cazes, Aurélie, Debray, Marie-Pierre, Cadranel, Jacques, Dieudé, Philippe, Degot, Tristan, Dominique, Stéphane, Gamez, Anne Sophie, Jaillet, Madeleine, Juge, Pierre-Antoine, Londono-Vallejo, Arturo, Mailleux, Arnaud, Mal, Herve, Boileau, Catherine, Ménard, Christelle, Nunes, Hilario, Prevot, Grégoire, Quetant, Sébastien, Revy, Patrick, Traclet, Julie, Wemeau-Stervinou, Lidwine, Wislez, Marie, Kannengiesser, Caroline, Crestani, Bruno, Immunité et cancer (U932), Institut Curie-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Biologie Computationnelle et Quantitative = Laboratory of Computational and Quantitative Biology (LCQB), Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut Curie, Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Institut Bergonié - Département de médecine, Université Bordeaux Segalen - Bordeaux 2-Centre régional de lutte contre le cancer [CRLCC], Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Conditions Extrêmes et Matériaux : Haute Température et Irradiation (CEMHTI), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Centre Commun de Mesures Imagerie Cellulaire, Université de Lille, Sciences et Technologies, Telomeres and Cancer Laboratory, Centre Génomique Fonctionnelle Bordeaux [Bordeaux] (CGFB), Institut Polytechnique de Bordeaux-Université de Bordeaux Ségalen [Bordeaux 2], Acides Nucléiques : Régulations Naturelle et Artificielle (ARNA), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'Anatomie Pathologique Générale, CHU Strasbourg-Hôpital de Hautepierre [Strasbourg], Plateforme de génétique moléculaire des cancers d'Aquitaine, Institut Bergonié - CRLCC Bordeaux, University of Glasgow, Régulation et dynamique des génomes, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie et Epidémiologie des Maladies Respiratoires (PHERE (UMR_S_1152 / U1152)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de pneumologie [Avicenne], Hôpital Avicenne, Rétrovirus et Pathologie Comparée (RPC), Institut National de la Recherche Agronomique (INRA)-École pratique des hautes études (EPHE)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Ecole Nationale Vétérinaire de Lyon (ENVL), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Université Paris Diderot - Paris 7 (UPD7), Service de pneumologie et réanimation [CHU Tenon], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Tenon [APHP], Service de rhumatologie [Bichat], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7), Service de pneumologie, oncologie thoracique et soins intensifs respiratoires [Rouen], Hôpital Charles Nicolle [Rouen]-CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU), Département des Maladies Respiratoires [Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Arnaud de Villeneuve, Biologie de l'Os et du Cartilage : Régulations et Ciblages Thérapeutiques (BIOSCAR (UMR_S_1132 / U1132)), Dynamique de l'information génétique : bases fondamentales et cancer (DIG CANCER), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Curie-Centre National de la Recherche Scientifique (CNRS), Service de pneumologie B, Université Paris Descartes - Paris 5 (UPD5), CHU, Hôpital Larrey, Respiratory Disease, CHU Grenoble-Hôpital Michallon, Developpement Normal et Pathologique du Système Immunitaire, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service de Pneumologie et Immuno-Allergologie, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Theranoscan, Université Pierre et Marie Curie - Paris 6 (UPMC), Hôpital Bichat - Claude Bernard, Physiopathologie et Epidemiologie de l'Insuffisance Respiratoire, ANR-10-LABX-77, LABEX VRI, ANR-10-IDEX-0001-02 PSL∗, LABEX DCBIOL, ACTERIA FoundationACTERIA Foundation, Fondation Schlumberger pour l’Education et la Recherche, ECTZ36691, ANRSANRS, VIH2016126002, SidactionSidaction, DIM Biothérapies, 727408 STIMUNITY, European Research CouncilEuropean Research Council, French Ministry of Education, Research, and Technology, DCBIO 751735, Marie Skłodowska-Curie Individual Fellowship, ALTF 1298-2016, EMBO Long-term fellowship, ANR INNATENUCLEOTIDES, Fondation BMS, Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut Curie [Paris], Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut Bergonié [Bordeaux], UNICANCER, UNICANCER-UNICANCER, Hôpital Avicenne [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut National de la Recherche Agronomique (INRA)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Claude Bernard Lyon 1 (UCBL), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Tenon [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université-Sorbonne Université, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Université Pierre et Marie Curie - Paris 6 (UPMC), Service de Pneumologie et Immuno-Allergologie [CHU LIlle], Pole Cardio-vasculaire et pulmonaire [CHU Lille], Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Biologie Cellulaire et Cancer, Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Sorbonne Université (SU), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Université de Rouen Normandie (UNIROUEN), and Normandie Université (NU)-Normandie Université (NU)-Hôpital Charles Nicolle [Rouen]-CHU Rouen

Subjects
0301 basic medicine, Male, [SDV]Life Sciences [q-bio], [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], chemistry.chemical_compound, Mice, 0302 clinical medicine, ComputingMilieux_MISCELLANEOUS, 0303 health sciences, Transfection, interferon, nuclear envelope, Compartmentalization (psychology), Nucleotidyltransferases, Cell biology, Nuclear DNA, 3. Good health, centromere, Female, Adult, Satellite DNA, Guanosine, LINE, satellite DNA, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, DNA, Satellite, General Biochemistry, Genetics and Molecular Biology, Article, Cell Line, 03 medical and health sciences, Protein Domains, Animals, Humans, dendritic cells, 030304 developmental biology, Cell Nucleus, Innate immune system, DNA, IRF3, Immunity, Innate, Mice, Inbred C57BL, 030104 developmental biology, chemistry, cGAMP, 030217 neurology & neurosurgery, HeLa Cells, cGAS, STING
Abstract

Summary Cytosolic DNA activates cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS), an innate immune sensor pivotal in anti-microbial defense, senescence, auto-immunity, and cancer. cGAS is considered to be a sequence-independent DNA sensor with limited access to nuclear DNA because of compartmentalization. However, the nuclear envelope is a dynamic barrier, and cGAS is present in the nucleus. Here, we identify determinants of nuclear cGAS localization and activation. We show that nuclear-localized cGAS synthesizes cGAMP and induces innate immune activation of dendritic cells, although cGAMP levels are 200-fold lower than following transfection with exogenous DNA. Using cGAS ChIP-seq and a GFP-cGAS knockin mouse, we find nuclear cGAS enrichment on centromeric satellite DNA, confirmed by imaging, and to a lesser extent on LINE elements. The non-enzymatic N-terminal domain of cGAS determines nucleo-cytoplasmic localization, enrichment on centromeres, and activation of nuclear-localized cGAS. These results reveal a preferential functional association of nuclear cGAS with centromeres., Graphical Abstract, Highlights • Nuclear-localized cGAS activates a cellular innate immune response • Nuclear cGAS is 200-fold less active toward self-DNA than exogenous cytosolic DNA • Nuclear cGAS is enriched on centromeric satellite and LINE DNA repeats • The non-enzymatic N-terminal of cGAS determines nuclear localization and activity, cGAS is a well-established innate immune sensor of cytosolic DNA, but its presence in the nucleus is poorly understood. Gentili et al. find that nuclear cGAS is active and enriched on centromeres and LINE DNA repeats. Nuclear-cytoplasmic distribution, centromere association, and nuclear activation are determined by its non-enzymatic N-terminal domain.

Published
2019

27. Telomere Maintenance Is a Critical Determinant in the Physiopathology of Pulmonary Hypertension

Author

Izikki, Mohamed, primary, Hoang, Eric, additional, Draskovic, Irena, additional, Mercier, Olaf, additional, Lecerf, Florence, additional, Lamrani, Lilia, additional, Liu, Win-Yan, additional, Guignabert, Christophe, additional, Fadel, Elie, additional, Dorfmuller, Peter, additional, Humbert, Marc, additional, Londoño-Vallejo, Arturo, additional, and Eddahibi, Saadia, additional

Published
2015
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28. FISH in chips: turning microfluidic fluorescence in situ hybridization into a quantitative and clinically reliable molecular diagnosis tool

Author

Perez-Toralla, Karla, primary, Mottet, Guillaume, additional, Guneri, Ezgi Tulukcuoglu, additional, Champ, Jérôme, additional, Bidard, François-Clément, additional, Pierga, Jean-Yves, additional, Klijanienko, Jerzy, additional, Draskovic, Irena, additional, Malaquin, Laurent, additional, Viovy, Jean-Louis, additional, and Descroix, Stéphanie, additional

Published
2015
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34. Mutant Mice Lacking the p53 C-Terminal Domain Model Telomere Syndromes

Author

Simeonova, Iva, primary, Jaber, Sara, additional, Draskovic, Irena, additional, Bardot, Boris, additional, Fang, Ming, additional, Bouarich-Bourimi, Rachida, additional, Lejour, Vincent, additional, Charbonnier, Laure, additional, Soudais, Claire, additional, Bourdon, Jean-Christophe, additional, Huerre, Michel, additional, Londono-Vallejo, Arturo, additional, and Toledo, Franck, additional

Published
2013
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39. EASYcareGIDS-project

Author

Perry, Marieke, primary, Theunisse, Leny, additional, Draskovic, Irena, additional, and Olde Rikkert, Marcel, additional

Published
2007
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42. Improving person-centred care in nursing homes through dementia-care mapping: design of a cluster-randomised controlled trial.

Author

de Ven, Geertje van, Draskovic, Irena, Adang, Eddy M. M., Donders, Rogier A. R. T., Post, Aukje, Zuidema, Sytse U., Koopmans, Raymond T. C. M, and Vernooij-Dassen, Myrra J. F. J.

Subjects
CARE of dementia patients, COST effectiveness, CLINICAL trials, NURSING home care, HEALTH outcome assessment, NURSING care facilities
Abstract

Background: The effectiveness and efficiency of nursing-home dementia care are suboptimal: there are high rates of neuropsychiatric symptoms among the residents and work-related stress among the staff. Dementia-care mapping is a person-centred care method that may alleviate both the resident and the staff problems. The main objective of this study is to evaluate the effectiveness and cost-effectiveness of dementia-care mapping in nursinghome dementia care. Methods/Design: The study is a cluster-randomised controlled trial, with nursing homes grouped in clusters. Studywise minimisation is the allocation method. Nursing homes in the intervention group will receive a dementia-care-mapping intervention, while the control group will receive usual care. The primary outcome measure is resident agitation, to be assessed with the Cohen-Mansfield Agitation Inventory. The secondary outcomes are resident neuropsychiatric symptoms, assessed with the Neuropsychiatric Inventory - Nursing Homes and quality of life, assessed with Qualidem and the EQ-5D. The staff outcomes are stress reactions, job satisfaction and job-stress-related absenteeism, and staff turnover rate, assessed with the Questionnaire about Experience and Assessment of Work, the General Health Questionnaire-12, and the Maastricht Job Satisfaction Scale for Health Care, respectively. We will collect the data from the questionnaires and electronic registration systems. We will employ linear mixed-effect models and cost-effectiveness analyses to evaluate the outcomes. We will use structural equation modelling in the secondary analysis to evaluate the plausibility of a theoretical model regarding the effectiveness of the dementia-care mapping intervention. We will set up process analyses, including focus groups with staff, to determine the relevant facilitators of and barriers to implementing dementia-care mapping broadly. Discussion: A novelty of dementia-care mapping is that it offers an integral person-centred approach to dementia care in nursing homes. The major strengths of the study design are the large sample size, the clusterrandomisation, and the one-year follow-up. The generalisability of the implementation strategies may be questionable because the motivation for person-centred care in both the intervention and control nursing homes is above average. The results of this study may be useful in improving the quality of care and are relevant for policymakers. [ABSTRACT FROM AUTHOR]

Published
2012
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45. Modulation of the ATM/autophagy pathway by a G-quadruplex ligand tips the balance between senescence and apoptosis in cancer cells.

Author

Beauvarlet J, Bensadoun P, Darbo E, Labrunie G, Rousseau B, Richard E, Draskovic I, Londono-Vallejo A, Dupuy JW, Nath Das R, Guédin A, Robert G, Orange F, Croce S, Valesco V, Soubeyran P, Ryan KM, Mergny JL, and Djavaheri-Mergny M

Subjects
A549 Cells, Animals, Apoptosis genetics, Autophagy genetics, Cell Line, Tumor, Cellular Senescence genetics, DNA Damage drug effects, HeLa Cells, Humans, Ligands, Male, Mice, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Neoplasms genetics, Signal Transduction drug effects, Signal Transduction genetics, Xenograft Model Antitumor Assays, Apoptosis drug effects, Ataxia Telangiectasia Mutated Proteins antagonists & inhibitors, Ataxia Telangiectasia Mutated Proteins metabolism, Autophagy drug effects, Cellular Senescence drug effects, G-Quadruplexes, Neoplasms pathology
Abstract

G-quadruplex ligands exert their antiproliferative effects through telomere-dependent and telomere-independent mechanisms, but the inter-relationships among autophagy, cell growth arrest and cell death induced by these ligands remain largely unexplored. Here, we demonstrate that the G-quadruplex ligand 20A causes growth arrest of cancer cells in culture and in a HeLa cell xenografted mouse model. This response is associated with the induction of senescence and apoptosis. Transcriptomic analysis of 20A treated cells reveals a significant functional enrichment of biological pathways related to growth arrest, DNA damage response and the lysosomal pathway. 20A elicits global DNA damage but not telomeric damage and activates the ATM and autophagy pathways. Loss of ATM following 20A treatment inhibits both autophagy and senescence and sensitizes cells to death. Moreover, disruption of autophagy by deletion of two essential autophagy genes ATG5 and ATG7 leads to failure of CHK1 activation by 20A and subsequently increased cell death. Our results, therefore, identify the activation of ATM by 20A as a critical player in the balance between senescence and apoptosis and autophagy as one of the key mediators of such regulation. Thus, targeting the ATM/autophagy pathway might be a promising strategy to achieve the maximal anticancer effect of this compound., (© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.)

Published
2019
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46. Human RTEL1 stabilizes long G-overhangs allowing telomerase-dependent over-extension.

Author

Porreca RM, Glousker G, Awad A, Matilla Fernandez MI, Gibaud A, Naucke C, Cohen SB, Bryan TM, Tzfati Y, Draskovic I, and Londoño-Vallejo A

Subjects
Cell Line, Guanine analysis, Humans, Shelterin Complex, Telomere chemistry, Telomere metabolism, Telomere-Binding Proteins chemistry, Telomere-Binding Proteins metabolism, DNA Helicases physiology, Telomerase metabolism, Telomere Homeostasis
Abstract

Telomere maintenance protects the cell against genome instability and senescence. Accelerated telomere attrition is a characteristic of premature aging syndromes including Dyskeratosis congenita (DC). Mutations in hRTEL1 are associated with a severe form of DC called Hoyeraal-Hreidarsson syndrome (HHS). HHS patients carry short telomeres and HHS cells display telomere damage. Here we investigated how hRTEL1 contributes to telomere maintenance in human primary as well as tumor cells. Transient depletion of hRTEL1 resulted in rapid telomere shortening only in the context of telomerase-positive cells with very long telomeres and high levels of telomerase. The effect of hRTEL1 on telomere length is telomerase dependent without impacting telomerase biogenesis or targeting of the enzyme to telomeres. Instead, RTEL1 depletion led to a decrease in both G-overhang content and POT1 association with telomeres with limited telomere uncapping. Strikingly, overexpression of POT1 restored telomere length but not the overhang, demonstrating that G-overhang loss is the primary defect caused by RTEL1 depletion. We propose that hRTEL1 contributes to the maintenance of long telomeres by preserving long G-overhangs, thereby facilitating POT1 binding and elongation by telomerase.

Published
2018
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47. FISH-in-CHIPS: A Microfluidic Platform for Molecular Typing of Cancer Cells.

Author

Perez-Toralla K, Mottet G, Tulukcuoglu-Guneri E, Champ J, Bidard FC, Pierga JY, Klijanienko J, Draskovic I, Malaquin L, Viovy JL, and Descroix S

Subjects
Cell Line, Tumor, Equipment Design, Humans, Image Processing, Computer-Assisted methods, In Situ Hybridization, Fluorescence instrumentation, Microfluidic Analytical Techniques instrumentation, Microfluidics instrumentation, Microscopy, Fluorescence, Molecular Typing instrumentation, Neoplasms diagnosis, Neoplasms genetics, Optical Imaging, Software, In Situ Hybridization, Fluorescence methods, Microfluidic Analytical Techniques methods, Microfluidics methods, Molecular Typing methods
Abstract

Microfluidics offer powerful tools for the control, manipulation, and analysis of cells, in particular for the assessment of cell malignancy or the study of cell subpopulations. However, implementing complex biological protocols on chip remains a challenge. Sample preparation is often performed off chip using multiple manually performed steps, and protocols usually include different dehydration and drying steps that are not always compatible with a microfluidic format.Here, we report the implementation of a Fluorescence in situ Hybridization (FISH) protocol for the molecular typing of cancer cells in a simple and low-cost device. The geometry of the chip allows integrating the sample preparation steps to efficiently assess the genomic content of individual cells using a minute amount of sample. The FISH protocol can be fully automated, thus enabling its use in routine clinical practice.

Published
2017
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48. Telomere recombination and alternative telomere lengthening mechanisms.

Author

Draskovic I and Londono Vallejo A

Subjects
Animals, DNA Helicases metabolism, DNA Methylation physiology, Exodeoxyribonucleases metabolism, Genomic Instability, Heterochromatin metabolism, Humans, Mice, RecQ Helicases metabolism, Recombination, Genetic, Shelterin Complex, Telomerase metabolism, Telomere Shortening, Telomere-Binding Proteins physiology, Werner Syndrome Helicase, Telomere metabolism, Telomere Homeostasis physiology
Abstract

Telomeres are nucleoprotein structures at the ends of linear chromosomes that protect them from being recognized as DNA double stranded breaks. Telomeres shorten with every cell division and in the absence of the checkpoint mechanisms critical telomere shortening leads to chromosome end fusions and genomic instability. Cancer cells achieve immortality by engaging in one of the two known mechanisms for telomere maintenance: elongation by telomerase or through recombination. Recombination based elongation of telomeres, also known as alternative lengthening of telomeres or ALT, is prevalent among cancers of mesenchymal origin. However, the conditions favoring ALT emergence are not known. Here we will discuss possible players in ALT mechanisms, including recruitment of telomeres to recombination centers, alterations of telomere associated proteins and modifications at the level of chromatin that could generate recombination permissive conditions at telomeres.

Published
2013
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