BESOIN D’AIDE POUR ANALYSER ET INTERPRÉTER VOS DONNÉES ?
AltraBio est une société de recherche contractuelle spécialisée dans l’analyse de données biologiques et médicales grâce à l’utilisation de méthodes statistiques et d’intelligence artificielle.
Elle est reconnue mondialement comme un partenaire de confiance pour les projets de recherche et développement menés par de grandes entreprises et des hôpitaux universitaires de premier plan évoluant dans divers secteurs tels que les produits pharmaceutiques, les dispositifs médicaux, le diagnostic et les dermato-cosmétiques.
COMMENT TRAVAILLER ENSEMBLE?
Partenariat
Développement d’outils informatiques pour l’analyse de données au sein de consortiums régionaux / nationaux / internationaux.
Exemples de projets réalisés ou en cours:
Sous-traitance
Analyse de données pour des entreprises ou des instituts hospitalo-universitaires.
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Des centaines de projets réalisés
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Des clients réguliers incluant les plus grandes pharmas et les leaders de la cosmétique
FINANCEMENTS
NOUVELLES
novembre 2023
Congrès annuel de l’AFC
AltraBio est ravi d’annoncer sa présence au prochain congrès [...]
octobre 2023
Innovative Therapies Days
AltraBio est heureux d'annoncer sa présence aux prochains Innovative Therapies [...]
juillet 2023
The multi-level regulation of clownfish metamorphosis by thyroid hormones
Félicitations aux équipes de Vincent Laudet de l'Okinawa Institute [...]
mai 2023
AltraBio et Tercen annoncent leur partenariat pour le gating automatique dans les études cliniques.
AltraBio SAS, a leading company in data analysis and [...]
DERNIERES PUBLICATIONS
2016
Bachy, Emmanuel; Urb, Mirjam; Chandra, Shilpi; Robinot, Rémy; Bricard, Gabriel; de Bernard, Simon; Traverse-Glehen, Alexandra; Gazzo, Sophie; Blond, Olivier; Khurana, Archana; Baseggio, Lucile; Heavican, Tayla; Ffrench, Martine; Crispatzu, Giuliano; Mondière, Paul; Schrader, Alexandra; Taillardet, Morgan; Thaunat, Olivier; Martin, Nadine; Dalle, Stéphane; Garff-Tavernier, Magali Le; Salles, Gilles; Lachuer, Joel; Hermine, Olivier; Asnafi, Vahid; Roussel, Mikael; Lamy, Thierry; Herling, Marco; Iqbal, Javeed; Buffat, Laurent; Marche, Patrice N; Gaulard, Philippe; Kronenberg, Mitchell; Defrance, Thierry; Genestier, Laurent
CD1d-restricted peripheral T cell lymphoma in mice and humans Article de journal
Dans: J Exp Med, vol. 213, no. 5, p. 841–857, 2016, ISSN: 1540-9538.
@article{pmid27069116,
title = {CD1d-restricted peripheral T cell lymphoma in mice and humans},
author = {Emmanuel Bachy and Mirjam Urb and Shilpi Chandra and Rémy Robinot and Gabriel Bricard and Simon de Bernard and Alexandra Traverse-Glehen and Sophie Gazzo and Olivier Blond and Archana Khurana and Lucile Baseggio and Tayla Heavican and Martine Ffrench and Giuliano Crispatzu and Paul Mondière and Alexandra Schrader and Morgan Taillardet and Olivier Thaunat and Nadine Martin and Stéphane Dalle and Magali Le Garff-Tavernier and Gilles Salles and Joel Lachuer and Olivier Hermine and Vahid Asnafi and Mikael Roussel and Thierry Lamy and Marco Herling and Javeed Iqbal and Laurent Buffat and Patrice N Marche and Philippe Gaulard and Mitchell Kronenberg and Thierry Defrance and Laurent Genestier},
doi = {10.1084/jem.20150794},
issn = {1540-9538},
year = {2016},
date = {2016-05-01},
urldate = {2016-05-01},
journal = {J Exp Med},
volume = {213},
number = {5},
pages = {841--857},
abstract = {Peripheral T cell lymphomas (PTCLs) are a heterogeneous entity of neoplasms with poor prognosis, lack of effective therapies, and a largely unknown pathophysiology. Identifying the mechanism of lymphomagenesis and cell-of-origin from which PTCLs arise is crucial for the development of efficient treatment strategies. In addition to the well-described thymic lymphomas, we found that p53-deficient mice also developed mature PTCLs that did not originate from conventional T cells but from CD1d-restricted NKT cells. PTCLs showed phenotypic features of activated NKT cells, such as PD-1 up-regulation and loss of NK1.1 expression. Injections of heat-killed Streptococcus pneumonia, known to express glycolipid antigens activating NKT cells, increased the incidence of these PTCLs, whereas Escherichia coli injection did not. Gene expression profile analyses indicated a significant down-regulation of genes in the TCR signaling pathway in PTCL, a common feature of chronically activated T cells. Targeting TCR signaling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged mice survival. Importantly, we identified human CD1d-restricted lymphoma cells within Vδ1 TCR-expressing PTCL. These results define a new subtype of PTCL and pave the way for the development of blocking anti-CD1d antibody for therapeutic purposes in humans.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2015
Helden, Mary J; Goossens, Steven; Daussy, Cécile; Mathieu, Anne-Laure; Faure, Fabrice; cais, Antoine Marc; Vandamme, Niels; Farla, Natalie; Mayol, Katia; Viel, Sébastien; Degouve, Sophie; Debien, Emilie; Seuntjens, Eve; Conidi, Andrea; Chaix, Julie; Mangeot, Philippe; Bernard, Simon; Buffat, Laurent; Haigh, Jody J; Huylebroeck, Danny; Lambrecht, Bart N; Berx, Geert; Walzer, Thierry
Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection Article de journal
Dans: J. Exp. Med., vol. 212, no. 12, p. 2015–2025, 2015.
@article{Van_Helden2015-zx,
title = {Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection},
author = {Mary J Helden and Steven Goossens and Cécile Daussy and Anne-Laure Mathieu and Fabrice Faure and Antoine Marc cais and Niels Vandamme and Natalie Farla and Katia Mayol and Sébastien Viel and Sophie Degouve and Emilie Debien and Eve Seuntjens and Andrea Conidi and Julie Chaix and Philippe Mangeot and Simon Bernard and Laurent Buffat and Jody J Haigh and Danny Huylebroeck and Bart N Lambrecht and Geert Berx and Thierry Walzer},
doi = {10.1084/jem.20150809},
year = {2015},
date = {2015-11-01},
urldate = {2015-11-01},
journal = {J. Exp. Med.},
volume = {212},
number = {12},
pages = {2015--2025},
publisher = {Rockefeller University Press},
abstract = {Natural killer (NK) cell maturation is a tightly controlled
process that endows NK cells with functional competence and the
capacity to recognize target cells. Here, we found that the
transcription factor (TF) Zeb2 was the most highly induced TF
during NK cell maturation. Zeb2 is known to control epithelial
to mesenchymal transition, but its role in immune cells is
mostly undefined. Targeted deletion of Zeb2 resulted in impaired
NK cell maturation, survival, and exit from the bone marrow. NK
cell function was preserved, but mice lacking Zeb2 in NK cells
were more susceptible to B16 melanoma lung metastases.
Reciprocally, ectopic expression of Zeb2 resulted in a higher
frequency of mature NK cells in all organs. Moreover, the
immature phenotype of Zeb2(-/-) NK cells closely resembled that
of Tbx21(-/-) NK cells. This was caused by both a dependence of
Zeb2 expression on T-bet and a probable cooperation of these
factors in gene regulation. Transgenic expression of Zeb2 in
Tbx21(-/-) NK cells partially restored a normal maturation,
establishing that timely induction of Zeb2 by T-bet is an
essential event during NK cell differentiation. Finally, this
novel transcriptional cascade could also operate in human as
T-bet and Zeb2 are similarly regulated in mouse and human NK
cells.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
process that endows NK cells with functional competence and the
capacity to recognize target cells. Here, we found that the
transcription factor (TF) Zeb2 was the most highly induced TF
during NK cell maturation. Zeb2 is known to control epithelial
to mesenchymal transition, but its role in immune cells is
mostly undefined. Targeted deletion of Zeb2 resulted in impaired
NK cell maturation, survival, and exit from the bone marrow. NK
cell function was preserved, but mice lacking Zeb2 in NK cells
were more susceptible to B16 melanoma lung metastases.
Reciprocally, ectopic expression of Zeb2 resulted in a higher
frequency of mature NK cells in all organs. Moreover, the
immature phenotype of Zeb2(-/-) NK cells closely resembled that
of Tbx21(-/-) NK cells. This was caused by both a dependence of
Zeb2 expression on T-bet and a probable cooperation of these
factors in gene regulation. Transgenic expression of Zeb2 in
Tbx21(-/-) NK cells partially restored a normal maturation,
establishing that timely induction of Zeb2 by T-bet is an
essential event during NK cell differentiation. Finally, this
novel transcriptional cascade could also operate in human as
T-bet and Zeb2 are similarly regulated in mouse and human NK
cells.
van Helden, Mary J; Goossens, Steven; Daussy, Cécile; Mathieu, Anne-Laure; Faure, Fabrice; Marçais, Antoine; Vandamme, Niels; Farla, Natalie; Mayol, Katia; Viel, Sébastien; Degouve, Sophie; Debien, Emilie; Seuntjens, Eve; Conidi, Andrea; Chaix, Julie; Mangeot, Philippe; de Bernard, Simon; Buffat, Laurent; Haigh, Jody J; Huylebroeck, Danny; Lambrecht, Bart N; Berx, Geert; Walzer, Thierry
Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection Article de journal
Dans: J Exp Med, vol. 212, no. 12, p. 2015–2025, 2015, ISSN: 1540-9538.
@article{pmid26503444,
title = {Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection},
author = {Mary J van Helden and Steven Goossens and Cécile Daussy and Anne-Laure Mathieu and Fabrice Faure and Antoine Marçais and Niels Vandamme and Natalie Farla and Katia Mayol and Sébastien Viel and Sophie Degouve and Emilie Debien and Eve Seuntjens and Andrea Conidi and Julie Chaix and Philippe Mangeot and Simon de Bernard and Laurent Buffat and Jody J Haigh and Danny Huylebroeck and Bart N Lambrecht and Geert Berx and Thierry Walzer},
doi = {10.1084/jem.20150809},
issn = {1540-9538},
year = {2015},
date = {2015-11-01},
urldate = {2015-11-01},
journal = {J Exp Med},
volume = {212},
number = {12},
pages = {2015--2025},
abstract = {Natural killer (NK) cell maturation is a tightly controlled process that endows NK cells with functional competence and the capacity to recognize target cells. Here, we found that the transcription factor (TF) Zeb2 was the most highly induced TF during NK cell maturation. Zeb2 is known to control epithelial to mesenchymal transition, but its role in immune cells is mostly undefined. Targeted deletion of Zeb2 resulted in impaired NK cell maturation, survival, and exit from the bone marrow. NK cell function was preserved, but mice lacking Zeb2 in NK cells were more susceptible to B16 melanoma lung metastases. Reciprocally, ectopic expression of Zeb2 resulted in a higher frequency of mature NK cells in all organs. Moreover, the immature phenotype of Zeb2(-/-) NK cells closely resembled that of Tbx21(-/-) NK cells. This was caused by both a dependence of Zeb2 expression on T-bet and a probable cooperation of these factors in gene regulation. Transgenic expression of Zeb2 in Tbx21(-/-) NK cells partially restored a normal maturation, establishing that timely induction of Zeb2 by T-bet is an essential event during NK cell differentiation. Finally, this novel transcriptional cascade could also operate in human as T-bet and Zeb2 are similarly regulated in mouse and human NK cells.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}