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AltraBio is a contract research company expert in the analysis of biological and medical data through the use of statistical methods and artificial intelligence.
AltraBio is trusted worldwide as a partner for research and development projects by leading companies and university hospitals operating in various sectors including pharmaceuticals, medical devices, diagnostics, and dermato-cosmetics.
How can we work together?
Partnership
Development of computational tools for data analysis in regional/national/international consortia.
Examples of current and completed projects:
Subcontracting
Data analysis for companies and university hospitals.
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Hundreds of completed projects
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Regular customers including top 10 pharmas and leaders in cosmetics
Funding
NEWS
July 2023
The multi-level regulation of clownfish metamorphosis by thyroid hormones.
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LATEST PUBLICATIONS
2013
Mahe, Yann F; Perez, Marie-Jesus; Tacheau, Charlotte; Fanchon, Chantal; Martin, Richard; Rousset, Françoise; Seite, Sophie
In: Clin Cosmet Investig Dermatol, vol. 6, pp. 191–196, 2013, ISSN: 1178-7015.
@article{pmid24039440,
title = {A new Vitreoscilla filiformis extract grown on spa water-enriched medium activates endogenous cutaneous antioxidant and antimicrobial defenses through a potential Toll-like receptor 2/protein kinase C, zeta transduction pathway},
author = {Yann F Mahe and Marie-Jesus Perez and Charlotte Tacheau and Chantal Fanchon and Richard Martin and Françoise Rousset and Sophie Seite},
doi = {10.2147/CCID.S47324},
issn = {1178-7015},
year = {2013},
date = {2013-01-01},
urldate = {2013-01-01},
journal = {Clin Cosmet Investig Dermatol},
volume = {6},
pages = {191--196},
abstract = {Vitreoscilla filiformis (VF) biomass (VFB) has been widely used in cosmetic preparations and shown to modulate the major inducible free-radical scavenger mitochondrial superoxide dismutase in skin cells. By adding La Roche-Posay (LRP) thermal spring water to the VF culture medium, we obtained a biomass (LRP-VFB) with a similar mitochondrial superoxide dismutase activation capacity to VF. Also, the new biomass more powerfully stimulated mRNA expression and antimicrobial peptides in reconstructed epidermis. Interestingly, a predictive computer model that analyzed transducing events within skin epidermal cells suggested that this protective activity may involve the Toll-like receptor 2/protein kinase C, zeta transduction pathway. Protein kinase C, zeta inhibition was effectively shown to abolish VFB-induced gene stimulation and confirmed this hypothesis. This thus opens new avenues for investigation into the improvement of skin homeostatic defense in relation to the control of its physiological microbiota and innate immunity.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Vitreoscilla filiformis (VF) biomass (VFB) has been widely used in cosmetic preparations and shown to modulate the major inducible free-radical scavenger mitochondrial superoxide dismutase in skin cells. By adding La Roche-Posay (LRP) thermal spring water to the VF culture medium, we obtained a biomass (LRP-VFB) with a similar mitochondrial superoxide dismutase activation capacity to VF. Also, the new biomass more powerfully stimulated mRNA expression and antimicrobial peptides in reconstructed epidermis. Interestingly, a predictive computer model that analyzed transducing events within skin epidermal cells suggested that this protective activity may involve the Toll-like receptor 2/protein kinase C, zeta transduction pathway. Protein kinase C, zeta inhibition was effectively shown to abolish VFB-induced gene stimulation and confirmed this hypothesis. This thus opens new avenues for investigation into the improvement of skin homeostatic defense in relation to the control of its physiological microbiota and innate immunity.
2012
Idbaih, Ahmed; cois Ducray, Franc; Dehais, Caroline; Courdy, Célia; Carpentier, Catherine; Bernard, Simon; Uro-Coste, Emmanuelle; Mokhtari, Karima; Jouvet, Anne; Honnorat, Jér^ome; Chinot, Olivier; Ramirez, Carole; Beauchesne, Patrick; Benouaich-Amiel, Alexandra; Godard, Jo"el; Eimer, Sandrine; Parker, Fabrice; Lechapt-Zalcman, Emmanuelle; Colin, Philippe; Loussouarn, Delphine; Faillot, Thierry; Dam-Hieu, Phong; Elouadhani-Hamdi, Selma; Bauchet, Luc; Langlois, Olivier; Guerinel, Caroline Le; Fontaine, Denys; Vauleon, Elodie; Menei, Philippe; Fotso, Marie Janette Motsuo; Desenclos, Christine; Verrelle, Pierre; cois Ghiringhelli, Franc; Noel, Georges; cois Labrousse, Franc; Carpentier, Antoine; Dhermain, Frédéric; Delattre, Jean-Yves; Figarella-Branger, Dominique; Network, POLA
SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas Journal Article
In: PLoS One, vol. 7, no. 10, pp. e45950, 2012.
@article{Idbaih2012-ur,
title = {SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas},
author = {Ahmed Idbaih and Franc cois Ducray and Caroline Dehais and Célia Courdy and Catherine Carpentier and Simon Bernard and Emmanuelle Uro-Coste and Karima Mokhtari and Anne Jouvet and Jér^ome Honnorat and Olivier Chinot and Carole Ramirez and Patrick Beauchesne and Alexandra Benouaich-Amiel and Jo"el Godard and Sandrine Eimer and Fabrice Parker and Emmanuelle Lechapt-Zalcman and Philippe Colin and Delphine Loussouarn and Thierry Faillot and Phong Dam-Hieu and Selma Elouadhani-Hamdi and Luc Bauchet and Olivier Langlois and Caroline Le Guerinel and Denys Fontaine and Elodie Vauleon and Philippe Menei and Marie Janette Motsuo Fotso and Christine Desenclos and Pierre Verrelle and Franc cois Ghiringhelli and Georges Noel and Franc cois Labrousse and Antoine Carpentier and Frédéric Dhermain and Jean-Yves Delattre and Dominique Figarella-Branger and POLA Network},
doi = {10.1371/journal.pone.0045950},
year = {2012},
date = {2012-10-01},
urldate = {2012-10-01},
journal = {PLoS One},
volume = {7},
number = {10},
pages = {e45950},
publisher = {Public Library of Science (PLoS)},
abstract = {Anaplastic oligodendrogliomas (AOD) are rare glial tumors in
adults with relative homogeneous clinical, radiological and
histological features at the time of diagnosis but dramatically
various clinical courses. Studies have identified several
molecular abnormalities with clinical or biological relevance to
AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1
mutations).To better characterize the clinical and biological
behavior of this tumor type, the creation of a national
multicentric network, named ``Prise en charge des
OLigodendrogliomes Anaplasiques (POLA),'' has been supported by
the Institut National du Cancer (InCA). Newly diagnosed and
centrally validated AOD patients and their related biological
material (tumor and blood samples) were prospectively included
in the POLA clinical database and tissue bank, respectively.At
the molecular level, we have conducted a high-resolution single
nucleotide polymorphism array analysis, which included 83
patients. Despite a careful central pathological review, AOD
have been found to exhibit heterogeneous genomic features. A
total of 82% of the tumors exhibited a 1p/19q-co-deletion,
while 18% harbor a distinct chromosome pattern. Novel focal
abnormalities, including homozygously deleted, amplified and
disrupted regions, have been identified. Recurring copy neutral
losses of heterozygosity (CNLOH) inducing the modulation of gene
expression have also been discovered. CNLOH in the CDKN2A locus
was associated with protein silencing in 1/3 of the cases. In
addition, FUBP1 homozygous deletion was detected in one case
suggesting a putative tumor suppressor role of FUBP1 in AOD.Our
study showed that the genomic and pathological analyses of AOD
are synergistic in detecting relevant clinical and biological
subgroups of AOD.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Anaplastic oligodendrogliomas (AOD) are rare glial tumors in
adults with relative homogeneous clinical, radiological and
histological features at the time of diagnosis but dramatically
various clinical courses. Studies have identified several
molecular abnormalities with clinical or biological relevance to
AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1
mutations).To better characterize the clinical and biological
behavior of this tumor type, the creation of a national
multicentric network, named ``Prise en charge des
OLigodendrogliomes Anaplasiques (POLA),'' has been supported by
the Institut National du Cancer (InCA). Newly diagnosed and
centrally validated AOD patients and their related biological
material (tumor and blood samples) were prospectively included
in the POLA clinical database and tissue bank, respectively.At
the molecular level, we have conducted a high-resolution single
nucleotide polymorphism array analysis, which included 83
patients. Despite a careful central pathological review, AOD
have been found to exhibit heterogeneous genomic features. A
total of 82% of the tumors exhibited a 1p/19q-co-deletion,
while 18% harbor a distinct chromosome pattern. Novel focal
abnormalities, including homozygously deleted, amplified and
disrupted regions, have been identified. Recurring copy neutral
losses of heterozygosity (CNLOH) inducing the modulation of gene
expression have also been discovered. CNLOH in the CDKN2A locus
was associated with protein silencing in 1/3 of the cases. In
addition, FUBP1 homozygous deletion was detected in one case
suggesting a putative tumor suppressor role of FUBP1 in AOD.Our
study showed that the genomic and pathological analyses of AOD
are synergistic in detecting relevant clinical and biological
subgroups of AOD.
adults with relative homogeneous clinical, radiological and
histological features at the time of diagnosis but dramatically
various clinical courses. Studies have identified several
molecular abnormalities with clinical or biological relevance to
AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1
mutations).To better characterize the clinical and biological
behavior of this tumor type, the creation of a national
multicentric network, named ``Prise en charge des
OLigodendrogliomes Anaplasiques (POLA),'' has been supported by
the Institut National du Cancer (InCA). Newly diagnosed and
centrally validated AOD patients and their related biological
material (tumor and blood samples) were prospectively included
in the POLA clinical database and tissue bank, respectively.At
the molecular level, we have conducted a high-resolution single
nucleotide polymorphism array analysis, which included 83
patients. Despite a careful central pathological review, AOD
have been found to exhibit heterogeneous genomic features. A
total of 82% of the tumors exhibited a 1p/19q-co-deletion,
while 18% harbor a distinct chromosome pattern. Novel focal
abnormalities, including homozygously deleted, amplified and
disrupted regions, have been identified. Recurring copy neutral
losses of heterozygosity (CNLOH) inducing the modulation of gene
expression have also been discovered. CNLOH in the CDKN2A locus
was associated with protein silencing in 1/3 of the cases. In
addition, FUBP1 homozygous deletion was detected in one case
suggesting a putative tumor suppressor role of FUBP1 in AOD.Our
study showed that the genomic and pathological analyses of AOD
are synergistic in detecting relevant clinical and biological
subgroups of AOD.
Idbaih, Ahmed; Ducray, François; Dehais, Caroline; Courdy, Célia; Carpentier, Catherine; de Bernard, Simon; Uro-Coste, Emmanuelle; Mokhtari, Karima; Jouvet, Anne; Honnorat, Jérôme; Chinot, Olivier; Ramirez, Carole; Beauchesne, Patrick; Benouaich-Amiel, Alexandra; Godard, Joël; Eimer, Sandrine; Parker, Fabrice; Lechapt-Zalcman, Emmanuelle; Colin, Philippe; Loussouarn, Delphine; Faillot, Thierry; Dam-Hieu, Phong; Elouadhani-Hamdi, Selma; Bauchet, Luc; Langlois, Olivier; Guerinel, Caroline Le; Fontaine, Denys; Vauleon, Elodie; Menei, Philippe; Fotso, Marie Janette Motsuo; Desenclos, Christine; Verrelle, Pierre; Ghiringhelli, François; Noel, Georges; Labrousse, François; Carpentier, Antoine; Dhermain, Frédéric; Delattre, Jean-Yves; Figarella-Branger, Dominique
SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas Journal Article
In: PLoS One, vol. 7, no. 10, pp. e45950, 2012, ISSN: 1932-6203.
@article{pmid23071531,
title = {SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas},
author = {Ahmed Idbaih and François Ducray and Caroline Dehais and Célia Courdy and Catherine Carpentier and Simon de Bernard and Emmanuelle Uro-Coste and Karima Mokhtari and Anne Jouvet and Jérôme Honnorat and Olivier Chinot and Carole Ramirez and Patrick Beauchesne and Alexandra Benouaich-Amiel and Joël Godard and Sandrine Eimer and Fabrice Parker and Emmanuelle Lechapt-Zalcman and Philippe Colin and Delphine Loussouarn and Thierry Faillot and Phong Dam-Hieu and Selma Elouadhani-Hamdi and Luc Bauchet and Olivier Langlois and Caroline Le Guerinel and Denys Fontaine and Elodie Vauleon and Philippe Menei and Marie Janette Motsuo Fotso and Christine Desenclos and Pierre Verrelle and François Ghiringhelli and Georges Noel and François Labrousse and Antoine Carpentier and Frédéric Dhermain and Jean-Yves Delattre and Dominique Figarella-Branger},
doi = {10.1371/journal.pone.0045950},
issn = {1932-6203},
year = {2012},
date = {2012-01-01},
urldate = {2012-01-01},
journal = {PLoS One},
volume = {7},
number = {10},
pages = {e45950},
abstract = {Anaplastic oligodendrogliomas (AOD) are rare glial tumors in adults with relative homogeneous clinical, radiological and histological features at the time of diagnosis but dramatically various clinical courses. Studies have identified several molecular abnormalities with clinical or biological relevance to AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1 mutations).To better characterize the clinical and biological behavior of this tumor type, the creation of a national multicentric network, named "Prise en charge des OLigodendrogliomes Anaplasiques (POLA)," has been supported by the Institut National du Cancer (InCA). Newly diagnosed and centrally validated AOD patients and their related biological material (tumor and blood samples) were prospectively included in the POLA clinical database and tissue bank, respectively.At the molecular level, we have conducted a high-resolution single nucleotide polymorphism array analysis, which included 83 patients. Despite a careful central pathological review, AOD have been found to exhibit heterogeneous genomic features. A total of 82% of the tumors exhibited a 1p/19q-co-deletion, while 18% harbor a distinct chromosome pattern. Novel focal abnormalities, including homozygously deleted, amplified and disrupted regions, have been identified. Recurring copy neutral losses of heterozygosity (CNLOH) inducing the modulation of gene expression have also been discovered. CNLOH in the CDKN2A locus was associated with protein silencing in 1/3 of the cases. In addition, FUBP1 homozygous deletion was detected in one case suggesting a putative tumor suppressor role of FUBP1 in AOD.Our study showed that the genomic and pathological analyses of AOD are synergistic in detecting relevant clinical and biological subgroups of AOD.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Anaplastic oligodendrogliomas (AOD) are rare glial tumors in adults with relative homogeneous clinical, radiological and histological features at the time of diagnosis but dramatically various clinical courses. Studies have identified several molecular abnormalities with clinical or biological relevance to AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1 mutations).To better characterize the clinical and biological behavior of this tumor type, the creation of a national multicentric network, named "Prise en charge des OLigodendrogliomes Anaplasiques (POLA)," has been supported by the Institut National du Cancer (InCA). Newly diagnosed and centrally validated AOD patients and their related biological material (tumor and blood samples) were prospectively included in the POLA clinical database and tissue bank, respectively.At the molecular level, we have conducted a high-resolution single nucleotide polymorphism array analysis, which included 83 patients. Despite a careful central pathological review, AOD have been found to exhibit heterogeneous genomic features. A total of 82% of the tumors exhibited a 1p/19q-co-deletion, while 18% harbor a distinct chromosome pattern. Novel focal abnormalities, including homozygously deleted, amplified and disrupted regions, have been identified. Recurring copy neutral losses of heterozygosity (CNLOH) inducing the modulation of gene expression have also been discovered. CNLOH in the CDKN2A locus was associated with protein silencing in 1/3 of the cases. In addition, FUBP1 homozygous deletion was detected in one case suggesting a putative tumor suppressor role of FUBP1 in AOD.Our study showed that the genomic and pathological analyses of AOD are synergistic in detecting relevant clinical and biological subgroups of AOD.