@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}

}

@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}

}

@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}

}