Analyse de données omiques

@article{pmid25029475,

title = {A novel genomic signature with translational significance for human idiopathic pulmonary fibrosis},

author = {Yasmina Bauer and John Tedrow and Simon de Bernard and Magdalena Birker-Robaczewska and Kevin F Gibson and Brenda Juan Guardela and Patrick Hess and Axel Klenk and Kathleen O Lindell and Sylvie Poirey and Bérengère Renault and Markus Rey and Edgar Weber and Oliver Nayler and Naftali Kaminski},

doi = {10.1165/rcmb.2013-0310OC},

issn = {1535-4989},

year  = {2015},

date = {2015-02-01},

urldate = {2015-02-01},

journal = {Am J Respir Cell Mol Biol},

volume = {52},

number = {2},

pages = {217--231},

abstract = {The bleomycin-induced rodent lung fibrosis model is commonly used to study mechanisms of lung fibrosis and to test potential therapeutic interventions, despite the well recognized dissimilarities to human idiopathic pulmonary fibrosis (IPF). Therefore, in this study, we sought to identify genomic commonalities between the gene expression profiles from 100 IPF lungs and 108 control lungs that were obtained from the Lung Tissue Research Consortium, and rat lungs harvested at Days 3, 7, 14, 21, 28, 42, and 56 after bleomycin instillation. Surprisingly, the highest gene expression similarity between bleomycin-treated rat and IPF lungs was observed at Day 7. At this point of maximal rat-human commonality, we identified a novel set of 12 disease-relevant translational gene markers (C6, CTHRC1, CTSE, FHL2, GAL, GREM1, LCN2, MMP7, NELL1, PCSK1, PLA2G2A, and SLC2A5) that was able to separate almost all patients with IPF from control subjects in our cohort and in two additional IPF/control cohorts (GSE10667 and GSE24206). Furthermore, in combination with diffusing capacity of carbon monoxide measurements, four members of the translational gene marker set contributed to stratify patients with IPF according to disease severity. Significantly, pirfenidone attenuated the expression change of one (CTHRC1) translational gene marker in the bleomycin-induced lung fibrosis model, in transforming growth factor-β1-treated primary human lung fibroblasts and transforming growth factor-β1-treated human epithelial A549 cells. Our results suggest that a strategy focused on rodent model-human disease commonalities may identify genes that could be used to predict the pharmacological impact of therapeutic interventions, and thus facilitate the development of novel treatments for this devastating lung disease.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid25209580,

title = {Dramatic response of a BRAF V600E-mutated primary CNS histiocytic sarcoma to vemurafenib},

author = {Ahmed Idbaih and Karima Mokhtari and Jean-François Emile and Damien Galanaud and Hayat Belaid and Simon de Bernard and Neila Benameur and Vlad-Ciprian Barlog and Dimitri Psimaras and Jean Donadieu and Catherine Carpentier and Nadine Martin-Duverneuil and Julien Haroche and Loic Feuvret and Noel Zahr and Jean-Yves Delattre and Khê Hoang-Xuan},

doi = {10.1212/WNL.0000000000000880},

issn = {1526-632X},

year  = {2014},

date = {2014-10-01},

urldate = {2014-10-01},

journal = {Neurology},

volume = {83},

number = {16},

pages = {1478--1480},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid24516120,

title = {T-bet and Eomes instruct the development of two distinct natural killer cell lineages in the liver and in the bone marrow},

author = {Cécile Daussy and Fabrice Faure and Katia Mayol and Sébastien Viel and Georg Gasteiger and Emily Charrier and Jacques Bienvenu and Thomas Henry and Emilie Debien and Uzma A Hasan and Jacqueline Marvel and Keigyou Yoh and Satoru Takahashi and Immo Prinz and Simon de Bernard and Laurent Buffat and Thierry Walzer},

doi = {10.1084/jem.20131560},

issn = {1540-9538},

year  = {2014},

date = {2014-03-01},

urldate = {2014-03-01},

journal = {J Exp Med},

volume = {211},

number = {3},

pages = {563--577},

abstract = {Trail(+)DX5(-)Eomes(-) natural killer (NK) cells arise in the mouse fetal liver and persist in the adult liver. Their relationships with Trail(-)DX5(+) NK cells remain controversial. We generated a novel Eomes-GFP reporter murine model to address this question. We found that Eomes(-) NK cells are not precursors of classical Eomes(+) NK cells but rather constitute a distinct lineage of innate lymphoid cells. Eomes(-) NK cells are strictly dependent on both T-bet and IL-15, similarly to NKT cells. We observed that, in the liver, expression of T-bet in progenitors represses Eomes expression and the development of Eomes(+) NK cells. Reciprocally, the bone marrow (BM) microenvironment restricts T-bet expression in developing NK cells. Ectopic expression of T-bet forces the development of Eomes(-) NK cells, demonstrating that repression of T-bet is essential for the development of Eomes(+) NK cells. Gene profile analyses show that Eomes(-) NK cells share part of their transcriptional program with NKT cells, including genes involved in liver homing and NK cell receptors. Moreover, Eomes(-) NK cells produce a broad range of cytokines, including IL-2 and TNF in vitro and in vivo, during immune responses against vaccinia virus. Thus, mutually exclusive expression of T-bet and Eomes drives the development of different NK cell lineages with complementary functions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}