@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{Faugaret2014-ap,

title = {Granulomatous response to Coxiella burnetii, the agent of Q  fever: the lessons from gene expression analysis},

author = {Delphine Faugaret and Amira Ben Amara and Julie Alingrin and Aurélie Daumas and Amélie Delaby and Catherine Lépolard and Didier Raoult and Julien Textoris and Jean-Louis M`ege},

doi = {10.3389/fcimb.2014.00172},

year  = {2014},

date = {2014-12-01},

urldate = {2014-12-01},

journal = {Front. Cell. Infect. Microbiol.},

volume = {4},

pages = {172},

publisher = {Frontiers Media SA},

abstract = {The formation of granulomas is associated with the resolution of 

 Q fever, a zoonosis due to Coxiella burnetii; however the 

 molecular mechanisms of granuloma formation remain poorly 

 understood. We generated human granulomas with peripheral blood 

 mononuclear cells (PBMCs) and beads coated with C. burnetii, 

 using BCG extracts as controls. A microarray analysis showed 

 dramatic changes in gene expression in granuloma cells of which 

 more than 50% were commonly modulated genes in response to C. 

 burnetii and BCG. They included M1-related genes and genes 

 related to chemotaxis. The inhibition of the chemokines, CCL2 

 and CCL5, directly interfered with granuloma formation. C. 

 burnetii granulomas also expressed a specific transcriptional 

 profile that was essentially enriched in genes associated with 

 type I interferon response. Our results showed that granuloma 

 formation is associated with a core of transcriptional response 

 based on inflammatory genes. The specific granulomatous response 

 to C. burnetii is characterized by the activation of type 1 

 interferon pathway.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Idbaih2014-pa,

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

author = {Ahmed Idbaih and Karima Mokhtari and Jean-Franc cois Emile and Damien Galanaud and Hayat Belaid and Simon 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 Kh^e Hoang-Xuan},

doi = {10.1212/WNL.0000000000000880},

year  = {2014},

date = {2014-10-01},

urldate = {2014-10-01},

journal = {Neurology},

volume = {83},

number = {16},

pages = {1478--1480},

publisher = {Ovid Technologies (Wolters Kluwer Health)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}