Publications and patents

We have a track-record of peer-reviewed articles and patents in the field of clinical bioinformatics.

 

Clinical

  1. Julien Laurent, Cedric Touvrey, Silke Gillessen, Magali Joffraud, Manuela Vicari, Caroline Bertrand, Stefano Ongarello, Bernd Liedert, Elisa Gallerani and Joachim Beck.
    T-cell activation by treatment of cancer patients with EMD 521873 (Selectikine), an IL-2/anti-DNA fusion protein. J Transl Med 11(5), 2013.
    URL BibTeX

    @article{laurent_t-cell_2013,
    	title = "T-cell activation by treatment of cancer patients with {EMD} 521873 (Selectikine), an {IL-2/anti-DNA} fusion protein",
    	volume = 11,
    	url = "http://www.biomedcentral.com/content/pdf/1479-5876-11-5.pdf",
    	number = 5,
    	urldate = "2014-02-13",
    	journal = "J Transl Med",
    	author = "Laurent, Julien and Touvrey, Cedric and Gillessen, Silke and Joffraud, Magali and Vicari, Manuela and Bertrand, Caroline and Ongarello, Stefano and Liedert, Bernd and Gallerani, Elisa and Beck, Joachim",
    	year = 2013
    }
    
  2. A Valsesia, A Di Cara, A Berton, V Debailleul, J Wojcik, P Farmer and C H Ladel.
    Exploratory biomarker analysis reveals a genetic epistatic interaction in interleukin 1 receptor antagonist (IL1RN) gene associated to cartilage volume growth measured by MRI in response to sprifermin therapy in patients with knee radiographic osteoarthritis. Osteoarthritis and Cartilage 21:S76–S76, 2013.
    URL, DOI BibTeX

    @article{valsesia_exploratory_2013,
    	title = "Exploratory biomarker analysis reveals a genetic epistatic interaction in interleukin 1 receptor antagonist ({IL1RN)} gene associated to cartilage volume growth measured by {MRI} in response to sprifermin therapy in patients with knee radiographic osteoarthritis",
    	volume = 21,
    	issn = "1063-4584",
    	url = "http://www.oarsijournal.com/article/S1063-4584(13)00215-X/fulltext",
    	doi = "10.1016/j.joca.2013.02.165",
    	abstract = "No abstract is available. To read the body of this article, please view the Full Text online.",
    	urldate = "2014-02-13",
    	journal = "Osteoarthritis and Cartilage",
    	author = "Valsesia, A. and Di Cara, A. and Berton, A. and Debailleul, V. and Wojcik, J. and Farmer, P. and Ladel, C. H.",
    	month = "",
    	year = 2013,
    	pages = "S76--S76",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/DAK4S3IJ/abstract.html:text/html"
    }
    
  3. Casimiro Castillejo-López, Angélica M Delgado-Vega, Jerome Wojcik, Sergey V Kozyrev, Elangovan Thavathiru, Ying-Yu Wu, Elena Sánchez, David Pöllmann, Juan R López-Egido, Serena Fineschi, Nicolás Domínguez, Rufei Lu, Judith A James, Joan T Merrill, Jennifer A Kelly, Kenneth M Kaufman, Kathy L Moser, Gary Gilkeson, Johan Frostegård, Bernardo A Pons-Estel, Sandra D'Alfonso, Torsten Witte, José Luis Callejas, John B Harley, Patrick M Gaffney, Javier Martin, Joel M Guthridge and Marta E Alarcón-Riquelme.
    Genetic and physical interaction of the B-cell systemic lupus erythematosus-associated genes BANK1 and BLK. Annals of the rheumatic diseases 71(1):136–142, 2012.
    DOI BibTeX

    @article{castillejo-lopez_genetic_2012,
    	title = "Genetic and physical interaction of the B-cell systemic lupus erythematosus-associated genes {BANK1} and {BLK}",
    	volume = 71,
    	issn = "1468-2060",
    	doi = "10.1136/annrheumdis-2011-200085",
    	abstract = "{OBJECTIVES:} Altered signalling in B cells is a predominant feature of systemic lupus erythematosus ({SLE).} The genes {BANK1} and {BLK} were recently described as associated with {SLE.} {BANK1} codes for a B-cell-specific cytoplasmic protein involved in B-cell receptor signalling and {BLK} codes for an Src tyrosine kinase with important roles in B-cell development. To characterise the role of {BANK1} and {BLK} in {SLE}, a genetic interaction analysis was performed hypothesising that genetic interactions could reveal functional pathways relevant to disease pathogenesis. {METHODS:} The {GPAT16} method was used to analyse the gene-gene interactions of {BANK1} and {BLK.} Confocal microscopy was used to investigate co-localisation, and immunoprecipitation was used to verify the physical interaction of {BANK1} and {BLK.} {RESULTS:} Epistatic interactions between {BANK1} and {BLK} polymorphisms associated with {SLE} were observed in a discovery set of 279 patients and 515 controls from northern Europe. A meta-analysis with 4399 European individuals confirmed the genetic interactions between {BANK1} and {BLK.} As {BANK1} was identified as a binding partner of the Src tyrosine kinase {LYN}, the possibility that {BANK1} and {BLK} could also show a protein-protein interaction was tested. The co-immunoprecipitation and co-localisation of {BLK} and {BANK1} were demonstrated. In a Daudi cell line and primary naive B cells endogenous binding was enhanced upon B-cell receptor stimulation using anti-{IgM} antibodies. {CONCLUSION:} This study shows a genetic interaction between {BANK1} and {BLK}, and demonstrates that these molecules interact physically. The results have important consequences for the understanding of {SLE} and other autoimmune diseases and identify a potential new signalling pathway.",
    	language = "eng",
    	number = 1,
    	journal = "Annals of the rheumatic diseases",
    	author = "Castillejo-López, Casimiro and Delgado-Vega, Angélica M and Wojcik, Jerome and Kozyrev, Sergey V and Thavathiru, Elangovan and Wu, Ying-Yu and Sánchez, Elena and Pöllmann, David and López-Egido, Juan R and Fineschi, Serena and Domínguez, Nicolás and Lu, Rufei and James, Judith A and Merrill, Joan T and Kelly, Jennifer A and Kaufman, Kenneth M and Moser, Kathy L and Gilkeson, Gary and Frostegård, Johan and Pons-Estel, Bernardo A and {D'Alfonso}, Sandra and Witte, Torsten and Callejas, José Luis and Harley, John B and Gaffney, Patrick M and Martin, Javier and Guthridge, Joel M and Alarcón-Riquelme, Marta E",
    	month = "",
    	year = 2012,
    	note = "{PMID:} 21978998 {PMCID:} {PMC3268679}",
    	keywords = "Adaptor Proteins, Signal Transducing, B-Lymphocytes, Case-Control Studies, Epistasis, Genetic, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Lupus Erythematosus, Systemic, Male, Membrane Proteins, Polymorphism, Single Nucleotide, Protein Binding, Signal Transduction, src-Family Kinases",
    	pages = "136--142",
    	file = "2011_SLEinteraction_AnnRheumDis.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/IIC29G98/2011_SLEinteraction_AnnRheumDis.pdf:application/pdf"
    }
    
  4. F Martinelli-Boneschi, F Esposito, P Brambilla, E Lindstrom, G Lavorgna, J Stankovich, M Rodegher, R Capra, A Ghezzi, G Coniglio, B Colombo, M Sorosina, V Martinelli, D Booth, A B Oturai, G Stewart, H F Harbo, T J Kilpatrick, J Hillert, J P Rubio, H Abderrahim, J Wojcik and G Comi.
    A genome-wide association study in progressive multiple sclerosis. Multiple Sclerosis Journal 18(10):1384–1394, 2012.
    URL, DOI BibTeX

    @article{martinelli-boneschi_genome-wide_2012,
    	title = "A genome-wide association study in progressive multiple sclerosis",
    	volume = 18,
    	issn = "1352-4585, 1477-0970",
    	url = "http://msj.sagepub.com/cgi/doi/10.1177/1352458512439118",
    	doi = "10.1177/1352458512439118",
    	number = 10,
    	urldate = "2014-02-13",
    	journal = "Multiple Sclerosis Journal",
    	author = "Martinelli-Boneschi, F. and Esposito, F. and Brambilla, P. and Lindstrom, E. and Lavorgna, G. and Stankovich, J. and Rodegher, M. and Capra, R. and Ghezzi, A. and Coniglio, G. and Colombo, B. and Sorosina, M. and Martinelli, V. and Booth, D. and Oturai, A. B. and Stewart, G. and Harbo, H. F. and Kilpatrick, T. J. and Hillert, J. and Rubio, J. P. and Abderrahim, H. and Wojcik, J. and Comi, G.",
    	month = "",
    	year = 2012,
    	pages = "1384--1394",
    	file = "2012_MSPP_MultipleSclerosis.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/8GW6WERK/2012_MSPP_MultipleSclerosis.pdf:application/pdf"
    }
    
  5. Federica Esposito, Jerome Wojcik, Mariaemma Rodegher, Marta Radaelli, Lucia Moiola, Angelo Ghezzi, Ruggero Capra, Paola Brambilla, Melissa Sorosina, Giacomo Giacalone, Vittorio Martinelli, Giancarlo Comi, Hadi Abderrahim and Filippo Martinelli Boneschi.
    MGAT5 and disease severity in progressive multiple sclerosis. Journal of neuroimmunology 230(1-2):143–147, January 2011.
    DOI BibTeX

    @article{esposito_mgat5_2011,
    	title = "{MGAT5} and disease severity in progressive multiple sclerosis",
    	volume = 230,
    	issn = "1872-8421",
    	doi = "10.1016/j.jneuroim.2010.10.026",
    	abstract = "{MGAT5} was demonstrated to be associated to multiple sclerosis ({MS)} severity. We evaluated its role in progressive {MS.} We studied 11 {SNPs} mapping to {MGAT5} in an Italian cohort of primary progressive or progressive-relapsing patients. The rs1257169(G) allele is associated with lower disease severity (p-value = 0.02). Adding the age of onset as covariate, another {SNP}, rs539588, is nominally significant. None of the {SNPs} survived after multiple testing correction. These results, even if suggestive of {MGAT5} involvement also in progressive {MS} severity, require a bigger sample size to confirm and better explore the role of this locus in this rare disease course.",
    	language = "eng",
    	number = "1-2",
    	journal = "Journal of neuroimmunology",
    	author = "Esposito, Federica and Wojcik, Jerome and Rodegher, Mariaemma and Radaelli, Marta and Moiola, Lucia and Ghezzi, Angelo and Capra, Ruggero and Brambilla, Paola and Sorosina, Melissa and Giacalone, Giacomo and Martinelli, Vittorio and Comi, Giancarlo and Abderrahim, Hadi and Martinelli Boneschi, Filippo",
    	month = "jan",
    	year = 2011,
    	note = "{PMID:} 21115203",
    	keywords = "Adult, Age of Onset, Disease Progression, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Multiple Sclerosis, N-Acetylglucosaminyltransferases, Nerve Tissue Proteins, Polymorphism, Single Nucleotide",
    	pages = "143--147",
    	file = "2010_MGAT5PP_JNeuroimmunology.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/6SK683VK/2010_MGAT5PP_JNeuroimmunology.pdf:application/pdf"
    }
    
  6. R F Vollenhoven, N Kinnman, E Vincent, S Wax and J Bathon.
    Atacicept in patients with rheumatoid arthritis and an inadequate response to methotrexate: results of a phase II, randomized, placebo-controlled trial. Arthritis and rheumatism 63(7):1782–1792, 2011.
    DOI BibTeX

    @article{van_vollenhoven_atacicept_2011,
    	title = "Atacicept in patients with rheumatoid arthritis and an inadequate response to methotrexate: results of a phase {II}, randomized, placebo-controlled trial",
    	volume = 63,
    	issn = "1529-0131",
    	shorttitle = "Atacicept in patients with rheumatoid arthritis and an inadequate response to methotrexate",
    	doi = "10.1002/art.30372",
    	abstract = "{OBJECTIVE:} To assess the efficacy, safety, and biologic activity of atacicept in tumor necrosis factor antagonist-naive patients with rheumatoid arthritis ({RA)} in whom the response to methotrexate treatment was inadequate. {METHODS:} In this phase {II} study, patients with active {RA} (n = 311) were randomized 1:1:1:1 to receive placebo, atacicept 150 mg weekly with or without a 4-week loading period (twice-weekly dosing), or open-label adalimumab 40 mg every other week, for 25 weeks. The primary end point was 20\% improvement in disease severity according to the American College of Rheumatology criteria, assessed using the C-reactive protein level ({ACR20-CRP)}, at week 26. Secondary end points included additional assessments of efficacy, biologic activity, and safety. {RESULTS:} The proportion of patients meeting the primary end point ({ACR20-CRP} response) did not differ significantly in the atacicept groups and the placebo group (46\% in the placebo group, 45\% in the atacicept loading group, and 58\% in the atacicept nonloading group). In contrast, an {ACR20-CRP} response was observed in 71\% of patients in the adalimumab group (P {\textless} 0.001 versus placebo). {ACR50-CRP} response rates were significantly higher in all active-treatment groups compared with placebo, but {ACR70-CRP} response rates were superior only in the adalimumab group. Atacicept treatment reduced the levels of serum {IgG}, {IgA}, and {IgM} rheumatoid factor and the levels of circulating mature B cells and plasma cells. The effects of treatment were similar with and without loading. Immunoglobulin levels returned toward baseline values during the treatment-free followup period (week 38). The most frequent adverse events associated with atacicept represented common illnesses. No serious infections occurred among patients treated with atacicept. {CONCLUSION:} The primary end point ({ACR20-CRP} response) was not met despite significant biologic effects of atacicept that were consistent with its proposed mechanism of action. Modest effects of atacicept were seen for some secondary efficacy end points. Treatment with atacicept raised no new safety concerns.",
    	language = "eng",
    	number = 7,
    	journal = "Arthritis and rheumatism",
    	author = "van Vollenhoven, R F and Kinnman, N and Vincent, E and Wax, S and Bathon, J",
    	month = "",
    	year = 2011,
    	note = "{PMID:} 21452294",
    	keywords = "Adult, Aged, Antirheumatic Agents, Arthritis, Rheumatoid, Double-Blind Method, Female, Flow Cytometry, Humans, Intention to Treat Analysis, Male, Methotrexate, Middle Aged, Odds Ratio, Recombinant Fusion Proteins, Treatment Outcome",
    	pages = "1782--1792"
    }
    
  7. Pratyaksha Wirapati, Karl Forner, Angelica Delgado-Vega, Marta Alarcón-Riquelme, Mauro Delorenzi and Jérôme Wojcik.
    Detecting epistasis with restricted response patterns in pairs of biallelic loci. Annals of human genetics 75(1):133–145, January 2011.
    DOI BibTeX

    @article{wirapati_detecting_2011,
    	title = "Detecting epistasis with restricted response patterns in pairs of biallelic loci",
    	volume = 75,
    	issn = "1469-1809",
    	doi = "10.1111/j.1469-1809.2010.00625.x",
    	abstract = "Well-established examples of genetic epistasis between a pair of loci typically show characteristic patterns of phenotypic distributions in joint genotype tables. However, inferring epistasis given such data is difficult due to the lack of power in commonly used approaches, which decompose the epistatic patterns into main plus interaction effects followed by testing the interaction term. Testing additive-only or all terms may have more power, but they are sensitive to nonepistatic patterns. Alternatively, the epistatic patterns of interest can be enumerated and the best matching one is found by searching through the possibilities. Although this approach requires multiple testing correction over possible patterns, each pattern can be fitted with a regression model with just one degree of freedom and thus the overall power can still be high, if the number of possible patterns is limited. Here we compare the power of the linear decomposition and pattern search methods, by applying them to simulated data generated under several patterns of joint genotype effects with simple biological interpretations. Interaction-only tests are the least powerful; while pattern search approach is the most powerful if the range of possibilities is restricted, but still includes the true pattern.",
    	language = "eng",
    	number = 1,
    	journal = "Annals of human genetics",
    	author = "Wirapati, Pratyaksha and Forner, Karl and Delgado-Vega, Angelica and Alarcón-Riquelme, Marta and Delorenzi, Mauro and Wojcik, Jérôme",
    	month = "jan",
    	year = 2011,
    	note = "{PMID:} 21118193",
    	keywords = "Epistasis, Genetic, Humans, Models, Genetic, Polymorphism, Single Nucleotide, Quantitative Trait Loci",
    	pages = "133--145",
    	file = "2010_Epistasis_AnnalsHumanGenetics.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/DZT4SJUF/2010_Epistasis_AnnalsHumanGenetics.pdf:application/pdf"
    }
    
  8. B Brynedal, J Wojcik, F Esposito, V Debailleul, J Yaouanq, F Martinelli-Boneschi, G Edan, G Comi, J Hillert and H Abderrahim.
    MGAT5 alters the severity of multiple sclerosis. Journal of neuroimmunology 220(1-2):120–124, March 2010.
    DOI BibTeX

    @article{brynedal_mgat5_2010,
    	title = "{MGAT5} alters the severity of multiple sclerosis",
    	volume = 220,
    	issn = "1872-8421",
    	doi = "10.1016/j.jneuroim.2010.01.003",
    	abstract = "Multiple Sclerosis ({MS)} is a genetically complex immune mediated, demyelinating disease of the central nervous system. To date no genetic variants have been unambiguously linked to disease severity. We have conducted a genome wide screen, using Affymetrix Genechip {500K} technology, for severity in 1040 {MS} patients. Two markers within {MGAT5}, a gene coding for a glycosylation enzyme, were found to be significantly associated with outcome in the screening as well as in an independent population (combined p-values: 2.8 x 10(-6) and 1.5 x 10(-7)).",
    	language = "eng",
    	number = "1-2",
    	journal = "Journal of neuroimmunology",
    	author = "Brynedal, B and Wojcik, J and Esposito, F and Debailleul, V and Yaouanq, J and Martinelli-Boneschi, F and Edan, G and Comi, G and Hillert, J and Abderrahim, H",
    	month = "mar",
    	year = 2010,
    	note = "{PMID:} 20117844",
    	keywords = "Adult, Cohort Studies, Disability Evaluation, {DNA} Mutational Analysis, Europe, Female, Genetic Markers, Genetic Predisposition to Disease, Genetic Testing, Genetic Variation, Genome, Genome-Wide Association Study, Genotype, Glycosylation, Humans, Male, Multiple Sclerosis, N-Acetylglucosaminyltransferases, Nerve Tissue Proteins, Oligonucleotide Array Sequence Analysis, Severity of Illness Index",
    	pages = "120--124",
    	file = "2010_MSseverityscanMGAT5_JNeuroimmunology.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/VFHQ2B44/2010_MSseverityscanMGAT5_JNeuroimmunology.pdf:application/pdf"
    }
    
  9. D Colleselli, A E Pelzer, E Steiner, S Ongarello, G Schaefer, G Bartsch and C Schwentner.
    Upgrading of Gleason score 6 prostate cancers on biopsy after prostatectomy in the low and intermediate tPSA range. Prostate cancer and prostatic diseases 13(2):182–185, 2010.
    DOI BibTeX

    @article{colleselli_upgrading_2010,
    	title = "Upgrading of Gleason score 6 prostate cancers on biopsy after prostatectomy in the low and intermediate {tPSA} range",
    	volume = 13,
    	issn = "1476-5608",
    	doi = "10.1038/pcan.2009.54",
    	abstract = "When offering watchful waiting or active monitoring protocols to prostate cancer ({PCa)} patients, differentiation between Gleason scores ({GS)} 6 and 7 at biopsy is important. However, upgrading after prostatectomy is common. We investigated the impact of different {PSA} levels on misclassification in the {PSA} range of 2-3.9 and 4-10 ng ml(-1). A total of 448 patients with {GS} 6 {PCa} on prostate biopsy were evaluated by comparing biopsy and prostatectomy {GS.} Possible over diagnosis was defined as {GS} {\textless}7, pathological stage {pT2a} and negative surgical margins, and possible under diagnosis was defined as {pT3a} or greater, or positive surgical margins; the percentage of over- or under diagnosis was determined for correctly and upgraded tumors after prostatectomy. A match between biopsy and prostatectomy {GS} was found in 210 patients (46.9\%). Patients in the {PSA} range of 2.0-3.9 and 4.0-10.0 ng ml(-1) were upgraded in 32.6 and 44.0\%, respectively. Over diagnosis was more common than under diagnosis (23.2\% vs 15.6\%). When upgraded there was a significant increase in under diagnosis. As almost 40\% of {GS} 6 tumors on biopsy are {GS} 7 or higher after surgery with a significant rise in under diagnosis there is a risk of misclassification and subsequent delayed or even insufficient treatment, when relying on favorable biopsy {GS.}",
    	language = "eng",
    	number = 2,
    	journal = "Prostate cancer and prostatic diseases",
    	author = "Colleselli, D and Pelzer, A E and Steiner, E and Ongarello, S and Schaefer, G and Bartsch, G and Schwentner, C",
    	month = "",
    	year = 2010,
    	note = "{PMID:} 20029401",
    	keywords = "Adult, Aged, Biopsy, Diagnostic Errors, Humans, Male, Middle Aged, Neoplasm Staging, Prostate-Specific Antigen, Prostatectomy, Prostatic Neoplasms",
    	pages = "182--185"
    }
    
  10. Rosanna Pescini Gobert, Lara Joubert, Marie-Laure Curchod, Catherine Salvat, Isabelle Foucault, Catherine Jorand-Lebrun, Marc Lamarine, Hélène Peixoto, Chloé Vignaud, Christèle Frémaux, Thérèse Jomotte, Bernard Françon, Chantal Alliod, Lilia Bernasconi, Hadi Abderrahim, Dominique Perrin, Agnes Bombrun, Francisca Zanoguera, Christian Rommel and Rob Hooft van Huijsduijnen.
    Convergent functional genomics of oligodendrocyte differentiation identifies multiple autoinhibitory signaling circuits. Molecular and cellular biology 29(6):1538–1553, March 2009.
    DOI BibTeX

    @article{gobert_convergent_2009,
    	title = "Convergent functional genomics of oligodendrocyte differentiation identifies multiple autoinhibitory signaling circuits",
    	volume = 29,
    	issn = "1098-5549",
    	doi = "10.1128/MCB.01375-08",
    	abstract = "Inadequate remyelination of brain white matter lesions has been associated with a failure of oligodendrocyte precursors to differentiate into mature, myelin-producing cells. In order to better understand which genes play a critical role in oligodendrocyte differentiation, we performed time-dependent, genome-wide gene expression studies of mouse Oli-neu cells as they differentiate into process-forming and myelin basic protein-producing cells, following treatment with three different agents. Our data indicate that different inducers activate distinct pathways that ultimately converge into the completely differentiated state, where regulated gene sets overlap maximally. In order to also gain insight into the functional role of genes that are regulated in this process, we silenced 88 of these genes using small interfering {RNA} and identified multiple repressors of spontaneous differentiation of Oli-neu, most of which were confirmed in rat primary oligodendrocyte precursors cells. Among these repressors were {CNP}, a well-known myelin constituent, and three phosphatases, each known to negatively control mitogen-activated protein kinase cascades. We show that a novel inhibitor for one of the identified genes, dual-specificity phosphatase {DUSP10/MKP5}, was also capable of inducing oligodendrocyte differentiation in primary oligodendrocyte precursors. Oligodendrocytic differentiation feedback loops may therefore yield pharmacological targets to treat disease related to dysfunctional myelin deposition.",
    	language = "eng",
    	number = 6,
    	journal = "Molecular and cellular biology",
    	author = "Gobert, Rosanna Pescini and Joubert, Lara and Curchod, Marie-Laure and Salvat, Catherine and Foucault, Isabelle and Jorand-Lebrun, Catherine and Lamarine, Marc and Peixoto, Hélène and Vignaud, Chloé and Frémaux, Christèle and Jomotte, Thérèse and Françon, Bernard and Alliod, Chantal and Bernasconi, Lilia and Abderrahim, Hadi and Perrin, Dominique and Bombrun, Agnes and Zanoguera, Francisca and Rommel, Christian and Hooft van Huijsduijnen, Rob",
    	month = "mar",
    	year = 2009,
    	note = "{PMID:} 19139271 {PMCID:} {PMC2648232}",
    	keywords = "Animals, Cell Differentiation, Cells, Cultured, Colforsin, Dexamethasone, Dual-Specificity Phosphatases, Gene Regulatory Networks, Gene Silencing, Genome-Wide Association Study, Mice, Myelin Basic Protein, Neurogenesis, Oligodendroglia, Rats, Signal Transduction, Tretinoin",
    	pages = "1538--1553"
    }
    
  11. A-K Abelson, A M Delgado-Vega, S V Kozyrev, E Sánchez, R Velázquez-Cruz, N Eriksson, J Wojcik, M V P Linga Reddy, G Lima, S D'Alfonso, S Migliaresi, V Baca, L Orozco, T Witte, N Ortego-Centeno, AADEA group, H Abderrahim, B A Pons-Estel, C Gutiérrez, A Suárez, M F González-Escribano, J Martin and M E Alarcón-Riquelme.
    STAT4 associates with systemic lupus erythematosus through two independent effects that correlate with gene expression and act additively with IRF5 to increase risk. Annals of the rheumatic diseases 68(11):1746–1753, 2009.
    DOI BibTeX

    @article{abelson_stat4_2009,
    	title = "{STAT4} associates with systemic lupus erythematosus through two independent effects that correlate with gene expression and act additively with {IRF5} to increase risk",
    	volume = 68,
    	issn = "1468-2060",
    	doi = "10.1136/ard.2008.097642",
    	abstract = "{OBJECTIVES:} To confirm and define the genetic association of {STAT4} and systemic lupus erythematosus ({SLE)}, investigate the possibility of correlations with differential splicing and/or expression levels, and genetic interaction with {IRF5.} {METHODS:} 30 tag {SNPs} were genotyped in an independent set of Spanish cases and controls. {SNPs} surviving correction for multiple tests were genotyped in five new sets of cases and controls for replication. {STAT4} {cDNA} was analysed by 5'-{RACE} {PCR} and sequencing. Expression levels were measured by quantitative {PCR.} {RESULTS:} In the fine mapping, four {SNPs} were significant after correction for multiple testing, with rs3821236 and rs3024866 as the strongest signals, followed by the previously associated rs7574865, and by rs1467199. Association was replicated in all cohorts. After conditional regression analyses, two major independent signals, represented by {SNPs} rs3821236 and rs7574865, remained significant across the sets. These {SNPs} belong to separate haplotype blocks. High levels of {STAT4} expression correlated with {SNPs} rs3821236, rs3024866 (both in the same haplotype block) and rs7574865 but not with other {SNPs.} Transcription of alternative tissue-specific exons 1, indicating the presence of tissue-specific promoters of potential importance in the expression of {STAT4}, was also detected. No interaction with associated {SNPs} of {IRF5} was observed using regression analysis. {CONCLUSIONS:} These data confirm {STAT4} as a susceptibility gene for {SLE} and suggest the presence of at least two functional variants affecting levels of {STAT4.} The results also indicate that the genes {STAT4} and {IRF5} act additively to increase the risk for {SLE.}",
    	language = "eng",
    	number = 11,
    	journal = "Annals of the rheumatic diseases",
    	author = "Abelson, A-K and Delgado-Vega, A M and Kozyrev, S V and Sánchez, E and Velázquez-Cruz, R and Eriksson, N and Wojcik, J and Linga Reddy, M V P and Lima, G and {D'Alfonso}, S and Migliaresi, S and Baca, V and Orozco, L and Witte, T and Ortego-Centeno, N and {{AADEA} group} and Abderrahim, H and Pons-Estel, B A and Gutiérrez, C and Suárez, A and González-Escribano, M F and Martin, J and Alarcón-Riquelme, M E",
    	month = "",
    	year = 2009,
    	note = "{PMID:} 19019891 {PMCID:} {PMC3878433}",
    	keywords = "Adult, Alternative Splicing, Case-Control Studies, Child, Gene Expression Regulation, Genetic Predisposition to Disease, Genotype, Humans, Interferon Regulatory Factors, Lupus Erythematosus, Systemic, Polymorphism, Single Nucleotide, {RNA}, Messenger, {STAT4} Transcription Factor",
    	pages = "1746--1753",
    	file = "2009_STAT4_AnnRheumDis.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/UNNZR2P3/2009_STAT4_AnnRheumDis.pdf:application/pdf"
    }
    
  12. Alexandre E Pelzer, Daniela Colleselli, Jasmin Bektic, Georg Schaefer, Stefano Ongarello, Christian Schwentner, Leo Pallwein, Michael Mitterberger, Eberhard Steiner, Georg Bartsch and Wolfgang Horninger.
    Clinical and pathological features of screen vs non-screen-detected prostate cancers: is there a difference?. BJU international 102(1):24–27, July 2008.
    DOI BibTeX

    @article{pelzer_clinical_2008,
    	title = "Clinical and pathological features of screen vs non-screen-detected prostate cancers: is there a difference?",
    	volume = 102,
    	issn = "1464-{410X}",
    	shorttitle = "Clinical and pathological features of screen vs non-screen-detected prostate cancers",
    	doi = "10.1111/j.1464-410X.2008.07566.x",
    	abstract = "{OBJECTIVE:} To evaluate the clinical and pathological characteristics of screen vs non-screen-detected prostate cancers, to determine if there is a difference in the same prostate-specific antigen ({PSA)} range. {PATIENTS} {AND} {METHODS:} In all, 997 patients who had had a radical prostatectomy were evaluated; 806 were Tyrolean screening volunteers, and 191 were from outside Tyrol, representing the 'referred prostate cancer' group. {PSA} level, age, prostate volume and pathological characteristics were assessed, as was the amount of over- and under-diagnosis. {RESULTS:} There were no statistically significant differences in patient age or {PSA} levels in the two groups. Even in the same {PSA} range there were statistically significantly more extraprostatic cancers in the referral group, at 31.7\% and 17.4\%, respectively. In the referred and screening groups there was over-diagnosis in 7.9\% and 16.8\%, and under-diagnosis in 40.8\% and 27.8\%, respectively. {CONCLUSION:} This study suggests that screening volunteers have a statistically significantly higher rate of organ-confined prostate cancers, and a statistically significantly lower rate of extracapsular extension and positive surgical margins than their counterparts in the referral group even in the same {PSA} range. As the pathological stage and surgical margin status are significant predictors of recurrence, these findings support the concept of {PSA} screening.",
    	language = "eng",
    	number = 1,
    	journal = "{BJU} international",
    	author = "Pelzer, Alexandre E and Colleselli, Daniela and Bektic, Jasmin and Schaefer, Georg and Ongarello, Stefano and Schwentner, Christian and Pallwein, Leo and Mitterberger, Michael and Steiner, Eberhard and Bartsch, Georg and Horninger, Wolfgang",
    	month = "jul",
    	year = 2008,
    	note = "{PMID:} 18341623",
    	keywords = "Aged, Austria, Cohort Studies, Early Diagnosis, Humans, Male, Mass Screening, Middle Aged, Neoplasm Staging, Program Evaluation, Prostate-Specific Antigen, Prostatectomy, Prostatic Neoplasms",
    	pages = "24--27"
    }
    
  13. Alexandre E Pelzer, Daniela Colleselli, Jasmin Bektic, Eberhard Steiner, Reinhold Ramoner, Michael Mitterberger, Christian Schwentner, Georg Schaefer, Stefano Ongarello, Georg Bartsch and Wolfgang Horninger.
    Pathological features of Gleason score 6 prostate cancers in the low and intermediate range of prostate-specific antigen level: is there a difference?. BJU international 101(7):822–825, April 2008.
    DOI BibTeX

    @article{pelzer_pathological_2008,
    	title = "Pathological features of Gleason score 6 prostate cancers in the low and intermediate range of prostate-specific antigen level: is there a difference?",
    	volume = 101,
    	issn = "1464-{410X}",
    	shorttitle = "Pathological features of Gleason score 6 prostate cancers in the low and intermediate range of prostate-specific antigen level",
    	doi = "10.1111/j.1464-410X.2008.07454.x",
    	abstract = "{OBJECTIVE:} To assess the pathological features of Gleason score 6 prostate cancers after radical prostatectomy in the low ({\textless}4 {ng/mL)} and intermediate range of prostate-specific antigen level (4-10 {ng/mL)}, as such prostate cancers are considered to be well differentiated tumours with a low risk for recurrence after therapy. {PATIENTS} {AND} {METHODS:} In all, 1354 patients with T1c prostate cancer and {PSA} levels of {\textless}10.0 {ng/mL} had a radical retropubic prostatectomy. Patients with Gleason score 6 tumours were divided into two groups, those with {PSA} levels of {\textless}4 and 4.0-10.0 {ng/mL.} Extracapsular extension, positive surgical margins, biochemical recurrence ({BCR)} and mean time to {BCR} were evaluated. {RESULTS:} Of the 1354 patients, there were 437 (32.3\%) with Gleason score 6 prostate cancers. Patients in the low {PSA} group had less extraprostatic disease than those with a higher level (5.9\% vs 14.5\%) and both groups had an almost equal proportion of positive surgical margins (9.4\% vs 11.0\%). In the low {PSA} group there was statistically significantly shorter {BCR} than in the high {PSA} group, with a mean time to {BCR} of 1.7 vs 3.1 years. {CONCLUSIONS:} These results show a statistically significantly higher rate of extraprostatic disease and earlier {BCR} in men with a high than a low {PSA} level even in Gleason score 6 prostate cancer. As the rate of {BCR} and extracapsular extension are significantly related to prostate cancer mortality, these findings further support the concept of screening using low {PSA} levels.",
    	language = "eng",
    	number = 7,
    	journal = "{BJU} international",
    	author = "Pelzer, Alexandre E and Colleselli, Daniela and Bektic, Jasmin and Steiner, Eberhard and Ramoner, Reinhold and Mitterberger, Michael and Schwentner, Christian and Schaefer, Georg and Ongarello, Stefano and Bartsch, Georg and Horninger, Wolfgang",
    	month = "apr",
    	year = 2008,
    	note = "{PMID:} 18261154",
    	keywords = "Adult, Aged, Biopsy, Humans, Male, Middle Aged, Neoplasm Recurrence, Local, Neoplasm Staging, Prostate, Prostate-Specific Antigen, Prostatectomy, Prostatic Neoplasms",
    	pages = "822--825"
    }
    
  14. Sergey V Kozyrev, Anna-Karin Abelson, Jerome Wojcik, Ammar Zaghlool, Prasad M V Linga Reddy, Elena Sanchez, Iva Gunnarsson, Elisabet Svenungsson, Gunnar Sturfelt, Andreas Jönsen, Lennart Truedsson, Bernardo A Pons-Estel, Torsten Witte, Sandra D'Alfonso, Nadia Barizzone, Nadia Barrizzone, Maria Giovanna Danieli, Carmen Gutierrez, Ana Suarez, Peter Junker, Helle Laustrup, Maria Francisca González-Escribano, Javier Martin, Hadi Abderrahim and Marta E Alarcón-Riquelme.
    Functional variants in the B-cell gene BANK1 are associated with systemic lupus erythematosus. Nature genetics 40(2):211–216, 2008.
    DOI BibTeX

    @article{kozyrev_functional_2008,
    	title = "Functional variants in the B-cell gene {BANK1} are associated with systemic lupus erythematosus",
    	volume = 40,
    	issn = "1546-1718",
    	doi = "10.1038/ng.79",
    	abstract = "Systemic lupus erythematosus ({SLE)} is a prototypical autoimmune disease characterized by production of autoantibodies and complex genetic inheritance. In a genome-wide scan using 85,042 {SNPs}, we identified an association between {SLE} and a nonsynonymous substitution (rs10516487, {R61H)} in the B-cell scaffold protein with ankyrin repeats gene, {BANK1.} We replicated the association in four independent case-control sets (combined P = 3.7 x 10(-10); {OR} = 1.38). We analyzed {BANK1} {cDNA} and found two isoforms, one full-length and the other alternatively spliced and lacking exon 2 (Delta2), encoding a protein without a putative {IP3R-binding} domain. The transcripts were differentially expressed depending on a branch point-site {SNP}, rs17266594, in strong linkage disequilibrium ({LD)} with rs10516487. A third associated variant was found in the ankyrin domain (rs3733197, {A383T).} Our findings implicate {BANK1} as a susceptibility gene for {SLE}, with variants affecting regulatory sites and key functional domains. The disease-associated variants could contribute to sustained B cell-receptor signaling and B-cell hyperactivity characteristic of this disease.",
    	language = "eng",
    	number = 2,
    	journal = "Nature genetics",
    	author = "Kozyrev, Sergey V and Abelson, Anna-Karin and Wojcik, Jerome and Zaghlool, Ammar and Linga Reddy, M V Prasad and Sanchez, Elena and Gunnarsson, Iva and Svenungsson, Elisabet and Sturfelt, Gunnar and Jönsen, Andreas and Truedsson, Lennart and Pons-Estel, Bernardo A and Witte, Torsten and {D'Alfonso}, Sandra and Barizzone, Nadia and Barrizzone, Nadia and Danieli, Maria Giovanna and Gutierrez, Carmen and Suarez, Ana and Junker, Peter and Laustrup, Helle and González-Escribano, Maria Francisca and Martin, Javier and Abderrahim, Hadi and Alarcón-Riquelme, Marta E",
    	month = "",
    	year = 2008,
    	note = "{PMID:} 18204447",
    	keywords = "Adaptor Proteins, Signal Transducing, Alleles, Alternative Splicing, Amino Acid Motifs, Amino Acid Sequence, Amino Acid Substitution, Ankyrin Repeat, B-Lymphocytes, Case-Control Studies, Chromosomes, Human, Cohort Studies, {DNA}, Complementary, Exons, Gene Deletion, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Genome, Human, Haplotypes, Histidine, Humans, Introns, Linkage Disequilibrium, Logistic Models, Lupus Erythematosus, Systemic, Membrane Proteins, Molecular Sequence Data, Physical Chromosome Mapping, Polymorphism, Single Nucleotide, Protein Isoforms, Protein Structure, Tertiary, Sequence Analysis, {DNA}, Sweden",
    	pages = "211--216",
    	file = "2008_BANK1_NatureGenetics.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/MBRUTQXU/2008_BANK1_NatureGenetics.pdf:application/pdf"
    }
    
  15. Alexandre E Pelzer, Daniela Colleselli, Jasmin Bektic, Georg Schaefer, Stefano Ongarello, Christian Schwentner, Fritz Aigner, Michael Mitterberger, Eberhard Steiner, Georg Bartsch and Wolfgang Horninger.
    Over-diagnosis and under-diagnosis of screen- vs non-screen-detected prostate cancers with in men with prostate-specific antigen levels of 2.0-10.0 ng/mL. BJU international 101(10):1223–1226, 2008.
    DOI BibTeX

    @article{pelzer_over-diagnosis_2008,
    	title = "Over-diagnosis and under-diagnosis of screen- vs non-screen-detected prostate cancers with in men with prostate-specific antigen levels of 2.0-10.0 {ng/mL}",
    	volume = 101,
    	issn = "1464-{410X}",
    	doi = "10.1111/j.1464-410X.2007.07367.x",
    	abstract = "{OBJECTIVES:} To evaluate possible over- and under-diagnosis of prostate cancer in a screened vs a referral population in the same range of prostate-specific antigen ({PSA).} {PATIENTS} {AND} {METHODS:} In all, 1445 patients undergoing radical prostatectomy and with a {PSA} level of {\textless}10 {ng/mL} were evaluated; 237 were from outside Tyrol (Austria) and represented the unscreened group, and 1208 were Tyrolean screening volunteers. Over-diagnosis was defined as a pathological stage of {pT2a} and a Gleason score of {\textless}7 with no positive surgical margins. Under-diagnosis was defined as a pathological stage of {\textgreater}{or=pT3a} or positive surgical margins. The chi-square test was used to assess the differences, with P {\textless} 0.05 considered to indicate statistical significance. {RESULTS:} There were no significant differences in patient age or {PSA} levels between the study groups. There was over-diagnosis in the screening and referral groups in 17.4\% and 8.9\%, respectively, and under-diagnosis in 18.6\% and 42.2\%, respectively. {CONCLUSION:} This study suggests that patients with prostate cancer participating in a screening programme are less likely to be under-diagnosed or have extracapsular disease than their counterparts in a referral population, even in the same {PSA} range, after radical prostatectomy. Furthermore, there was more under-diagnosis in the referral group than over-diagnosis in the screened group.",
    	language = "eng",
    	number = 10,
    	journal = "{BJU} international",
    	author = "Pelzer, Alexandre E and Colleselli, Daniela and Bektic, Jasmin and Schaefer, Georg and Ongarello, Stefano and Schwentner, Christian and Aigner, Fritz and Mitterberger, Michael and Steiner, Eberhard and Bartsch, Georg and Horninger, Wolfgang",
    	month = "",
    	year = 2008,
    	note = "{PMID:} 18190631",
    	keywords = "Adult, Aged, Austria, Humans, Male, Mass Screening, Middle Aged, Prostate-Specific Antigen, Prostatectomy, Prostatic Neoplasms, Referral and Consultation",
    	pages = "1223--1226"
    }
    
  16. Alexandre E Pelzer, Jasmin Bektic, Thomas Akkad, Stefano Ongarello, Georg Schaefer, Christian Schwentner, Ferdinand Frauscher, Georg Bartsch and Wolfgang Horninger.
    Under Diagnosis and Over Diagnosis of Prostate Cancer in a Screening Population With Serum PSA 2 to 10 ng/ml. The Journal of Urology 178(1):93–97, July 2007.
    URL, DOI BibTeX

    @article{pelzer_under_2007,
    	title = "Under Diagnosis and Over Diagnosis of Prostate Cancer in a Screening Population With Serum {PSA} 2 to 10 ng/ml",
    	volume = 178,
    	issn = "0022-5347",
    	url = "http://www.jurology.com/article/S0022-5347(07)00529-0/abstract",
    	doi = "10.1016/j.juro.2007.03.021",
    	abstract = "Purpose Since the implementation of widespread serum total prostate specific antigen based screening, the risk of prostate cancer over diagnosis has become a concern. We evaluated the amount of possible over and under diagnosis of prostate cancer in an asymptomatic screening population with a total prostate specific antigen of 2.0 to 3.9 (lower range) and 4.0 to 10.0 ng/ml (higher range). Materials and Methods A total of 680 patients with prostate cancer were included. Possible over diagnosis was defined as Gleason score less than 7, pathological stage {pT2a} and negative surgical margins. Under diagnosis was defined as pathological stage {pT3} or greater, or positive surgical margins. Furthermore, insignificant tumors according to the Epstein criteria were evaluated in a small subset of patients for whom cancer volume information was available. Results In the lower and higher total prostate specific antigen ranges there was an over diagnosis rate of 19.7\% and 16.5\%, and an under diagnosis rate of 18.9\%* and 36.7\%, respectively (p {\textless}0.05). In the prostate specific antigen range of 2.0 to 10.0 ng/ml combined the rates of over and under diagnosis were 17.6\% and 30.3\%, respectively. In addition, 8.7\% of tumors with total prostate specific antigen 2.0 to 10.0 ng/ml met the Epstein criteria for insignificance. Conclusions These data show that the reported estimates of over diagnosis in the low total prostate specific antigen group are exaggerated in a screening population. Using our criteria prostate cancer under diagnosis occurs more frequently than over diagnosis in the total prostate specific antigen range of 4.0 to 10 ng/ml.",
    	number = 1,
    	urldate = "2014-02-13",
    	journal = "The Journal of Urology",
    	author = "Pelzer, Alexandre E. and Bektic, Jasmin and Akkad, Thomas and Ongarello, Stefano and Schaefer, Georg and Schwentner, Christian and Frauscher, Ferdinand and Bartsch, Georg and Horninger, Wolfgang",
    	month = "jul",
    	year = 2007,
    	note = "{PMID:} 17499288",
    	keywords = "Cvol, prostate cancer volume, diagnosis, {DRE}, digital rectal examination, {GS}, Gleason score, Mass Screening, {PCa}, prostate cancer, Prostate, Prostate-Specific Antigen, Prostatic Neoplasms, {PSA}, prostate specific antigen, {PV}, prostate volume, {RRP}, radical retropubic prostatectomy, {tPSA}, total {PSA}",
    	pages = "93--97"
    }
    
  17. Mickael Guedj, David Robelin, Mark Hoebeke, Marc Lamarine, Jérôme Wojcik and Gregory Nuel.
    Detecting local high-scoring segments: a first-stage approach for genome-wide association studies. Statistical applications in genetics and molecular biology 5:Article22, 2006.
    DOI BibTeX

    @article{guedj_detecting_2006,
    	title = "Detecting local high-scoring segments: a first-stage approach for genome-wide association studies",
    	volume = 5,
    	issn = "1544-6115",
    	shorttitle = "Detecting local high-scoring segments",
    	doi = "10.2202/1544-6115.1192",
    	abstract = "Genetic epidemiology aims at identifying biological mechanisms responsible for human diseases. Genome-wide association studies, made possible by recent improvements in genotyping technologies, are now promisingly investigated. In these studies, common first-stage strategies focus on marginal effects but lead to multiple-testing and are unable to capture the possibly complex interplay between genetic factors. We have adapted the use of the local score statistic, already successfully applied to analyse long molecular sequences. Via sum statistics, this method captures local and possible distant dependences between markers. Dedicated to genome-wide association studies, it is fast to compute, able to handle large datasets, circumvents the the multiple-testing problem and outlines a set of genomic regions (segments) for further analyses. Applied to simulated and real data, our approach outperforms classical Bonferroni and {FDR} corrections for multiple-testing. It is implemented in a software termed {LHiSA} for Local High-scoring Segments for Association and available at: http://stat.genopole.cnrs.fr/software/lhisa.",
    	language = "eng",
    	journal = "Statistical applications in genetics and molecular biology",
    	author = "Guedj, Mickael and Robelin, David and Hoebeke, Mark and Lamarine, Marc and Wojcik, Jérôme and Nuel, Gregory",
    	year = 2006,
    	note = "{PMID:} 17049033",
    	keywords = "Algorithms, Computer Simulation, Genetic Linkage, Genetic Predisposition to Disease, Genome, Human, Humans, Lod Score, Models, Genetic, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Research Design, Schizophrenia",
    	pages = "Article22",
    	file = "2006_LocalScore_StatAppliGenetMolBiol.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/Z9UHA4WI/2006_LocalScore_StatAppliGenetMolBiol.pdf:application/pdf"
    }
    

Methods

  1. Abhishek Garg, Kartik Mohanram, Alessandro Di Cara, Gwendoline Degueurce, Mark Ibberson, Julien Dorier and Ioannis Xenarios.
    Efficient computation of minimal perturbation sets in gene regulatory networks. Frontiers in physiology 4:361, 2013.
    DOI BibTeX

    @article{garg_efficient_2013,
    	title = "Efficient computation of minimal perturbation sets in gene regulatory networks",
    	volume = 4,
    	issn = "1664-{042X}",
    	doi = "10.3389/fphys.2013.00361",
    	abstract = "In the last few decades, technological and experimental advancements have enabled a more precise understanding of the mode of action of drugs with respect to human cell signaling pathways and have positively influenced the design of new drug compounds. However, as the design of compounds has become increasingly target-specific, the overall effects of a drug on adjacent cellular signaling pathways remain difficult to predict because of the complexity of the interactions involved. Off-target effects of drugs are known to influence their efficacy and safety. Similarly, drugs which are more target-specific also suffer from lack of efficacy because their scope might be too limited in the context of cellular signaling. Even in situations where the signaling pathways targeted by a drug are known, the presence of point mutations in some of the components of the pathways can render a therapy ineffective in a considerable target subpopulation. Some of these issues can be addressed by predicting Minimal Intervention Sets ({MIS)} of elements of the signaling pathways that when perturbed give rise to a pre-defined cellular phenotype. These minimal gene perturbation sets can then be further used to screen a library of drug compounds in order to discover effective drug therapies. This manuscript describes algorithms that can be used to discover {MIS} in a gene regulatory network that can lead to a defined cellular phenotype. Algorithms are implemented in our Boolean modeling toolbox, {GenYsis.} The software binaries of {GenYsis} are available for download from http://www.vital-{it.ch/software/genYsis/.}",
    	language = "eng",
    	journal = "Frontiers in physiology",
    	author = "Garg, Abhishek and Mohanram, Kartik and Di Cara, Alessandro and Degueurce, Gwendoline and Ibberson, Mark and Dorier, Julien and Xenarios, Ioannis",
    	year = 2013,
    	note = "{PMID:} 24391592 {PMCID:} {PMC3867968}",
    	pages = 361
    }
    
  2. Pratyaksha Wirapati, Karl Forner, Angelica Delgado-Vega, Marta Alarcón-Riquelme, Mauro Delorenzi and Jérôme Wojcik.
    Detecting epistasis with restricted response patterns in pairs of biallelic loci. Annals of human genetics 75(1):133–145, 2011.
    DOI BibTeX

    @article{wirapati_detecting_2011,
    	title = "Detecting epistasis with restricted response patterns in pairs of biallelic loci",
    	volume = 75,
    	issn = "1469-1809",
    	doi = "10.1111/j.1469-1809.2010.00625.x",
    	abstract = "Well-established examples of genetic epistasis between a pair of loci typically show characteristic patterns of phenotypic distributions in joint genotype tables. However, inferring epistasis given such data is difficult due to the lack of power in commonly used approaches, which decompose the epistatic patterns into main plus interaction effects followed by testing the interaction term. Testing additive-only or all terms may have more power, but they are sensitive to nonepistatic patterns. Alternatively, the epistatic patterns of interest can be enumerated and the best matching one is found by searching through the possibilities. Although this approach requires multiple testing correction over possible patterns, each pattern can be fitted with a regression model with just one degree of freedom and thus the overall power can still be high, if the number of possible patterns is limited. Here we compare the power of the linear decomposition and pattern search methods, by applying them to simulated data generated under several patterns of joint genotype effects with simple biological interpretations. Interaction-only tests are the least powerful; while pattern search approach is the most powerful if the range of possibilities is restricted, but still includes the true pattern.",
    	language = "eng",
    	number = 1,
    	journal = "Annals of human genetics",
    	author = "Wirapati, Pratyaksha and Forner, Karl and Delgado-Vega, Angelica and Alarcón-Riquelme, Marta and Delorenzi, Mauro and Wojcik, Jérôme",
    	month = "",
    	year = 2011,
    	note = "{PMID:} 21118193",
    	keywords = "Epistasis, Genetic, Humans, Models, Genetic, Polymorphism, Single Nucleotide, Quantitative Trait Loci",
    	pages = "133--145",
    	file = "2010_Epistasis_AnnalsHumanGenetics.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/DZT4SJUF/2010_Epistasis_AnnalsHumanGenetics.pdf:application/pdf"
    }
    
  3. Karl Forner, Marc Lamarine, Mickaël Guedj, Jérôme Dauvillier and Jérôme Wojcik.
    Universal false discovery rate estimation methodology for genome-wide association studies. Human heredity 65(4):183–194, 2008.
    DOI BibTeX

    @article{forner_universal_2008,
    	title = "Universal false discovery rate estimation methodology for genome-wide association studies",
    	volume = 65,
    	issn = "1423-0062",
    	doi = "10.1159/000112365",
    	abstract = "Genome-wide case-control association studies aim at identifying significant differential markers between sick and healthy populations. With the development of large-scale technologies allowing the genotyping of thousands of single nucleotide polymorphisms ({SNPs)} comes the multiple testing problem and the practical issue of selecting the most probable set of associated markers. Several False Discovery Rate ({FDR)} estimation methods have been developed and tuned mainly for differential gene expression studies. However they are based on hypotheses and designs that are not necessarily relevant in genetic association studies. In this article we present a universal methodology to estimate the {FDR} of genome-wide association results. It uses a single global probability value per {SNP} and is applicable in practice for any study design, using any statistic. We have benchmarked this algorithm on simulated data and shown that it outperforms previous methods in cases requiring non-parametric estimation. We exemplified the usefulness of the method by applying it to the analysis of experimental genotyping data of three Multiple Sclerosis case-control association studies.",
    	language = "eng",
    	number = 4,
    	journal = "Human heredity",
    	author = "Forner, Karl and Lamarine, Marc and Guedj, Mickaël and Dauvillier, Jérôme and Wojcik, Jérôme",
    	year = 2008,
    	note = "{PMID:} 18073488",
    	keywords = "Case-Control Studies, Data Interpretation, Statistical, False Positive Reactions, Female, Genetic Predisposition to Disease, Genome, Human, Genotype, Humans, Male, Models, Genetic, Multiple Sclerosis, Polymorphism, Single Nucleotide, Risk",
    	pages = "183--194",
    	file = "2007_PermutationFDR_HumanHeredity.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/9FTKHN5J/2007_PermutationFDR_HumanHeredity.pdf:application/pdf"
    }
    
  4. Nicolas Omont, Karl Forner, Marc Lamarine, Gwendal Martin, François Képès and Jérôme Wojcik.
    Gene-based bin analysis of genome-wide association studies. BMC proceedings 2 Suppl 4:S6, 2008.
    BibTeX

    @article{omont_gene-based_2008,
    	title = "Gene-based bin analysis of genome-wide association studies",
    	volume = "2 Suppl 4",
    	issn = "1753-6561",
    	abstract = "{BACKGROUND:} With the improvement of genotyping technologies and the exponentially growing number of available markers, case-control genome-wide association studies promise to be a key tool for investigation of complex diseases. However new analytical methods have to be developed to face the problems induced by this data scale-up, such as statistical multiple testing, data quality control and computational tractability. {RESULTS:} We present a novel method to analyze genome-wide association studies results. The algorithm is based on a Bayesian model that integrates genotyping errors and genomic structure dependencies. p-values are assigned to genomic regions termed bins, which are defined from a gene-biased partitioning of the genome, and the false-discovery rate is estimated. We have applied this algorithm to data coming from three genome-wide association studies of Multiple Sclerosis. {CONCLUSION:} The method practically overcomes the scale-up problems and permits to identify new putative regions statistically associated with the disease.",
    	language = "eng",
    	journal = "{BMC} proceedings",
    	author = "Omont, Nicolas and Forner, Karl and Lamarine, Marc and Martin, Gwendal and Képès, François and Wojcik, Jérôme",
    	year = 2008,
    	note = "{PMID:} 19091053 {PMCID:} {PMC2654974}",
    	pages = "S6",
    	file = "2008_NNBC_BMCProceedings.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/JSF868F7/2008_NNBC_BMCProceedings.pdf:application/pdf"
    }
    
  5. Jérôme Wojcik and Karl Forner.
    ExactFDR: exact computation of false discovery rate estimate in case-control association studies. Bioinformatics (Oxford, England) 24(20):2407–2408, 2008.
    DOI BibTeX

    @article{wojcik_exactfdr:_2008,
    	title = "{ExactFDR:} exact computation of false discovery rate estimate in case-control association studies",
    	volume = 24,
    	issn = "1367-4811",
    	shorttitle = "{ExactFDR}",
    	doi = "10.1093/bioinformatics/btn379",
    	abstract = "Genome-wide association studies require accurate and fast statistical methods to identify relevant signals from the background noise generated by a huge number of simultaneously tested hypotheses. It is now commonly accepted that exact computations of association probability value (P-value) are preferred to chi(2) and permutation-based approximations. Following the same principle, the {ExactFDR} software package improves speed and accuracy of the permutation-based false discovery rate ({FDR)} estimation method by replacing the permutation-based estimation of the null distribution by the generalization of the algorithm used for computing individual exact P-values. It provides a quick and accurate non-conservative estimator of the proportion of false positives in a given selection of markers, and is therefore an efficient and pragmatic tool for the analysis of genome-wide association studies.",
    	language = "eng",
    	number = 20,
    	journal = "Bioinformatics (Oxford, England)",
    	author = "Wojcik, Jérôme and Forner, Karl",
    	month = "",
    	year = 2008,
    	note = "{PMID:} 18662924",
    	keywords = "Algorithms, Case-Control Studies, Computational Biology, Data Interpretation, Statistical, False Positive Reactions, Gene Expression Profiling, Genetic Predisposition to Disease, Genome, Human, Humans, Models, Genetic, Software",
    	pages = "2407--2408",
    	file = "2008_exactfdr_Bioinformatics.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/26RRK2SE/2008_exactfdr_Bioinformatics.pdf:application/pdf"
    }
    
  6. Alessandro Di Cara, Abhishek Garg, Giovanni De Micheli, Ioannis Xenarios and Luis Mendoza.
    Dynamic simulation of regulatory networks using SQUAD. BMC bioinformatics 8:462, 2007.
    DOI BibTeX

    @article{di_cara_dynamic_2007,
    	title = "Dynamic simulation of regulatory networks using {SQUAD}",
    	volume = 8,
    	issn = "1471-2105",
    	doi = "10.1186/1471-2105-8-462",
    	abstract = "{BACKGROUND:} The ambition of most molecular biologists is the understanding of the intricate network of molecular interactions that control biological systems. As scientists uncover the components and the connectivity of these networks, it becomes possible to study their dynamical behavior as a whole and discover what is the specific role of each of their components. Since the behavior of a network is by no means intuitive, it becomes necessary to use computational models to understand its behavior and to be able to make predictions about it. Unfortunately, most current computational models describe small networks due to the scarcity of kinetic data available. To overcome this problem, we previously published a methodology to convert a signaling network into a dynamical system, even in the total absence of kinetic information. In this paper we present a software implementation of such methodology. {RESULTS:} We developed {SQUAD}, a software for the dynamic simulation of signaling networks using the standardized qualitative dynamical systems approach. {SQUAD} converts the network into a discrete dynamical system, and it uses a binary decision diagram algorithm to identify all the steady states of the system. Then, the software creates a continuous dynamical system and localizes its steady states which are located near the steady states of the discrete system. The software permits to make simulations on the continuous system, allowing for the modification of several parameters. Importantly, {SQUAD} includes a framework for perturbing networks in a manner similar to what is performed in experimental laboratory protocols, for example by activating receptors or knocking out molecular components. Using this software we have been able to successfully reproduce the behavior of the regulatory network implicated in T-helper cell differentiation. {CONCLUSION:} The simulation of regulatory networks aims at predicting the behavior of a whole system when subject to stimuli, such as drugs, or determine the role of specific components within the network. The predictions can then be used to interpret and/or drive laboratory experiments. {SQUAD} provides a user-friendly graphical interface, accessible to both computational and experimental biologists for the fast qualitative simulation of large regulatory networks for which kinetic data is not necessarily available.",
    	language = "eng",
    	journal = "{BMC} bioinformatics",
    	author = "Di Cara, Alessandro and Garg, Abhishek and De Micheli, Giovanni and Xenarios, Ioannis and Mendoza, Luis",
    	year = 2007,
    	note = "{PMID:} 18039375 {PMCID:} {PMC2238325}",
    	keywords = "Animals, Cell Differentiation, Cluster Analysis, Computer Graphics, Computer Simulation, Decision Trees, Enzymes, Homeostasis, Humans, Kinetics, Models, Biological, Nonlinear Dynamics, Protein Interaction Mapping, Signal Transduction, Software, Systems Biology, T-Lymphocytes, Helper-Inducer",
    	pages = 462
    }
    
  7. Alexandre E Pelzer, Isabel Feuerstein, Christian Fuchsberger, Stefano Ongarello, Jasmin Bektic, Christian Schwentner, Helmut Klocker, George Bartsch and Guenther K Bonn.
    Influence of blood sampling on protein profiling and pattern analysis using matrix-assisted laser desorption/ionisation mass spectrometry. BJU international 99(3):658–662, 2007.
    DOI BibTeX

    @article{pelzer_influence_2007,
    	title = "Influence of blood sampling on protein profiling and pattern analysis using matrix-assisted laser desorption/ionisation mass spectrometry",
    	volume = 99,
    	issn = "1464-4096",
    	doi = "10.1111/j.1464-410X.2006.06678.x",
    	abstract = "{OBJECTIVE:} To describe the influence of blood sampling/sampling tubes on mass spectrometric and clustering results, and on clinical blood variables, in blood samples collected from healthy volunteers and patients with prostate cancer. {PATIENTS}, {SUBJECTS} {AND} {METHODS:} Two venous blood samples were taken from 12 healthy volunteers and 12 patients with localized prostate cancer. Two blood samples were taken from each participant using two different venepuncture systems (group A and group B). The Kolmogorov-Smirnov test was used to identify the peaks distinguishing the different groups. In a 10-fold cross-validation study, decision trees for identifying discriminatory peaks that separate the benign from the malignant were constructed. {RESULTS:} The decision tree separated samples measured by matrix-assisted laser desorption/ionization mass spectrometry ({MALDI} {MS)} from healthy volunteers from those of patients with prostate cancer, with a sensitivity of 93.6\% and a specificity of 91.6\%. Of special interest is that one peak at 6941 m/z was produced during blood sample preparation and had a very powerful influence on the results of the classification. {CONCLUSION:} The results clearly showed that blood-sampling systems have a great influence on the recorded {MALDI} {MS} traces, and thus can markedly influence and confound the results of the {MS} analysis, whereas clinical variables might remain unchanged. {MS} profiling is a promising method of marker discovery, but as it could be shown well-designed studies are critical to allow proper interpretation for the identification of key variables as well as for the clinical use.",
    	language = "eng",
    	number = 3,
    	journal = "{BJU} international",
    	author = "Pelzer, Alexandre E and Feuerstein, Isabel and Fuchsberger, Christian and Ongarello, Stefano and Bektic, Jasmin and Schwentner, Christian and Klocker, Helmut and Bartsch, George and Bonn, Guenther K",
    	month = "",
    	year = 2007,
    	note = "{PMID:} 17407520",
    	keywords = "Decision Trees, Humans, Male, Prospective Studies, Prostate-Specific Antigen, Prostatic Neoplasms, Protein Array Analysis, Proteomics, Sensitivity and Specificity, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization",
    	pages = "658--662"
    }
    
  8. M Guedj, J Wojcik, E Della-Chiesa, G Nuel and K Forner.
    A fast, unbiased and exact allelic test for case-control association studies. Human heredity 61(4):210–221, 2006.
    DOI BibTeX

    @article{guedj_fast_2006,
    	title = "A fast, unbiased and exact allelic test for case-control association studies",
    	volume = 61,
    	issn = "0001-5652",
    	doi = "10.1159/000094776",
    	abstract = "Association studies are traditionally performed in the case-control framework. As a first step in the analysis process, comparing allele frequencies using the Pearson's chi-square statistic is often invoked. However such an approach assumes the independence of alleles under the hypothesis of no association, which may not always be the case. Consequently this method introduces a bias that deviates the expected type I error-rate. In this article we first propose an unbiased and exact test as an alternative to the biased allelic test. Available data require to perform thousands of such tests so we focused on its fast execution. Since the biased allelic test is still widely used in the community, we illustrate its pitfalls in the context of genome-wide association studies and particularly in the case of low-level tests. Finally, we compare the unbiased and exact test with the Cochran-Armitage test for trend and show it perfoms similarly in terms of power. The fast, unbiased and exact allelic test code is available in R, C++ and Perl at: http://stat.genopole.cnrs.fr/software/fueatest.",
    	language = "eng",
    	number = 4,
    	journal = "Human heredity",
    	author = "Guedj, M and Wojcik, J and Della-Chiesa, E and Nuel, G and Forner, K",
    	year = 2006,
    	note = "{PMID:} 16877868",
    	keywords = "Alleles, Case-Control Studies, Data Interpretation, Statistical, Gene Frequency",
    	pages = "210--221",
    	file = "2006_unbiasedAllelicTest_HumanHeredity.pdf:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/7RVGRXVX/2006_unbiasedAllelicTest_HumanHeredity.pdf:application/pdf"
    }
    
  9. J S Yu, S Ongarello, R Fiedler, X W Chen, G Toffolo, C Cobelli and Z Trajanoski.
    Ovarian cancer identification based on dimensionality reduction for high-throughput mass spectrometry data. Bioinformatics 21(10):2200–2209, March 2005.
    URL, DOI BibTeX

    @article{yu_ovarian_2005,
    	title = "Ovarian cancer identification based on dimensionality reduction for high-throughput mass spectrometry data",
    	volume = 21,
    	issn = "1367-4803, 1460-2059",
    	url = "http://bioinformatics.oxfordjournals.org/cgi/doi/10.1093/bioinformatics/bti370",
    	doi = "10.1093/bioinformatics/bti370",
    	number = 10,
    	urldate = "2014-02-13",
    	journal = "Bioinformatics",
    	author = "Yu, J. S. and Ongarello, S. and Fiedler, R. and Chen, X. W. and Toffolo, G. and Cobelli, C. and Trajanoski, Z.",
    	month = "mar",
    	year = 2005,
    	pages = "2200--2209"
    }
    

Patents

  1. Pascal Croteau, John Raelson, Jérôme Wojcik, Benoit Destenaves, Clément Olivier and Sonia Schnieper-Samec.
    Genomic Markers for Prediction of Long-Term Response to Growth Hormone (gh) Therapy. , 2012.
    URL BibTeX

    @article{croteau_genomic_2012,
    	title = "Genomic Markers for Prediction of Long-Term Response to Growth Hormone (gh) Therapy",
    	url = "http://patentscope.wipo.int/search/en/detail.jsf?docId=WO2012028633&recNum=2&office=&queryString=FP%3A%28wojcik+merck+serono%29&prevFilter=&sortOption=Pub+Date+Desc&maxRec=9",
    	abstract = "Genomic Markers for Prediction of Long-Term Response to Growth Hormone (gh) Therapy",
    	assignee = "{MERCK} {SERONO} {S.A.}, {CROTEAU}, Pascal, {RAELSON}, John, {WOJCIK}, Jérôme, {DESTENAVES}, Benoit, {OLIVIER}, Clément, {SCHNIEPER-SAMEC}, Sonia",
    	urldate = "2014-02-13",
    	author = "Croteau, Pascal and Raelson, John and Wojcik, Jérôme and Destenaves, Benoit and Olivier, Clément and Schnieper-Samec, Sonia",
    	month = "",
    	year = 2012,
    	keywords = "Genomic Markers for Prediction of Long-Term Response to Growth Hormone (gh) Therapy",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/4CAPEID9/detail.html:text/html"
    }
    
  2. Jérôme Wojcik and Emmanuel Monnet.
    Cladribine Treatment of Multiple Sclerosis in Patient Groups Defined by Genotype. (WO/2011/117267), 2011.
    URL BibTeX

    @article{wojcik_cladribine_2011,
    	title = "Cladribine Treatment of Multiple Sclerosis in Patient Groups Defined by Genotype",
    	url = "http://patentscope.wipo.int/search/en/detail.jsf?docId=WO2011117267&recNum=161&docAn=EP2011054388&queryString=(PA/Merck)%2520&maxRec=6591",
    	abstract = "The invention relates to a method for determining the capacity of a subject suffering from Relapsing-Remitting Multiple Sclerosis ({RRMS)} to respond to treatment with Cladribine, said method comprising determining the polymorphism genotype of the subject in at least one {SNP} located on chromosome X, particularly an {SNP} located in the Duchenne Muscular Dystrophy ({DMD)} gene, for example rs5971598. The invention also relates to Cladribine for use in treating Relapsing-Remitting Multiple Sclerosis ({RRMS)} in a subject, wherein the treatment is specifically adapted to the capacity of the subject to respond to Cladribine treatment, as predicted by genotype., Cette invention concerne une méthode permettant de déterminer la capacité d'un sujet atteint de sclérose en plaques récurrente-rémittente ({RRMS)} à répondre à un traitement à la cladribine, ladite méthode comprenant la détermination du génotype du polymorphisme du sujet dans au moins un {SNP} localisé sur le chromosome X, en particulier, un {SNP} localisé dans le gène de la dystrophie musculaire de Duchenne ({DMD)}, par exemple, rs5971598. Cette invention concerne également la Cladribine destinée à être utilisée pour traiter la sclérose en plaques récurrente-rémittente ({RRMS)} chez un sujet, le traitement étant spécifiquement conçu en fonction de la capacité du sujet à répondre au traitement à la cladribine, comme prédit par le génotype.",
    	language = "English ({EN)}",
    	assignee = "{MERCK} {SERONO} {SA}, {WOJCIK}, Jérôme, {MONNET}, Emmanuel",
    	number = "{WO/2011/117267}",
    	urldate = "2014-02-13",
    	author = "Wojcik, Jérôme and Monnet, Emmanuel",
    	month = "",
    	year = 2011,
    	keywords = "Cladribine Treatment of Multiple Sclerosis in Patient Groups Defined by Genotype",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/FS2JUB6D/detail.html:text/html"
    }
    
  3. Hadi Abderrahim, Jérôme Wojcik, Federica Esposito, Giancarlo Comi and Filippo Martinelli Boneschi.
    Genetic Markers for Diagnosing Primary Progressive Forms of Multiple Sclerosis. (WO/2010/094525), 2010.
    URL BibTeX

    @article{abderrahim_genetic_2010-1,
    	title = "Genetic Markers for Diagnosing Primary Progressive Forms of Multiple Sclerosis",
    	url = "http://patentscope.wipo.int/search/en/detail.jsf?docId=WO2010094525&recNum=8&office=&queryString=FP%3A%28wojcik+merck+serono%29&prevFilter=&sortOption=Pub+Date+Desc&maxRec=9",
    	abstract = "The present invention relates to the use of {SNPs} in Multiple Sclerosis., La présente invention concerne l'utilisation des {SNP} (Single Nucleotide polymorphisms ou polymorphismes d'une seule paire de bases) dans la sclérose en plaques.",
    	language = "English ({EN)}",
    	assignee = "Merck Serono {S.A.}, Abderrahim, Hadi, Wojcik, Jérôme, Esposito, Federica, Comi, Giancarlo, Martinelli Boneschi, Filippo",
    	number = "{WO/2010/094525}",
    	urldate = "2014-02-13",
    	author = "Abderrahim, Hadi and Wojcik, Jérôme and Esposito, Federica and Comi, Giancarlo and Martinelli Boneschi, Filippo",
    	month = "",
    	year = 2010,
    	keywords = "Genetic Markers for Diagnosing Primary Progressive Forms of Multiple Sclerosis",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/3FN7VXZV/detail.html:text/html"
    }
    
  4. Hadi Abderrahim, Jérôme Wojcik, Federica Esposito and Virginie Debailleul.
    Genetic Severity Markers in Multiple Sclerosis. (WO/2010/127906), 2010.
    URL BibTeX

    @article{abderrahim_genetic_2010,
    	title = "Genetic Severity Markers in Multiple Sclerosis",
    	url = "http://patentscope.wipo.int/search/en/detail.jsf?docId=WO2010127906&recNum=6&office=&queryString=FP%3A%28wojcik+merck+serono%29&prevFilter=&sortOption=Pub+Date+Desc&maxRec=9",
    	abstract = "The present invention relates to the use of {SNPs} in predicting susceptibility and/or severity of Multiple Sclerosis in an individual. The {SNPs} are located in the introns of the glycosylation enzymes {MGAT5} and {XYLTl}, 3' of {HIFlAN}, within introns of {MEGF11}, {FGF14}, {PDE9A} and {CDH13} and within desert regions of 4q34 and 17p13., La présente invention concerne l'utilisation de {SNP} pour prévoir la sensibilité à et/ou la gravité de la sclérose en plaques chez un individu. Les {SNP} sont situés dans les introns des enzymes de glycosylation {MGAT5} et {XYLTI}, 3' de {HIFIAN}, dans les introns de {MEGF11}, {FGP14}, {PDE9A} et {CDH13} et dans les régions désertes de 4q34 et 17p13.",
    	language = "English ({EN)}",
    	assignee = "{MERCK} {SERONO} {S.A.}, {ABDERRAHIM}, Hadi, {WOJCIK}, Jérôme, {ESPOSITO}, Federica, {DEBAILLEUL}, Virginie",
    	number = "{WO/2010/127906}",
    	urldate = "2014-02-13",
    	author = "Abderrahim, Hadi and Wojcik, Jérôme and Esposito, Federica and Debailleul, Virginie",
    	month = "",
    	year = 2010,
    	keywords = "Genetic Severity Markers in Multiple Sclerosis",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/NS3ZRNKB/detail.html:text/html"
    }
    
  5. Ursula Boschert, Amanda Proudfoot, Linda Kadi, Pierre Alain Vitte and Jérôme Wojcik.
    Use of Sdf-1 for the Treatment and/or Prevention of Neurological Diseases. (WO/2007/051785), 2007.
    URL BibTeX

    @article{boschert_use_2007,
    	title = "Use of Sdf-1 for the Treatment and/or Prevention of Neurological Diseases",
    	url = "http://patentscope.wipo.int/search/en/detail.jsf?docId=WO2007051785&recNum=9&office=&queryString=FP%3A%28wojcik+merck+serono%29&prevFilter=&sortOption=Pub+Date+Desc&maxRec=9",
    	abstract = "The invention relates to the use of {SDF-1} , or of an agonist of {SDF-1} activity, for the treatment and/or prevention of a neurological disease., L'invention concerne l'utilisation de {SDF-1}, ou d'un antagoniste de l'activité de {SDF-1}, pour le traitement et/ou la prévention d'une maladie neurologique.",
    	language = "English ({EN)}",
    	assignee = "{LABORATOIRE} {SERONO} {S.A.}, {BOSCHERT}, Ursula, {PROUDFOOT}, Amanda, {KADI}, Linda, {VITTE}, Pierre Alain, {WOJCIK}, Jérôme",
    	number = "{WO/2007/051785}",
    	urldate = "2014-02-13",
    	author = "Boschert, Ursula and Proudfoot, Amanda and Kadi, Linda and Vitte, Pierre Alain and Wojcik, Jérôme",
    	month = "",
    	year = 2007,
    	keywords = "Use of Sdf-1 for the Treatment and/or Prevention of Neurological Diseases",
    	file = "Snapshot:/Users/adicara/Library/Application Support/Zotero/Profiles/t5o1rvx6.default/zotero/storage/U9FD5TU7/detail.html:text/html"
    }