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Your search keyword '"Sheridan, E. (Eamonn)"' showing total 3 results
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3 results on '"Sheridan, E. (Eamonn)"'

1. Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia

Author

Vijayakrishnan, J. (Jayaram), Studd, J. (James), Broderick, P. (Peter), Kinnersley, B. (Ben), Holroyd, A. (Amy), Law, P.J. (Philip J.), Kumar, R., Allan, J.M. (James M.), Harrison, C.J. (Christine), Moorman, A.V. (Anthony), Vora, A. (Ajay), Roman, E. (Eve), Rachakonda, S. (Sivaramakrishna), Kinsey, S.E. (Sally E.), Sheridan, E. (Eamonn), Thompson, P.D. (Pamela D.), Irving, J. (Julie), Koehler, R. (Rolf), Hoffmann, P. (Per), Nöthen, M.M. (Markus), Heilmann-Heimbach, S. (Stefanie), JöCkel, K.-H. (Karl-Heinz), Easton, D.F. (Douglas), Pharaoh, P.D.P. (Paul), Dunning, A.M. (Alison), Peto, J. (Julian), Canzian, F. (Frederico), Swerdlow, A.J. (Anthony ), Eeles, R.A. (Rosalind A.), Kote-Jarai, Z., Muir, K. (Kenneth), Pashayan, N. (Nora), Greaves, M.F. (Mel), Zimmerman, M. (Martin), Bartram, C.R. (Claus), Schrappe, M. (Martin), Stanulla, M. (Martin), Hemminki, K. (Kari), Houlston, R.S. (Richard S.), Vijayakrishnan, J. (Jayaram), Studd, J. (James), Broderick, P. (Peter), Kinnersley, B. (Ben), Holroyd, A. (Amy), Law, P.J. (Philip J.), Kumar, R., Allan, J.M. (James M.), Harrison, C.J. (Christine), Moorman, A.V. (Anthony), Vora, A. (Ajay), Roman, E. (Eve), Rachakonda, S. (Sivaramakrishna), Kinsey, S.E. (Sally E.), Sheridan, E. (Eamonn), Thompson, P.D. (Pamela D.), Irving, J. (Julie), Koehler, R. (Rolf), Hoffmann, P. (Per), Nöthen, M.M. (Markus), Heilmann-Heimbach, S. (Stefanie), JöCkel, K.-H. (Karl-Heinz), Easton, D.F. (Douglas), Pharaoh, P.D.P. (Paul), Dunning, A.M. (Alison), Peto, J. (Julian), Canzian, F. (Frederico), Swerdlow, A.J. (Anthony ), Eeles, R.A. (Rosalind A.), Kote-Jarai, Z., Muir, K. (Kenneth), Pashayan, N. (Nora), Greaves, M.F. (Mel), Zimmerman, M. (Martin), Bartram, C.R. (Claus), Schrappe, M. (Martin), Stanulla, M. (Martin), Hemminki, K. (Kari), and Houlston, R.S. (Richard S.)

Abstract

Genome-wide association studies (GWAS) have advanced our understanding of susceptibility to B-cell precursor acute lymphoblastic leukemia (BCP-ALL); however, much of the heritable risk remains unidentified. Here, we perform a GWAS and conduct a meta-analysis with two existing GWAS, totaling 2442 cases and 14,609 controls. We identify risk loci for BCP-ALL at 8q24.21 (rs28665337, P = 3.86 × 10-9, odds ratio (OR) = 1.34) and for ETV6-RUNX1 fusion-positive BCP-ALL at 2q22.3 (rs17481869, P = 3.20 × 10-8, OR = 2.14). Our findings provide further insights into genetic susceptibility to ALL and its biology.

Published
2018
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2. Risk-benefit trade-offs in revascularisation choices

Author

Federspiel, J.J. (Jerome), Stearns, S.C. (Sally), Domburg, R.T. (Ron) van, Sheridan, E. (Eamonn), Lund, J.L. (Jennifer), Serruys, P.W.J.C. (Patrick), Federspiel, J.J. (Jerome), Stearns, S.C. (Sally), Domburg, R.T. (Ron) van, Sheridan, E. (Eamonn), Lund, J.L. (Jennifer), and Serruys, P.W.J.C. (Patrick)

Abstract

Aims: When patients choose percutaneous coronary intervention (PCI) over coronary artery bypass grafting (CABG), they accept an increased long-term risk of repeat revascularisation in exchange for short-term morbidity benefits. This paper quantifies the risk-benefit trade-off faced by patients with multiple vessel coronary artery disease. Methods and results: Data from the Arterial Revascularisation Therapies Study are used to generate risk-benefit acceptability curves for PCI versus CABG. Risks are measured by the long-term likelihood of repeat revascularisation while benefits are measured by short-term reductions in pain or improvements in health-related quality of life (HRQL). PCI patients faced a risk of 0.81 additional revascularisation events over three years in exchange for being pain-free at one month. A patient would need to be willing to tolerate a risk of 1.06 additional revascularisation events at three years, in exchange for being pain free at one month to be 95% confident that choosing PCI over CABG is risk-effective for him/her. Conclusions: The risk-benefit framework outlined in this study provides information to enable physicians to help their patients weigh directly each procedure's risks and benefits. While trade-offs are typically measured in quality-adjusted life years, using pain reduction to reflect benefits may provide a more tangible framework for patients.

Published
2011
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3. Glucose transporter-1 deficiency syndrome: The expanding clinical and genetic spectrum of a treatable disorder

Author

Leen, W.G. (Wilhelmina), Klepper, J. (Joerg), Verbeek, M.M. (Marcel), Leferink, M. (Maike), Hofste, T. (Tom), Engelen, B.G.M. (Baziel) van, Wevers, R.A. (Ron), Arthur, T. (Todd), Bahi-Buisson, N. (Nadia), Ballhausen, D. (Diana), Bekhof, J. (Jolita), Bogaert, P. (Patrick) van, Carrilho, I. (Inês), Chabrol, B. (Brigitte), Champion, M.P. (Michael), Coldwell, J. (James), Clayton, P. (Peter), Donner, E. (Elizabeth), Evangeliou, A. (Athanasios), Ebinger, F. (Friedrich), Farrell, K. (Kevin), Forsyth, R.J. (Rob), Goede, C.G.E.L. (Christian) de, Gross, S. (Stephanie), Grünewald, S. (Sonja), Holthausen, H. (Hans), Jayawant, S. (Sandeep), Lachlan, K. (Katherine), Laugel, V. (Vincent), Leppig, K. (Kathy), Lim, M.J. (Ming), Mancini, G.M.S. (Grazia), Marina, A.D., Martorell, L. (Loreto), McMenamin, J. (Joe), Meuwissen, M.E.C. (Marije), Mundy, H. (Helen), Nilsson, N.O. (Nils), Panzer, A. (Axel), Poll-The, B.T., Rauscher, C. (Christian), Rouselle, C.M.R. (Christophe), Sandvig, I. (Inger), Scheffner, T. (Thomas), Sheridan, E. (Eamonn), Simpson, N. (Neil), Sykora, P. (Parol), Tomlinson, R. (Richard), Trounce, J. (John), Webb, D.W.M. (David), Weschke, B. (Bernhard), Scheffer, H. (Hans), Willemsen, M.A. (Michél), Leen, W.G. (Wilhelmina), Klepper, J. (Joerg), Verbeek, M.M. (Marcel), Leferink, M. (Maike), Hofste, T. (Tom), Engelen, B.G.M. (Baziel) van, Wevers, R.A. (Ron), Arthur, T. (Todd), Bahi-Buisson, N. (Nadia), Ballhausen, D. (Diana), Bekhof, J. (Jolita), Bogaert, P. (Patrick) van, Carrilho, I. (Inês), Chabrol, B. (Brigitte), Champion, M.P. (Michael), Coldwell, J. (James), Clayton, P. (Peter), Donner, E. (Elizabeth), Evangeliou, A. (Athanasios), Ebinger, F. (Friedrich), Farrell, K. (Kevin), Forsyth, R.J. (Rob), Goede, C.G.E.L. (Christian) de, Gross, S. (Stephanie), Grünewald, S. (Sonja), Holthausen, H. (Hans), Jayawant, S. (Sandeep), Lachlan, K. (Katherine), Laugel, V. (Vincent), Leppig, K. (Kathy), Lim, M.J. (Ming), Mancini, G.M.S. (Grazia), Marina, A.D., Martorell, L. (Loreto), McMenamin, J. (Joe), Meuwissen, M.E.C. (Marije), Mundy, H. (Helen), Nilsson, N.O. (Nils), Panzer, A. (Axel), Poll-The, B.T., Rauscher, C. (Christian), Rouselle, C.M.R. (Christophe), Sandvig, I. (Inger), Scheffner, T. (Thomas), Sheridan, E. (Eamonn), Simpson, N. (Neil), Sykora, P. (Parol), Tomlinson, R. (Richard), Trounce, J. (John), Webb, D.W.M. (David), Weschke, B. (Bernhard), Scheffer, H. (Hans), and Willemsen, M.A. (Michél)

Abstract

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene in the majority of patients and results in impaired glucose transport into the brain. From 2004-2008, 132 requests for mutational analysis of the SLC2A1 gene were studied by automated Sanger sequencing and multiplex ligation-dependent probe amplification. Mutation

Published
2010
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