Now showing items 1-5 of 5

    • Genetic and regulatory mechanism of susceptibility to high-hyperdiploid acute lymphoblastic leukaemia at 10p21.2. 

      Studd, JB; Vijayakrishnan, J; Yang, M; Migliorini, G; Paulsson, K; Houlston, RS (2017-03-03)
      Despite high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL) being the most common subgroup of paediatric ALL, its aetiology remains unknown. Genome-wide association studies have demonstrated association at 10q21.2. ...
    • Genetic predisposition to B-cell acute lymphoblastic leukemia at 14q11.2 is mediated by a CEBPE promoter polymorphism. 

      Studd, JB; Yang, M; Li, Z; Vijayakrishnan, J; Lu, Y; Yeoh, AE-J; Paulsson, K; Houlston, RS (2019-01)
      Acute lymphoblastic leukaemia (ALL) is the most common paediatric malignancy. Genome-wide association studies have shown variation at 14q11.2 influences ALL risk. We sought to decipher causal variant(s) at 14q11.2 and the ...
    • A genome-wide association study identifies risk loci for childhood acute lymphoblastic leukemia at 10q26.13 and 12q23.1. 

      Vijayakrishnan, J; Kumar, R; Henrion, MY; Moorman, AV; Rachakonda, PS; Hosen, I; da Silva Filho, MI; Holroyd, A; Dobbins, SE; Koehler, R; Thomsen, H; Irving, JA; Allan, JM; Lightfoot, T; Roman, E; Kinsey, SE; Sheridan, E; Thompson, PD; Hoffmann, P; Nöthen, MM; Heilmann-Heimbach, S; Karl-Heinz, J; Greaves, M; Harrison, CJ; Bartram, CR; Schrappe, M; Stanulla, M; Hemminki, K; Houlston, RS (2016-10-03)
      Genome-wide association studies (GWASs) have shown that common genetic variation contributes to the heritable risk of childhood acute lymphoblastic leukemia (ALL). To identify new susceptibility loci for the largest subtype ...
    • Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia (vol 9, 1340, 2018) 

      Vijayakrishnan, J; Studd, J; Broderick, P; Kinnersley, B; Holroyd, A; Law, PJ; Kumar, R; Allan, JM; Harrison, CJ; Moorman, AV; Vora, A; Roman, E; Rachakonda, S; Kinsey, SE; Sheridan, E; Thompson, PD; Irving, JA; Koehler, R; Hoffmann, P; Noethen, MM; Heilmann-Heimbach, S; Joeckel, K-H; Easton, DF; Pharaoh, PDP; Dunning, AM; Peto, J; Canzian, F; Swerdlow, A; Eeles, RA; Kote-Jarai, Z; Muir, K; Pashayan, N; Henderson, BE; Haiman, CA; Benlloch, S; Schumacher, FR; Al Olama, AA; Berndt, SI; Conti, DV; Wiklund, F; Chanock, S; Stevens, VL; Tangen, CM; Batra, J; Clements, J; Gronberg, H; Schleutker, J; Albanes, D; Weinstein, S; Wolk, A; West, C; Mucci, L; Cancel-Tassin, G; Koutros, S; Sorensen, KD; Maehle, L; Neal, DE; Travis, RC; Hamilton, RJ; Ingles, SA; Rosenstein, B; Lu, Y-J; Giles, GG; Kibel, AS; Vega, A; Kogevinas, M; Penney, KL; Park, JY; Stanford, JL; Cybulski, C; Nordestgaard, BG; Brenner, H; Maier, C; Kim, J; John, EM; Teixeira, MR; Neuhausen, SL; De Ruyck, K; Razack, A; Newcomb, LF; Lessel, D; Kaneva, R; Usmani, N; Claessens, F; Townsend, PA; Gago-Dominguez, M; Roobol, MJ; Menegaux, F; Greaves, M; Zimmerman, M; Bartram, CR; Schrappe, M; Stanulla, M; Hemminki, K; Houlston, RS; Consortium, PRACTICAL (2019-01-21)
    • Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia. 

      Vijayakrishnan, J; Studd, J; Broderick, P; Kinnersley, B; Holroyd, A; Law, PJ; Kumar, R; Allan, JM; Harrison, CJ; Moorman, AV; Vora, A; Roman, E; Rachakonda, S; Kinsey, SE; Sheridan, E; Thompson, PD; Irving, JA; Koehler, R; Hoffmann, P; Nöthen, MM; Heilmann-Heimbach, S; Jöckel, K-H; Easton, DF; Pharaoh, PDP; Dunning, AM; Peto, J; Canzian, F; Swerdlow, A; Eeles, RA; Kote-Jarai, Z; Muir, K; Pashayan, N; PRACTICAL Consortium; Greaves, M; Zimmerman, M; Bartram, CR; Schrappe, M; Stanulla, M; Hemminki, K; Houlston, RS (2018-04-09)
      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 ...