Now showing items 1-4 of 4

    • Dickkopf-3 links HSF1 and YAP/TAZ signalling to control aggressive behaviours in cancer-associated fibroblasts. 

      Ferrari, N; Ranftl, R; Chicherova, I; Slaven, ND; Moeendarbary, E; Farrugia, AJ; Lam, M; Semiannikova, M; Westergaard, MCW; Tchou, J; Magnani, L; Calvo, F (2019-01-10)
      Aggressive behaviours of solid tumours are highly influenced by the tumour microenvironment. Multiple signalling pathways can affect the normal function of stromal fibroblasts in tumours, but how these events are coordinated ...
    • Genetic Predisposition to Chronic Lymphocytic Leukemia Is Mediated by a BMF Super-Enhancer Polymorphism. 

      Kandaswamy, R; Sava, GP; Speedy, HE; Beà, S; Martín-Subero, JI; Studd, JB; Migliorini, G; Law, PJ; Puente, XS; Martín-García, D; Salaverria, I; Gutiérrez-Abril, J; López-Otín, C; Catovsky, D; Allan, JM; Campo, E; Houlston, RS (2016-08-11)
      Chronic lymphocytic leukemia (CLL) is an adult B cell malignancy. Genome-wide association studies show that variation at 15q15.1 influences CLL risk. We deciphered the causal variant at 15q15.1 and the mechanism by which ...
    • Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci. 

      Law, PJ; Sud, A; Mitchell, JS; Henrion, M; Orlando, G; Lenive, O; Broderick, P; Speedy, HE; Johnson, DC; Kaiser, M; Weinhold, N; Cooke, R; Sunter, NJ; Jackson, GH; Summerfield, G; Harris, RJ; Pettitt, AR; Allsup, DJ; Carmichael, J; Bailey, JR; Pratt, G; Rahman, T; Pepper, C; Fegan, C; von Strandmann, EP; Engert, A; Försti, A; Chen, B; Filho, MIDS; Thomsen, H; Hoffmann, P; Noethen, MM; Eisele, L; Jöckel, K-H; Allan, JM; Swerdlow, AJ; Goldschmidt, H; Catovsky, D; Morgan, GJ; Hemminki, K; Houlston, RS (2017-01-23)
      B-cell malignancies (BCM) originate from the same cell of origin, but at different maturation stages and have distinct clinical phenotypes. Although genetic risk variants for individual BCMs have been identified, an agnostic, ...
    • Genome-wide association study identifies multiple susceptibility loci for multiple myeloma. 

      Mitchell, JS; Li, N; Weinhold, N; Försti, A; Ali, M; van Duin, M; Thorleifsson, G; Johnson, DC; Chen, B; Halvarsson, B-M; Gudbjartsson, DF; Kuiper, R; Stephens, OW; Bertsch, U; Broderick, P; Campo, C; Einsele, H; Gregory, WA; Gullberg, U; Henrion, M; Hillengass, J; Hoffmann, P; Jackson, GH; Johnsson, E; Jöud, M; Kristinsson, SY; Lenhoff, S; Lenive, O; Mellqvist, U-H; Migliorini, G; Nahi, H; Nelander, S; Nickel, J; Nöthen, MM; Rafnar, T; Ross, FM; da Silva Filho, MI; Swaminathan, B; Thomsen, H; Turesson, I; Vangsted, A; Vogel, U; Waage, A; Walker, BA; Wihlborg, A-K; Broyl, A; Davies, FE; Thorsteinsdottir, U; Langer, C; Hansson, M; Kaiser, M; Sonneveld, P; Stefansson, K; Morgan, GJ; Goldschmidt, H; Hemminki, K; Nilsson, B; Houlston, RS (2016-07)
      Multiple myeloma (MM) is a plasma cell malignancy with a significant heritable basis. Genome-wide association studies have transformed our understanding of MM predisposition, but individual studies have had limited power ...