Browsing ICR Divisions by author "Studd, James"
Now showing items 1-9 of 9
-
Association analyses identify 31 new risk loci for colorectal cancer susceptibility.
Law, PJ; Timofeeva, M; Fernandez-Rozadilla, C; Broderick, P; Studd, J; et al. (NATURE PUBLISHING GROUP, 2019-05-14)Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide, and has a strong heritable basis. We report a genome-wide association analysis of 34,627 CRC cases and 71,379 controls of European ancestry that ... -
Cancer drivers and clonal dynamics in acute lymphoblastic leukaemia subtypes
Studd, J; Cornish, A; Hoang, P; Law, P; Houlston, R (2021-04-15)To obtain a comprehensive picture of composite genetic drivers events and clonal dynamics in subtypes of paediatric acute lymphoblastic leukaemia (ALL) we analysed tumour-normal whole genome sequencing and expression data ... -
Cancer drivers and clonal dynamics in acute lymphoblastic leukaemia subtypes.
Studd, JB; Cornish, AJ; Hoang, PH; Law, P; Kinnersley, B; et al. (SPRINGERNATURE, 2021-11-09)To obtain a comprehensive picture of composite genetic driver events and clonal dynamics in subtypes of paediatric acute lymphoblastic leukaemia (ALL) we analysed tumour-normal whole genome sequencing and expression data ... -
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; et al. (NATURE PORTFOLIO, 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; et al. (SPRINGERNATURE, 2019-01-01)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 ... -
Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia.
Vijayakrishnan, J; Studd, J; Broderick, P; Kinnersley, B; Holroyd, A; et al. (NATURE PORTFOLIO, 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 ... -
Identification of four novel associations for B-cell acute lymphoblastic leukaemia risk.
Vijayakrishnan, J; Qian, M; Studd, JB; Yang, W; Kinnersley, B; et al. (NATURE PORTFOLIO, 2019-11-25)There is increasing evidence for a strong inherited genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children. To identify new risk variants for B-cell ALL (B-ALL) we conducted a meta-analysis with ... -
Multiple myeloma risk variant at 7p15.3 creates an IRF4-binding site and interferes with CDCA7L expression.
Li, N; Johnson, DC; Weinhold, N; Studd, JB; Orlando, G; et al. (NATURE PUBLISHING GROUP, 2016-11-24)Genome-wide association studies have identified several risk loci for multiple myeloma (MM); however, the mechanisms by which they influence MM are unknown. Here by using genetic association data and functional characterization, ... -
The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression.
Liu, NQ; Ter Huurne, M; Nguyen, LN; Peng, T; Wang, S-Y; et al. (NATURE PORTFOLIO, 2017-02-14)Genome-wide association studies have identified a great number of non-coding risk variants for colorectal cancer (CRC). To date, the majority of these variants have not been functionally studied. Identification of ...