Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia

Elli Papaemmanuil; Fay J. Hosking; Jayaram Vijayakrishnan; Amy Price; Bianca Olver; Eammon Sheridan; Sally E. Kinsey; Tracy Lightfoot; Eve Roman; Julie A E Irving; James M. Allan; Ian P. Tomlinson; Malcolm Taylor; Mel Greaves; Richard S. Houlston

doi:10.1038/ng.430

Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia

Elli Papaemmanuil, Fay J. Hosking, Jayaram Vijayakrishnan, Amy Price, Bianca Olver, Eammon Sheridan, Sally E. Kinsey, Tracy Lightfoot, Eve Roman, Julie A E Irving, James M. Allan, Ian P. Tomlinson, Malcolm Taylor, Mel Greaves, Richard S. Houlston

Research output: Contribution to journal › Article › peer-review

Abstract

To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 (IKZF1, rs4132601, odds ratio (OR) = 1.69, P = 1.20 × 10 -19), 10q21.2 (ARID5B, rs7089424, OR = 1.65, P = 6.69 × 10 -19) and 14q11.2 (CEBPE, rs2239633, OR = 1.34, P = 2.88 × 10 -7). The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer. Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors. © 2009 Nature America, Inc. All rights reserved.

Original language	English
Pages (from-to)	1006-1010
Number of pages	4
Journal	Nature Genetics
Volume	41
Issue number	9
DOIs	https://doi.org/10.1038/ng.430
Publication status	Published - Sept 2009

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/ng.430

Cite this

Papaemmanuil, E., Hosking, F. J., Vijayakrishnan, J., Price, A., Olver, B., Sheridan, E., Kinsey, S. E., Lightfoot, T., Roman, E., Irving, J. A. E., Allan, J. M., Tomlinson, I. P., Taylor, M., Greaves, M., & Houlston, R. S. (2009). Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia. Nature Genetics, 41(9), 1006-1010. https://doi.org/10.1038/ng.430

@article{71a5cc63e3304ed682dd04cc7fcd20c3,

title = "Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia",

abstract = "To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 (IKZF1, rs4132601, odds ratio (OR) = 1.69, P = 1.20 × 10 -19), 10q21.2 (ARID5B, rs7089424, OR = 1.65, P = 6.69 × 10 -19) and 14q11.2 (CEBPE, rs2239633, OR = 1.34, P = 2.88 × 10 -7). The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer. Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors. {\textcopyright} 2009 Nature America, Inc. All rights reserved.",

author = "Elli Papaemmanuil and Hosking, \{Fay J.\} and Jayaram Vijayakrishnan and Amy Price and Bianca Olver and Eammon Sheridan and Kinsey, \{Sally E.\} and Tracy Lightfoot and Eve Roman and Irving, \{Julie A E\} and Allan, \{James M.\} and Tomlinson, \{Ian P.\} and Malcolm Taylor and Mel Greaves and Houlston, \{Richard S.\}",

year = "2009",

month = sep,

doi = "10.1038/ng.430",

language = "English",

volume = "41",

pages = "1006--1010",

journal = "Nature Genetics",

issn = "1061-4036",

publisher = "Nature Research",

number = "9",

}

Papaemmanuil, E, Hosking, FJ, Vijayakrishnan, J, Price, A, Olver, B, Sheridan, E, Kinsey, SE, Lightfoot, T, Roman, E, Irving, JAE, Allan, JM, Tomlinson, IP, Taylor, M, Greaves, M & Houlston, RS 2009, 'Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia', Nature Genetics, vol. 41, no. 9, pp. 1006-1010. https://doi.org/10.1038/ng.430

TY - JOUR

T1 - Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia

AU - Papaemmanuil, Elli

AU - Hosking, Fay J.

AU - Vijayakrishnan, Jayaram

AU - Price, Amy

AU - Olver, Bianca

AU - Sheridan, Eammon

AU - Kinsey, Sally E.

AU - Lightfoot, Tracy

AU - Roman, Eve

AU - Irving, Julie A E

AU - Allan, James M.

AU - Tomlinson, Ian P.

AU - Taylor, Malcolm

AU - Greaves, Mel

AU - Houlston, Richard S.

PY - 2009/9

Y1 - 2009/9

N2 - To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 (IKZF1, rs4132601, odds ratio (OR) = 1.69, P = 1.20 × 10 -19), 10q21.2 (ARID5B, rs7089424, OR = 1.65, P = 6.69 × 10 -19) and 14q11.2 (CEBPE, rs2239633, OR = 1.34, P = 2.88 × 10 -7). The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer. Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors. © 2009 Nature America, Inc. All rights reserved.

AB - To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 (IKZF1, rs4132601, odds ratio (OR) = 1.69, P = 1.20 × 10 -19), 10q21.2 (ARID5B, rs7089424, OR = 1.65, P = 6.69 × 10 -19) and 14q11.2 (CEBPE, rs2239633, OR = 1.34, P = 2.88 × 10 -7). The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer. Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors. © 2009 Nature America, Inc. All rights reserved.

UR - https://www.scopus.com/pages/publications/69349101565

U2 - 10.1038/ng.430

DO - 10.1038/ng.430

M3 - Article

SN - 1061-4036

VL - 41

SP - 1006

EP - 1010

JO - Nature Genetics

JF - Nature Genetics

IS - 9

ER -

Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia

Abstract

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this