Identification of four new susceptibility loci for testicular germ cell tumour

Kevin Litchfield, Amy Holroyd, Amy Lloyd, Peter Broderick, Jérémie Nsengimana, Rosalind Eeles, Douglas F Easton, Darshna Dudakia, D. Timothy Bishop, Alison Reid, Robert A. Huddart, Tom Grotmol, Fredrik Wiklund, Janet Shipley, Richard S. Houlston and Clare Turnbull ()
Additional contact information
Kevin Litchfield: The Institute of Cancer Research
Amy Holroyd: The Institute of Cancer Research
Amy Lloyd: The Institute of Cancer Research
Peter Broderick: The Institute of Cancer Research
Jérémie Nsengimana: Section of Epidemiology and Biostatistics, Leeds Institute of Cancer and Pathology
Rosalind Eeles: The Institute of Cancer Research
Douglas F Easton: Cancer Research UK, Genetic Epidemiology Unit, Strangeways Research Laboratory
Darshna Dudakia: The Institute of Cancer Research
D. Timothy Bishop: Section of Epidemiology and Biostatistics, Leeds Institute of Cancer and Pathology
Alison Reid: Academic Radiotherapy Unit, Institute of Cancer Research
Robert A. Huddart: Academic Radiotherapy Unit, Institute of Cancer Research
Tom Grotmol: Cancer Registry of Norway
Fredrik Wiklund: Karolinska Institutet
Janet Shipley: The Institute of Cancer Research
Richard S. Houlston: The Institute of Cancer Research
Clare Turnbull: The Institute of Cancer Research

Nature Communications, 2015, vol. 6, issue 1, 1-8

Abstract: Abstract Genome-wide association studies (GWAS) have identified multiple risk loci for testicular germ cell tumour (TGCT), revealing a polygenic model of disease susceptibility strongly influenced by common variation. To identify additional single-nucleotide polymorphisms (SNPs) associated with TGCT, we conducted a multistage GWAS with a combined data set of >25,000 individuals (6,059 cases and 19,094 controls). We identified new risk loci for TGCT at 3q23 (rs11705932, TFDP2, P=1.5 × 10−9), 11q14.1 (rs7107174, GAB2, P=9.7 × 10−11), 16p13.13 (rs4561483, GSPT1, P=1.6 × 10−8) and 16q24.2 (rs55637647, ZFPM1, P=3.4 × 10−9). We additionally present detailed functional analysis of these loci, identifying a statistically significant relationship between rs4561483 risk genotype and increased GSPT1 expression in TGCT patient samples. These findings provide additional support for a polygenic model of TGCT risk and further insight into the biological basis of disease development.

Date: 2015
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DOI: 10.1038/ncomms9690

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