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Your search keyword '"Steven J Lubbe"' showing total 4 results
Start Over Author "Steven J Lubbe" Journal nature genetics
4 results on '"Steven J Lubbe"'

1. A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3

Author

Sari Tuupanen, Melissa C. Southey, Ian Chandler, Enric Domingo, Paul D.P. Pharoah, Luis G. Carvajal-Carmona, D. Gareth Evans, Malcolm G. Dunlop, Trinidad Caldés, Graham G. Giles, Zoe Kemp, Harry Campbell, David J. Kerr, Alan M. Pittman, Eamonn R. Maher, D. Timothy Bishop, Jayaram Vijayakrishnan, Hans Morreau, Albert Tenesa, Asta Försti, Jean-Baptiste Cazier, Kimberley Howarth, Ella Barclay, Rebecca A. Barnetson, Tom van Wezel, Juul T. Wijnen, James G. D. Prendergast, Maggie Gorman, Julian Peto, Anneke Lucassen, Antoni Castells, Jochen Hampe, José A. G. Agúndez, Susan M. Farrington, Kate Sullivan, Henry Völzke, Richard Gray, Ulrich John, King Yip Cheng, Pavel Vodicka, Emma Jaeger, Peter Broderick, Judy W. C. Ho, Mobshra Qureshi, Lauri A. Aaltonen, Stephan Buch, Sarah Fielding, Sarah L. Spain, Lynn Martin, Andrew Rowan, Wendy Wood, Emily L. Webb, John M. Luk, Angel Carracedo, Clara Ruiz-Ponte, Alessio Naccarati, Steven J. Lubbe, Ian Tomlinson, Lara Lipton, John L. Hopper, Iina Niittymäki, Axel Walther, José M. Ladero, Pak C. Sham, Stefan Schreiber, Sergi Castellví-Bel, Miguel de la Hoya, Clemens Schafmayer, Gianluca Severi, Auli Karhu, Steven Penegar, Thibaud Koessler, Kari Hemminki, Richard S. Houlston, and Huw Thomas

Subjects
Adult, Male, Genetic Linkage, Colorectal cancer, Eukaryotic Initiation Factor-3, Single-nucleotide polymorphism, Genome-wide association study, Locus (genetics), Biology, Polymorphism, Single Nucleotide, 03 medical and health sciences, 0302 clinical medicine, Genetic linkage, Genetics, medicine, Humans, Genetic Predisposition to Disease, Allele, Genotyping, Alleles, Aged, 030304 developmental biology, 0303 health sciences, Chromosomes, Human, Pair 10, Genome, Human, Cancer, Middle Aged, medicine.disease, Pedigree, 3. Good health, 030220 oncology & carcinogenesis, Female, Colorectal Neoplasms, Chromosomes, Human, Pair 8
Abstract

To identify colorectal cancer (CRC) susceptibility alleles, we conducted a genome-wide association study. In phase 1, we genotyped 550,163 tagSNPs in 940 familial colorectal tumor cases (627 CRC, 313 high-risk adenoma) and 965 controls. In phase 2, we genotyped 42,708 selected SNPs in 2,873 CRC cases and 2,871 controls. In phase 3, we evaluated 11 SNPs showing association at P < 10(-4) in a joint analysis of phases 1 and 2 in 4,287 CRC cases and 3,743 controls. Two SNPs were taken forward to phase 4 genotyping (10,731 CRC cases and 10,961 controls from eight centers). In addition to the previously reported 8q24, 15q13 and 18q21 CRC risk loci, we identified two previously unreported associations: rs10795668, located at 10p14 (P = 2.5 x 10(-13) overall; P = 6.9 x 10(-12) replication), and rs16892766, at 8q23.3 (P = 3.3 x 10(-18) overall; P = 9.6 x 10(-17) replication), which tags a plausible causative gene, EIF3H. These data provide further evidence for the 'common-disease common-variant' model of CRC predisposition.

Published
2008

2. A genome-wide association study shows that common alleles of SMAD7 influence colorectal cancer risk

Author

Jayaram Vijayakrishnan, Ella Barclay, Maggie Gorman, Julian Peto, Andrew Rowan, Peter Broderick, Richard S. Houlston, Zoe Kemp, Luis G. Carvajal-Carmona, Sarah L. Spain, Emily L. Webb, Enric Domingo, Ian Chandler, Kate Sullivan, Steven J. Lubbe, Alan M. Pittman, Kimberley Howarth, Elli Papaemmanuil, Lynn Martin, Richard Gray, Gabrielle S. Sellick, Oliver M. Sieber, Sarah Fielding, Wendy Wood, Emma Jaeger, David J. Kerr, Steven Penegar, Ian Tomlinson, Jean-Baptiste Cazier, Mobshra Qureshi, and Ana Teixeira

Subjects
Genetics, Genotype, Genetic Linkage, Genome, Human, Colorectal cancer, Case-control study, Cancer, Single-nucleotide polymorphism, Genome-wide association study, Biology, medicine.disease, Polymorphism, Single Nucleotide, digestive system diseases, Smad7 Protein, Risk Factors, Polymorphism (computer science), Case-Control Studies, medicine, Humans, Genetic Predisposition to Disease, Colorectal Neoplasms, Genotyping, Alleles
Abstract

To identify risk variants for colorectal cancer (CRC), we conducted a genome-wide association study, genotyping 550,163 tag SNPs in 940 individuals with familial colorectal tumor (627 CRC, 313 advanced adenomas) and 965 controls. We evaluated selected SNPs in three replication sample sets (7,473 cases, 5,984 controls) and identified three SNPs in SMAD7 (involved in TGF-beta and Wnt signaling) associated with CRC. Across the four sample sets, the association between rs4939827 and CRC was highly statistically significant (P(trend) = 1.0 x 10(-12)).

Published
2007

3. Common genetic variants at the CRAC1 (HMPS) locus on chromosome 15q13.3 influence colorectal cancer risk

Author

Zoe Kemp, Axel Walther, Steven J. Lubbe, Ian Tomlinson, Alan M. Pittman, Lynn Martin, Luis G. Carvajal-Carmona, Richard S. Houlston, Andrew Rowan, Albert Tenesa, Sarah L. Spain, Susan M. Farrington, Kate Sullivan, Huw Thomas, Julian Peto, David J. Kerr, Emily L. Webb, Ian Chandler, Karl Heinimann, Enric Domingo, Emma Jaeger, Malcolm G. Dunlop, Ella Barclay, Jean-Baptiste Cazier, Steven Penegar, Harry Campbell, Maggie Gorman, Richard Gray, Peter Broderick, Wendy Wood, Kimberley Howarth, Elli Papaemmanuil, Jayaram Vijayakrishnan, and Mobshra Qureshi

Subjects
Adenoma, Genetics, Chromosomes, Human, Pair 15, education.field_of_study, Colorectal cancer, Population, Chromosome, Cancer, Genome-wide association study, Locus (genetics), Single-nucleotide polymorphism, Biology, medicine.disease, Polymorphism, Single Nucleotide, Chromosome 15, Cell Line, Tumor, Jews, medicine, Humans, Genetic Predisposition to Disease, Colorectal Neoplasms, education, Cells, Cultured
Abstract

We mapped a high-penetrance gene (CRAC1; also known as HMPS) associated with colorectal cancer (CRC) in the Ashkenazi population to a 0.6-Mb region on chromosome 15 containing SCG5 (also known as SGNE1), GREM1 and FMN1. We hypothesized that the CRAC1 locus harbored low-penetrance variants that increased CRC risk in the general population. In a large series of colorectal cancer cases and controls, SNPs near GREM1 and SCG5 were strongly associated with increased CRC risk (for rs4779584, P = 4.44 x 10(-14)).

Published
2008

4. A genome-wide association scan of tag SNPs identifies a susceptibility variant for colorectal cancer at 8q24.21

Author

Sarah Fielding, Richard Gray, Wendy Wood, Elaine C. Johnstone, David J. Kerr, Kimberley Howarth, Ruth Wild, Richard A. Hubner, Emma Jaeger, Luis G. Carvajal-Carmona, Ian Chandler, Ian Tomlinson, Ella Barclay, Steven J. Lubbe, Andrew Rowan, Wendy Atkin, Sarah L. Spain, Gabrielle S. Sellick, Julian Peto, Oliver M. Sieber, Richard F A Logan, Zoe Kemp, Lynn Martin, Jean-Baptiste Cazier, Kenneth Muir, Richard S. Houlston, Huw Thomas, Emily L. Webb, Steven Penegar, Andrew Silver, Maggie Gorman, and Peter Broderick

Subjects
Genetics, Male, Genotype, Colorectal cancer, Single-nucleotide polymorphism, Colorectal adenoma, Odds ratio, Biology, Middle Aged, medicine.disease, Polymorphism, Single Nucleotide, Polymorphism (computer science), medicine, SNP, Humans, Female, Genetic Predisposition to Disease, Allele, Colorectal Neoplasms, Aged, Chromosomes, Human, Pair 8
Abstract

Much of the variation in inherited risk of colorectal cancer (CRC) is probably due to combinations of common low risk variants. We conducted a genome- wide association study of 550,000 tag SNPs in 930 familial colorectal tumor cases and 960 controls. The most strongly associated SNP (P = 1.72 x 10(-7), allelic test) was rs6983267 at 8q24.21. To validate this finding, we genotyped rs6983267 in three additional CRC case-control series (4,361 affected individuals and 3,752 controls; 1,901 affected individuals and 1,079 controls; 1,072 affected individuals and 415 controls) and replicated the association, providing P = 1.27 x 10(-14) (allelic test) overall, with odds ratios (ORs) of 1.27 (95% confidence interval (c.i.): 1.16-1.39) and 1.47 (95% c.i.: 1.34-1.62) for heterozygotes and rare homozygotes, respectively. Analyses based on 1,477 individuals with colorectal adenoma and 2,136 controls suggest that susceptibility to CRC is mediated through development of adenomas (OR = 1.21, 95% c.i.: 1.10-1.34; P = 6.89 x 10(-5)). These data show that common, low-penetrance susceptibility alleles predispose to colorectal neoplasia.

Published
2007

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