Genomes and Genes
Ian Pm Tomlinson
Affiliation: Cancer Research UK
- Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH/MUTYH mutationsC Thirlwell
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, 44, Lincoln s Inn Fields, London WC2A 3PX, UK
Br J Cancer 96:1729-34. 2007..We suggest that, at least in some cases, the MCRA phenotype results from germline variation that acts subsequent to tumour initiation, perhaps by causing more rapid or more likely progression from microadenoma to macroadenoma...
- A genome-wide association scan of tag SNPs identifies a susceptibility variant for colorectal cancer at 8q24.21Ian Tomlinson
Molecular and Population Genetics Laboratory, Cancer Research UK, London WC2A 3PX, UK
Nat Genet 39:984-8. 2007..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...
- A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3Ian P M Tomlinson
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London WC2A 3PX, UK
Nat Genet 40:623-30. 2008..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...
- The FH mutation database: an online database of fumarate hydratase mutations involved in the MCUL (HLRCC) tumor syndrome and congenital fumarase deficiencyJean Pierre Bayley
Department of Human Genetics, Leiden University Medical Center, P, O, Box 9503, 2300 RA, Leiden, The Netherlands
BMC Med Genet 9:20. 2008....
- EPHB2 germline variants in patients with colorectal cancer or hyperplastic polyposisAntti Kokko
Department of Medical Genetics, Molecular and Cancer Biology Research Program, P, O, Box 63, 00014 University of Helsinki, Finland
BMC Cancer 6:145. 2006..Inactivation of the gene has been shown to correlate with progression of colorectal tumorigenesis, and somatic mutations have been reported in both colorectal and prostate tumors...