Affiliation: University of Oxford
- Common and rare variants in multifactorial susceptibility to common diseasesWalter Bodmer
Cancer and Immunogenetics Laboratory, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK
Nat Genet 40:695-701. 2008....
- Cytostatic drug treatment causes seeding of gene promoter methylationAnders Bredberg
Cancer Research UK Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
Eur J Cancer 43:947-54. 2007..Taken together, our findings suggest activation in cancer cells of an epigenetic process enabling a tumour to generate drug-resistant variant cells...
- Sam Karlin: a personal appreciationWalter Bodmer
Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK
Theor Popul Biol 75:230-2. 2009..Subsequently Karlin established a similar programme in Israel. The overall contributions of Karlin to population genetics and molecular biology are briefly reviewed from a personal perspective...
- Cancer genetics: colorectal cancer as a modelWalter F Bodmer
CR UK Cancer and Immunogenetics Laboratory, Weatherall Institute for Molecular Medicine, Oxford University, Oxford, OX3 9DS, UK
J Hum Genet 51:391-6. 2006..The evidence for this from our work on multiple adenoma cases, and certain other examples, is discussed...
- Prostate Cancer Charitable Trust 2004 Forum: a personal overviewW Bodmer
CRUK Cancer and Immunogenetics Laboratory, Weatherall Institute for Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK
Prostate Cancer Prostatic Dis 7:277-81. 2004
- RA Fisher, statistician and geneticist extraordinary: a personal viewWalter Bodmer
Sir Walter Bodmer, Hertford College, Catte Street, Oxford OX1 3BW
Int J Epidemiol 32:938-42; discussion 945-8. 2003
- The Eurasian heartland: a continental perspective on Y-chromosome diversityR S Wells
Imperial Cancer Research Fund Cancer and Immunogenetics Laboratory and Wellcome Trust Centre for Human Genetics, University of Oxford, Headington OX3 9DS, United Kingdom
Proc Natl Acad Sci U S A 98:10244-9. 2001..The genetic results are interpreted in the context of Eurasian linguistic patterns...
- A mutated HLA-A*0101 allele in the colorectal cell line HCA-7D C Bicknell
Cancer and Immunogenetics Laboratory, Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK
Tissue Antigens 66:231-7. 2005..This has probably then been selected for in the tumour to enable escape from immune attack against an HLA-A*0101-restricted tumour-specific determinant that has also arisen as a result of the tumour being MMR defective...
- The HLA-A,B,C genotype of the class I negative cell line Daudi reveals novel HLA-A and -B allelesM J Browning
Cancer Immunology Laboratory, ICRF, John Radcliffe Hospital, Oxford, United Kingdom
Tissue Antigens 45:177-87. 1995..Thus the novel A and B alleles are not specific to the Daudi tumor. Overall, this analysis of a single East African cell illustrates the power of molecular methods to define new class I HLA alleles in non-caucasoid populations...
- Nomenclature for factors of the HLA system, 1998J G Bodmer
ICRF Cancer and Immunogenetics Laboratory, Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, United Kingdom
Tissue Antigens 53:407-46. 1999
- Alkaline-mediated differential interaction (AMDI): a simple automatable single-nucleotide polymorphism assayS Bartlett
Imperial Cancer Research Fund Cancer and Immunogenetics Laboratory, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
Proc Natl Acad Sci U S A 98:2694-7. 2001..We believe the detection system that we call AMDI (alkaline-mediated differential interaction) satisfies the above criteria and is suitable for general high-throughput SNP typing...
- Multiple rare variants in different genes account for multifactorial inherited susceptibility to colorectal adenomasNicola S Fearnhead
Cancer Research UK Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, England
Proc Natl Acad Sci U S A 101:15992-7. 2004..This overall difference is highly significant, suggesting that many rare variants collectively contribute to the inherited susceptibility to colorectal adenomas...
- Genotyping possible polymorphic variants of human mismatch repair genes in healthy Korean individuals and sporadic colorectal cancer patientsJin C Kim
Department of Surgery, University of Ulsan College of Medicine, and Laboratory of Cancer Biology and Genetics, Asan Institute for Life Sciences, 388 1 Poongnap 2 Dong Songpa Ku, Seoul 138 736, Korea
Fam Cancer 3:129-37. 2004..Further verification in other ethnic groups may provide the genotypic and phenotypic significance of single nucleotide variants found in mismatch repair genes...
- Examples of mathematical modeling: tales from the cryptMatthew D Johnston
Centre for Mathematical Biology, Mathematical Institute, University of Oxford, Oxford, UK
Cell Cycle 6:2106-12. 2007..We use the model to argue why tumorigenesis is observed to occur in stages with long lag phases between periods of rapid growth, and we identify the key parameters...
- Rare variant hypothesis for multifactorial inheritance: susceptibility to colorectal adenomas as a modelNicola S Fearnhead
Cancer Research U.K. Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, Oxford, UK
Cell Cycle 4:521-5. 2005..Recent evidence suggests that a quarter of patients with multiple adenomatous polyps are due to rare but functionally important variants in just five genes...
- Mathematical modeling of cell population dynamics in the colonic crypt and in colorectal cancerMatthew D Johnston
Centre for Mathematical Biology, Mathematical Institute, University of Oxford, 24 29 St Giles, Oxford OX1 3LB, United Kingdom
Proc Natl Acad Sci U S A 104:4008-13. 2007..The second model can be used to explain the long lag phases in tumor growth, during which new, higher equilibria are reached, before unlimited growth in cell numbers ensues...
- Cell growth, global phosphotyrosine elevation, and c-Met phosphorylation through Src family kinases in colorectal cancer cellsMuhammad Emaduddin
Cell Signalling Group and Cancer and Immunogenetics Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headley Way, Oxford OX3 9DS, United Kingdom
Proc Natl Acad Sci U S A 105:2358-62. 2008..If this also is true for CRC patients, tumors with low-SFK activity may be particularly sensitive to SFK inhibitors, and such patients should be targeted in clinical trials testing SFK inhibitors...
- Multigene amplification and massively parallel sequencing for cancer mutation discoveryFredrik Dahl
Stanford Genome Technology Center, Stanford University, Palo Alto, CA 94304, USA
Proc Natl Acad Sci U S A 104:9387-92. 2007..Seven cancer cell lines and one normal genomic DNA sample were studied with multiple mutations and polymorphisms identified among the 10 genes. Mutations and polymorphisms in the TP53 gene were confirmed by traditional sequencing...
- Enhancement of colorectal tumor targeting using a novel biparatopic monoclonal antibody against carcinoembryonic antigen in experimental radioimmunoguided surgeryJin C Kim
Department of Surgery, University of Ulsan College of Medicine and Asan Institute for Life Sciences, Seoul, Korea
Int J Cancer 97:542-7. 2002..The biparatopic MAb using 2 anti-CEA MAbs against different epitopes achieved a great affinity and avidity with accurate localization of colorectal carcinoma in experimental radioimmunoguided surgery...
- Analysis of P53 mutations and their expression in 56 colorectal cancer cell linesYing Liu
Cancer Research UK Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, UK
Proc Natl Acad Sci U S A 103:976-81. 2006....
- Genetics of colorectal cancer: hereditary aspects and overview of colorectal tumorigenesisNicola S Fearnhead
Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DZ, UK
Br Med Bull 64:27-43. 2002..The latter part of this paper focuses on the key genetic events underlying this process and provides an overview of the genetic mechanisms responsible for colorectal tumorigenesis...
- Germline mutations but not somatic changes at the MYH locus contribute to the pathogenesis of unselected colorectal cancersSarah E R Halford
Molecular and Population Genetics Laboratory, London Institute, Cancer Research United Kingdom, London, UK
Am J Pathol 162:1545-8. 2003..Somatic inactivation of the DNA glycosylases involved in the BER pathway however does not appear to be involved in colorectal tumorigenesis...
- Bottom-up histogenesis of colorectal adenomas: origin in the monocryptal adenoma and initial expansion by crypt fissionSean L Preston
Histopathology Unit, London Research Institute, Cancer Research UK, London WC2A 3PX, United Kingdom
Cancer Res 63:3819-25. 2003..Both sporadic and FAP adenomas start as a unicryptal adenomas and grow initially by crypt fission--a bottom-up pattern. Later, in sporadic adenomas, there is evidence of growth down into adjacent crypts (top-down)...
- The generation and utilization of a cancer-oriented representation of the human transcriptome by using expressed sequence tagsHelena Brentani
, Departmento de Radiologia, , , 4deg, Brazil
Proc Natl Acad Sci U S A 100:13418-23. 2003....
- MSI-low, a real phenomenon which varies in frequency among cancer typesSarah E R Halford
Molecular and Population Genetics Laboratory, Cancer Research UK, 44 Lincoln's Inn Fields, London WC2A 3PX, UK
J Pathol 201:389-94. 2003..PCR artefact was also found to masquerade as MSI-L; criteria for the assessment of MSI-L are suggested to eliminate this problem...