Sheila A Rodwell
Affiliation: University of Cambridge
- Increased tumorigenesis associated with loss of the tumor suppressor gene Cadm1Louise van der Weyden
Experimental Cancer Genetics, The Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1HH, UK
Mol Cancer 11:29. 2012..Inactivation of CADM1, either by promoter hypermethylation or loss of heterozygosity, has been reported in a wide variety of tumor types, thus it has been postulated as a tumor suppressor gene...
- Pathways of colorectal carcinogenesisMark J Arends
Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK
Appl Immunohistochem Mol Morphol 21:97-102. 2013....
- Activation of K-RAS by co-mutation of codons 19 and 20 is transformingAdam Naguib
Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge, UK, CB2 0QQ, UK
J Mol Signal 6:2. 2011..This demonstrated the synergistic effects of co-mutation of codons 19 and 20 and illustrated that co-mutation of these codons is functionally significant...
- Differential expression of selected histone modifier genes in human solid cancersHilal Ozdag
Department of Oncology, Hutchison MRC Research Centre, University of Cambridge, Cambridge CB2 2XZ, UK
BMC Genomics 7:90. 2006..Expression of each gene in 225 samples (135 primary tumours, 47 cancer cell lines, and 43 normal tissues) was analysedby QRT-PCR, normalized with 8 housekeeping genes, and given as a ratio by comparison with a universal reference RNA...
- The pro-apoptotic K-Ras 4A proto-oncoprotein does not affect tumorigenesis in the ApcMin/+ mouse small intestineCharles E Patek
Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK
BMC Gastroenterol 8:24. 2008..By this means tumorigenesis in the small intestine was compared between ApcMin/+, K-ras+/+ and ApcMin/+, K-rastmDelta4A/tmDelta4A mice that can, and cannot, express the K-ras 4A proto-oncoprotein respectively...
- Alterations in PTEN and PIK3CA in colorectal cancers in the EPIC Norfolk study: associations with clinicopathological and dietary factorsAdam Naguib
Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 0QQ, UK
BMC Cancer 11:123. 2011....
- Lifestyle factors and p53 mutation patterns in colorectal cancer patients in the EPIC-Norfolk studyJin Young Park
Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
Mutagenesis 25:351-8. 2010..001). Our results suggest that p53 mutations accelerate progression of CRC to advanced Dukes' stage in association with higher meat especially red meat intakes...
- Inhibition of lipoprotein-associated phospholipase A2 diminishes the death-inducing effects of oxidised LDL on human monocyte-macrophagesK L Carpenter
Department of Pathology, University of Cambridge, UK
FEBS Lett 505:357-63. 2001..Hydrolysis products of oxidised phospholipids thus account for over a third of the cytotoxic and apoptosis-inducing effects of oxidised LDL on macrophages...
- A novel immunohistochemical method for estimating cell cycle phase distribution in ovarian serous neoplasms: implications for the histopathological assessment of paraffin-embedded specimensI S Scott
MRC Cancer Cell Unit, Hutchison MRC Research Centre, Hills Road, Cambridge CB2 2XZ, UK
Br J Cancer 90:1583-90. 2004..Immunohistochemical estimates of the S-phase fraction may identify serous borderline tumours likely to exhibit malignant progression and/or select serous cystadenocarcinomas likely to respond to adjuvant therapy...
- Dietary, lifestyle and clinicopathological factors associated with BRAF and K-ras mutations arising in distinct subsets of colorectal cancers in the EPIC Norfolk studyAdam Naguib
Department of Pathology, University of Cambridge, Addenbrooke s Hospital, Cambridge CB22QQ, UK
BMC Cancer 10:99. 2010..This study investigates the associations between BRAF and K-ras mutations and clinicopathological, lifestyle and dietary factors in colorectal cancers...
- Using surrogate biomarkers to improve measurement error models in nutritional epidemiologyRuth H Keogh
MRC Biostatistics Unit, Cambridge, U K MRC Centre for Nutritional Epidemiology in Cancer Prevention and Survival, Department of Public Health and Primary Care, University of Cambridge, Cambridge, U K Department of Medical Statistics, London School of Hygiene and Tropical Medicine, London, U K
Stat Med 32:3838-61. 2013....
- A conditional model of MLL-AF4 B-cell tumourigenesis using invertor technologyM Metzler
MRC Laboratory of Molecular Biology, Cambridge, UK
Oncogene 25:3093-103. 2006..These findings show that the MLL-AF4 fusion protein does not have a mandatory role in multi-potent haematopoietic stem cells to cause cancer and indicates that MLL-AF4 has an instructive function in the phenotype of the tumour...
- Mutation analysis of CBP and PCAF reveals rare inactivating mutations in cancer cell lines but not in primary tumoursH Ozdag
Cancer Genomics Program, Department of Oncology, University of Cambridge, Hutchison MRC Research Centre, Cambridge CB2 2XZ, UK
Br J Cancer 87:1162-5. 2002..We identified two CBP truncations (both in cell lines), seven PCAF missense variants and four CBP intronic microdeletions. These data suggest that neither gene is commonly inactivated in human epithelial cancers...
- Renal allograft recipients with high susceptibility to cutaneous malignancy have an increased prevalence of human papillomavirus DNA in skin tumours and a greater risk of anogenital malignancyM J Arends
Department of Pathology, Edinburgh University Medical School, UK
Br J Cancer 75:722-8. 1997..005) or the low-susceptibility group (0%)...
- Prevalence of human papillomavirus DNA in cutaneous neoplasms from renal allograft recipients supports a possible viral role in tumour promotionL A Stark
Department of Pathology, University of Edinburgh, UK
Br J Cancer 69:222-9. 1994....
- Accumulation of p53 is associated with tumour progression in cutaneous lesions of renal allograft recipientsL A Stark
Department of Pathology, Edinburgh University Medical School, UK
Br J Cancer 70:662-7. 1994..These data imply that factors other than p53 gene mutation play a part in accumulation of p53 in skin cancers...
- The RASSF1A isoform of RASSF1 promotes microtubule stability and suppresses tumorigenesisL van der Weyden
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom
Mol Cell Biol 25:8356-67. 2005..Thus, our results demonstrate that Rassf1A acts as a tumor suppressor gene...