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Harris E.J.,Institute of Cancer Research Sutton | Mukesh M.B.,University of Cambridge | Mukesh M.B.,Colchester Hospital University Trust | Donovan E.M.,Royal Marsden Hospital NHS Foundation Trust | And 14 more authors.
British Journal of Radiology | Year: 2015

Objective: To determine if subsets of patients may benefit from smaller or larger margins when using laser setup and bony anatomy verification of breast tumour bed (TB) boost radiotherapy (RT). Methods: Verification imaging data acquired using cone-beam CT, megavoltage CT or two-dimensional kilovoltage imaging on 218 patients were used (1574 images). TB setup errors for laser-only setup (dlaser) and for bony anatomy verification (dbone) were determined using clips implanted into the TB as a gold standard for the TB position. Cases were grouped by centre-, patientand treatment-related factors, incluDing breast volume, TB position, seroma visibility and surgical technique. Systematic (S) and random (s) TB setup errors were compared between groups, and TB planning target volume margins (MTB) were calculated. Results: For the study population, Slaser was between 2.8 and 3.4mm, and Sbone was between 2.2 and 2.6mm, respectively. Females with larger breasts (p50.03), easily visible seroma (p#0.02) and open surgical technique (p#0.04) had larger Slaser. Sbone was larger for females with larger breasts (p50.02) and lateral tumours (p50.04). Females with medial tumours (p,0.01) had smaller Sbone. Conclusion: If clips are not used, margins should be 8 and 10mm for bony anatomy verification and laser setup, respectively. Individualization of TB margins may be considered based on breast volume, TB and seroma visibility. Advances in knowledge: Setup accuracy using lasers and bony anatomy is influenced by patient and treatment factors. Some patients may benefit from clip-based image guidance more than others. © 2015 The Authors. Published by the British Institute of Radiology.

Teerlink C.C.,University of Utah | Thibodeau S.N.,Mayo Clinic ICPCG Group | Thibodeau S.N.,Mayo Medical School | McDonnell S.K.,Mayo Clinic ICPCG Group | And 65 more authors.
Human Genetics | Year: 2014

Previous GWAS studies have reported significant associations between various common SNPs and prostate cancer risk using cases unselected for family history. How these variants influence risk in familial prostate cancer is not well studied. Here, we analyzed 25 previously reported SNPs across 14 loci from prior prostate cancer GWAS. The International Consortium for Prostate Cancer Genetics (ICPCG) previously validated some of these using a family-based association method (FBAT). However, this approach suffered reduced power due to the conditional statistics implemented in FBAT. Here, we use a case-control design with an empirical analysis strategy to analyze the ICPCG resource for association between these 25 SNPs and familial prostate cancer risk. Fourteen sites contributed 12,506 samples (9,560 prostate cancer cases, 3,368 with aggressive disease, and 2,946 controls from 2,283 pedigrees). We performed association analysis with Genie software which accounts for relationships. We analyzed all familial prostate cancer cases and the subset of aggressive cases. For the familial prostate cancer phenotype, 20 of the 25 SNPs were at least nominally associated with prostate cancer and 16 remained significant after multiple testing correction (p ≤ 1E -3) occurring on chromosomal bands 6q25, 7p15, 8q24, 10q11, 11q13, 17q12, 17q24, and Xp11. For aggressive disease, 16 of the SNPs had at least nominal evidence and 8 were statistically significant including 2p15. The results indicate that the majority of common, low-risk alleles identified in GWAS studies for all prostate cancer also contribute risk for familial prostate cancer, and that some may contribute risk to aggressive disease. © 2013 Springer-Verlag Berlin Heidelberg.

Speedy H.E.,Institute of Cancer Research Sutton | Sava G.,Institute of Cancer Research Sutton | Houlston R.S.,Institute of Cancer Research Sutton
Advances in Experimental Medicine and Biology | Year: 2013

Chronic lymphocytic leukaemia (CLL) is the most common lymphoid malignancy in Western countries, accounting for around a quarter of all leukaemias. Despite a strong familial basis to CLL, with risks in first-degree relatives of CLL cases being increased around sevenfold, the inherited genetic basis of CLL is currently largely unknown. The failure of genetic studies of CLL families to provide support for a major disease-causing locus has suggested a model of susceptibility based on the co-inheritance of multiple low-risk variants, some of which will be common. Recent genome-wide association studies of CLL have vindicated this model of inherited susceptibility to CLL, identifying common variants at multiple independent loci influencing risk. Here we review the evidence for inherited genetic predisposition to CLL and what the currently identified risk loci are telling us about the biology of CLL development. © 2013 Springer Science+Business Media New York.

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