Publications
288 results found
Sloane J, Ranchod P, Williams G, et al., 2013, Familial adenomatous polyposis: not all masses are desmoids., Fam Cancer, Vol: 12, Pages: 525-528
Familial adenomatous polyposis (FAP) is a multi-system disease characterised by the development of hundreds to thousands of colorectal adenomas which inevitably progress to carcinoma without treatment. It is commonly associated with extra colonic lesions including osteomas, epidermoid cysts and desmoid tumours. Desmoid tumours are troublesome due to their size and bulk and are a significant cause of morbidity and mortality in FAP. This series highlights three cases in which patients with FAP developed masses thought initially to be manifestations of the condition. Further investigation in fact demonstrated neurofibromatosis type 1 in all three patients. All masses in FAP patients cannot be assumed to be disease related (desmoid, osteoma, epidermoid cyst or carcinoma).
McLaughlin SD, Culkin A, Cole J, et al., 2013, Exclusive elemental diet impacts on the gastrointestinal microbiota and improves symptoms in patients with chronic pouchitis, JOURNAL OF CROHNS & COLITIS, Vol: 7, Pages: 460-466, ISSN: 1873-9946
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- Citations: 21
Bhangu A, Beynon J, Brown G, et al., 2013, Consensus statement on the multidisciplinary management of patients with recurrent and primary rectal cancer beyond total mesorectal excision planes, BRITISH JOURNAL OF SURGERY, Vol: 100, Pages: E1-E33, ISSN: 0007-1323
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- Citations: 185
Brigic A, Symons NRA, Faiz O, et al., 2013, SYSTEMATIC REVIEW OF ENDOSCOPIC FULL THICKNESS RESECTION (EFTR) TECHNIQUES FOR COLONIC LESIONS, Annual General Meeting of the British-Society-of-Gastroenterology, Publisher: BMJ PUBLISHING GROUP, Pages: A48-A49, ISSN: 0017-5749
Davis HL, Cuadrado PR, Bardella C, et al., 2013, Aberrant Epithelial Expression of the BMP Antagonist GREMLIN1 in Human Colorectal Lesions and a Mouse Model of Hereditary Mixed Polyposis Syndrome (HMPS) Acts via Promotion of a Stem-Cell Phenotype, Digestive Disease Week / 28th Annual Residents and Fellows Research Conference of the Society-for-Surgery-of-the-Alimentary-Tract (SSAT), Publisher: W B SAUNDERS CO-ELSEVIER INC, Pages: S26-S26, ISSN: 0016-5085
Bhandari S, Onganer PU, Romero D, et al., 2013, In vitro studies of the Wnt signalling pathways in FAP desmoid tumour, Joint Meeting of the Section-of-Surgery of the Royal-Society-of-Medicine / Annual Meeting of the Society-of-Academic-and-Research-Surgery, Publisher: WILEY-BLACKWELL, Pages: 38-38, ISSN: 0007-1323
Palles C, Cazier J-B, Howarth KM, et al., 2013, Germline mutations affecting the proofreading domains of POLE and POLD1 predispose to colorectal adenomas and carcinomas, NATURE GENETICS, Vol: 45, Pages: 136-144, ISSN: 1061-4036
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- Citations: 695
Irving GRB, Howells LM, Sale S, et al., 2013, Prolonged Biologically Active Colonic Tissue Levels of Curcumin Achieved After Oral Administration-A Clinical Pilot Study Including Assessment of Patient Acceptability, CANCER PREVENTION RESEARCH, Vol: 6, Pages: 119-128, ISSN: 1940-6207
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- Citations: 73
Latchford AR, Maeda Y, Clark SK, 2013, Nonsteroidal anti-inflammatory drugs (NSAID) and aspirin for preventing colorectal adenomas and carcinomas in patients with previous adenomas and/or genetic disposition, Cochrane Database of Systematic Reviews, Vol: 2013
This is the protocol for a review and there is no abstract. The objectives are as follows: To determine if administration of nonsteroidal anti-inflammatory drugs (NSAID) and/or aspirin is effective as chemoprevention for colorectal adenomas and carcinomas in patients with previous colorectal adenomas and/or those who have genetic predispositions, compared to currently available other agents or no intervention and to assess adverse effects associated with the intervention. The following hypotheses will be tested: 1. NSAID and/or aspirin is better than no intervention 2. NSAID and/or aspirin is better than a placebo/sham intervention; 3. Aspirin with combination of resistant starch is better than no intervention; 4. One type of NSAID is better than another type; 5. Increased dose of NSAID and/or aspirin is better than another dose.
Latchford AR, Maeda Y, Clark SK, 2013, Nonsteroidal anti-inflammatory drugs (NSAID) and aspirin for preventing recurrence and metachronous colorectal carcinomas in patients previously treated for colorectal cancer, Cochrane Database of Systematic Reviews, Vol: 2013
This is the protocol for a review and there is no abstract. The objectives are as follows: To determine if administration of nonsteroidal anti-inflammatory drugs (NSAID) and/or aspirin is effective as chemoprevention for colorectal cancer in patients with previous colorectal carcinomas, compared to currently available other agents or no intervention and to assess adverse effects associated with the intervention. The following hypotheses will be tested: 1. NSAID and/or aspirin is better than no intervention 2. NSAID and/or aspirin is better than a placebo/sham intervention; 3. Aspirin with combination of resistant starch is better than no intervention; 4. One type of NSAID is better than another type; 5. Increased dose of NSAID and/or aspirin is better than another dose.
Tsang FJ, Mallappa S, Teh W, et al., 2013, Peutz-Jeghers Syndrome and carcinoma of the breast: call for new breast imaging surveillance guidelines, Annual Scientific Meeting of the British-Society-of-Breast-Radiology (BSBR), Publisher: BMC, ISSN: 1465-542X
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- Citations: 1
Balmforth DC, Phillips RKS, Clark SK, 2012, Advanced duodenal disease in familial adenomatous polyposis: how frequently should patients be followed up after successful therapy?, Fam Cancer, Vol: 11, Pages: 553-557
Duodenal polyposis is found in the majority of patients with familial adenomatous polyposis. Endoscopic surveillance programmes grade the severity of duodenal disease according to the Spigelman classification (stages 0-IV) to identify patients at risk of developing adenocarcinoma. To evaluate the progression of duodenal polyposis in patients with a previous diagnosis of Spigelman stage IV disease who have been downstaged by endoscopic or pharmacological means. A database search of a large polyposis registry identified patients who had been downstaged from stage IV disease and had further opportunity for disease progression. These patients were divided into three groups according to their new Spigelman stage. A measure of a patient's disease progression was obtained by the increase in stage over the recommended follow up time period for their new, reduced, Spigelman stage. Group 1 (n = 16) were downstaged to stage III disease, with 50 % progressing back to stage IV over the recommended 1-year follow up period. Group 2 (n = 19) were downstaged to stage II disease, with 84 % progressing over the recommended 3-year follow up period. Group 3 (n = 6) were downstaged to stage I disease, with 100 % progressing over the recommended 5-year follow up period. Patients downstaged from Spigelman stage IV demonstrate an increased rate of disease progression in comparison to reported rates of primary disease progression. An amendment to the current endoscopic surveillance protocol is recommended to ensure that once a patient has been diagnosed with stage IV disease they are treated as a high-risk patient in perpetuity.
Bhandari S, Sinha A, Tam E, et al., 2012, Diffusion tensor imaging (DTI) of desmoid tumours in familial adenomatous polyposis: initial experience., Eur J Radiol, Vol: 81, Pages: 3646-3651
PURPOSE: To assess the feasibility of diffusion tensor imaging (DTI) of desmoid tumours in familial adenomatous polyposis (FAP). MATERIALS AND METHODS: Following ethical approval and informed consent, FAP patients with desmoids underwent DTI. Fractional anisotropy (FA), relative anisotropy (RA) and apparent diffusion coefficient (ADC) were compared to control muscle using Mann-Whitney test; and to tumour site and signal intensity using one way analysis of variance (ANOVA). Imaging was repeated after 1 year. RESULTS: 15 desmoids (6 intra-abdominal; 6 abdominal wall, 3 extra-abdominal; size range: 1.6-22.9 cm) were evaluated in 9 patients. DTI was successful in 12/15 desmoid tumours. Median (range) of RA, FA and ADC were 0.23×10(-3) mm2/s (0.17-0.26); 0.27×10(-3) mm2/s (0.21-0.31); and 1.65×10(-3) mm2/s (1.39-1.91) for desmoids, significantly different from muscle: 0.27×10(-3) mm2/s (0.23-0.40), 0.32×10(-3) mm2/s (0.28-0.46), and 1.45×10(-3) mm2/s (0.92-1.63) (p=0.0001, p=0.0001, p=0.0016, respectively). There was no difference in RA, FA or ADC between tumour sites, or signal intensity (p>0.05). One year later, 2 patients had died. Tumour increased in size in 1 patient (+61%). DTI quantification was possible in only 8/13 tumours. FA, RA and ADC were not significantly different from baseline (p=0.77, 0.71 and 0.34, respectively). CONCLUSIONS: Assessment of water diffusion has the potential to provide insight into tumour microstructure and is feasible in desmoids. Desmoid tumours demonstrate anisotropy but diffusion is less restricted and less directional than in muscle.
Latchford AR, Neale K, Phillips RKS, et al., 2012, Juvenile Polyposis Syndrome: A Study of Genotype, Phenotype, and Long-term Outcome, DISEASES OF THE COLON & RECTUM, Vol: 55, Pages: 1038-1043, ISSN: 0012-3706
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- Citations: 104
Bhandari S, Taylor NJ, Sinha A, et al., 2012, Can Combined <SUP>18</SUP>F-FDG-PET and Dynamic Contrast-Enhanced MRI Predict Behavior of Desmoid Tumors in Patients With Familial Adenomatous Polyposis?, DISEASES OF THE COLON & RECTUM, Vol: 55, Pages: 1032-1037, ISSN: 0012-3706
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- Citations: 6
Cornish J, Wooding K, Tan E, et al., 2012, Study of sexual, urinary, and fecal function in females following restorative proctocolectomy, INFLAMMATORY BOWEL DISEASES, Vol: 18, Pages: 1601-1607, ISSN: 1078-0998
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- Citations: 20
Bhandari S, Ranchod P, Sinha A, et al., 2012, Familial Adenomatous Polyposis-Related Desmoids Presenting With Air-Fluid Level: A Clinical Review and Management Algorithm, DISEASES OF THE COLON & RECTUM, Vol: 55, Pages: 810-814, ISSN: 0012-3706
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- Citations: 2
Sinha A, Hansmann A, Bhandari S, et al., 2012, Imaging assessment of desmoid tumours in familial adenomatous polyposis: is state-of-the-art 1.5 T MRI better than 64-MDCT?, BRITISH JOURNAL OF RADIOLOGY, Vol: 85, Pages: E254-E261, ISSN: 0007-1285
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- Citations: 18
Landy J, Al-Hassi HO, Peake ST, et al., 2012, INAPPROPRIATE INFLAMMATORY RESPONSES IN THE ILEUM OF ULCERATIVE COLITIS PATIENTS, GUT, Vol: 61, Pages: A222-A222, ISSN: 0017-5749
Smith JJ, Netuveli G, Sleight SP, et al., 2012, Development of a social morbidity score in patients with chronic ulcerative colitis as a potential guide to treatment, COLORECTAL DISEASE, Vol: 14, Pages: e250-e257, ISSN: 1462-8910
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- Citations: 8
McNicol FJ, Kennedy RH, Phillips RKS, et al., 2012, Laparoscopic total colectomy and ileorectal anastomosis (IRA), supported by an enhanced recovery programme in cases of familial adenomatous polyposis, COLORECTAL DISEASE, Vol: 14, Pages: 458-462, ISSN: 1462-8910
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- Citations: 19
Bhandari S, Sinha A, Moonrose J, et al., 2012, Can combined fluorine-18 flurodeoxyglucose positron emission tomography (18f-FDG PET) and dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) predict behaviour of desmoid tumours in familial adenomatous polyposis (FAP) patients?, Annual Meeting of the Society-of-Academic-and-Research-Surgery, Publisher: WILEY-BLACKWELL, Pages: 48-48, ISSN: 0007-1323
Lynch PM, Rodriguez-Bigas M, Burke CA, et al., 2012, An International, Randomized Trial of Celecoxib Versus Celecoxib Plus Difluoromethylornithine in Patients With Familial Adenomatous Polyposis, Digestive Disease Week (DDW), Publisher: MOSBY-ELSEVIER, Pages: 285-285, ISSN: 0016-5107
Soobrah R, Clark SK, 2012, Your patient information website: how good is it?, COLORECTAL DISEASE, Vol: 14, Pages: e90-e94, ISSN: 1462-8910
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- Citations: 33
Clark S, 2012, Outcome of right- and left-sided colonic and rectal cancer following surgical resection. Suttie SA, Shaikh I, Mullen R et al. Colorectal Dis 2011; 13: 884-9., Colorectal Dis, Vol: 14
Sorelli PG, Clark SK, Jenkins JT, 2012, Laparoscopic repair of primary perineal hernias: the approach of choice in the 21st century, COLORECTAL DISEASE, Vol: 14, Pages: e72-e73, ISSN: 1462-8910
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- Citations: 13
Tudyka VN, Clark SK, 2012, Surgical treatment in familial adenomatous polyposis., Ann Gastroenterol, Vol: 25, Pages: 201-206, ISSN: 1108-7471
Familial adenomatous polyposis (FAP) is a dominantly inherited condition caused by germline mutation of the APC gene resulting in formation of numerous large bowel adenomas in late childhood or adolescence. Unless these are removed, colorectal cancer inevitably develops. Prophylactic surgical treatment is required to prevent this. In surgical decision making, considerations should include genotype-phenotype correlation, perioperative morbidity and risk of impaired sexual and reproductive function in young patients after major pelvic surgery. Colectomy with ileorectal anastomosis remains an appropriate prophylactic procedure in many patients. However, in those with high-density polyposis or a genotype predictive of aggressive disease, restorative proctocolectomy is preferable. There is a range of other features, as FAP is essentially a systemic disease. These include duodenal and peri-ampullary adenomas and carcinoma, desmoid tumors, papillary-type thyroid carcinoma and pancreatic carcinoma among others. With improved management that reduces the risk of colorectal cancer, these extracolonic manifestations have become of increasing clinical significance. For all FAP patients, including those undergoing proctocolectomy, thorough surveillance is of vital importance as there remains a risk of developing neoplasia. Despite advances in surgical techniques, screening and surveillance, life expectancy in patients with FAP is still less than that of the general population.
Clark SK, 2012, Colorectal Cancer Screening and Surveillance, Contemporary Coloproctology, Publisher: Springer London, Pages: 109-121, ISBN: 9780857298881
Bernardo D, Mann ER, Al-Hassi HO, et al., 2012, Human gut-specific homeostatic dendritic cells are generated from blood precursors by the gut microenvironment., Inflammatory Bowel Diseases, Vol: 7, Pages: 1275-1286
BACKGROUND: Dendritic cells (DC) dictate not only the type of T-cell immunity, but also homing patterns of T cells in mice. In humans, we characterized normal human gut DC and tested whether gut-specific homeostatic DC could be generated from blood precursors by factors in the gut microenvironment.METHODS: We characterized the phenotype and function of healthy human gut DC compared with blood and skin DC, and studied whether conditioning of blood DC in the presence of colonic biopsy supernatants (Bx-SN) induced gut-like phenotype and functions.RESULTS: Blood DC mostly expressed both gut and skin homing markers, indicating potential to migrate to both major immune surface organs, and induced multi-homing T cells. However, DC within gut or skin did not demonstrate this multi-homing phenotype, were tissue-specific, and induced tissue-specific T cells. Human gut DC were less stimulatory for allogeneic T cells than their dermal and blood counterparts. Human blood DC cultured in vitro lost homing marker expression. Conditioning of human enriched blood DC with colonic Bx-SN from healthy controls induced a gut-homing phenotype and a homeostatic profile. Moreover, Bx-SN-conditioned DC demonstrated a restricted T-cell stimulatory capacity and preferentially induced gut-specific T cells. Retinoic acid and transforming growth factor beta (TGF-β) mediated the acquisition of the gut-homing and homeostatic properties, respectively, induced by colonic Bx-SN on blood enriched DC.CONCLUSIONS: Tissue-specific factors manipulate immunity via modulating characteristics of DC and may provide tools to generate tissue-specific immunotherapy. (Inflamm Bowel Dis 2011;).
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