Robin K. S. Phillips

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BACKGROUND Patients with familial adenomatous polyposis have a nearly 100 percent risk of colorectal cancer. In this disease, the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. METHODS We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in(More)
BACKGROUND Germ-line mutations in the base-excision-repair gene MYH have been associated with recessive inheritance of multiple colorectal adenomas. Tumors from affected persons displayed excess somatic transversions of a guanine-cytosine pair to a thymine-adenine pair (G:C-->T:A) in the APC gene. METHODS We screened for germ-line MYH mutations in 152(More)
BACKGROUND Familial adenomatous polyposis (FAP) is a well-described inherited syndrome, which is responsible for <1% of all colorectal cancer (CRC) cases. The syndrome is characterised by the development of hundreds to thousands of adenomas in the colorectum. Almost all patients will develop CRC if they are not identified and treated at an early stage. The(More)
BACKGROUND Although an increased cancer risk in Peutz-Jeghers syndrome is established, data on the spectrum of tumors associated with the disease and the influence of germ-line STK11/LKB1 (serine/threonine kinase) mutation status are limited. EXPERIMENTAL DESIGN We analyzed the incidence of cancer in 419 individuals with Peutz-Jeghers syndrome, and 297(More)
102 patients with familial adenomatous polyposis underwent upper gastrointestinal endoscopy as a screening test for gastroduodenal adenomas. 100 had duodenal abnormalities (dysplasia in 94, and hyperplasia in 6), usually in the second and third parts of the duodenum (91%). The periampullary area was abnormal in 87 of 97 patients who had a biopsy specimen(More)
Peutz-Jeghers syndrome (PJS, MIM175200) is an autosomal dominant condition defined by the development of characteristic polyps throughout the gastrointestinal tract and mucocutaneous pigmentation. The majority of patients that meet the clinical diagnostic criteria have a causative mutation in the STK11 gene, which is located at 19p13.3. The cancer risks in(More)
The Large Bowel Cancer Project is a collaborative prospective study of 4228 patients with a histologically proven adenocarcinoma, of whom 2336 (55 per cent) survived a 'curative' resection. Follow-up information is available on 2220 patients (95 per cent). Subsequently, 309 (14 per cent) have developed a local recurrence confirmed by: biopsy (127; 41 per(More)
Of 4583 patients in the Large Bowel Cancer Project, 713 (16 per cent) were obstructed. The site of greatest risk was the splenic flexure (49 per cent). Advanced stage was neither the full reason why some patients obstructed nor for their subsequent poor prospects (age-adjusted 5-year survival: not obstructed, 45 per cent; obstructed, 25 per cent). Also,(More)
Familial adenomatous polyposis (FAP) is a dominantly inherited colorectal tumor predisposition that results from germ-line mutations in the APC gene (chromosome 5q21). FAP shows substantial phenotypic variability: classical polyposis patients develop more than 100 colorectal adenomas, whereas those with attenuated polyposis (AAPC) have fewer than 100(More)
BACKGROUND Desmoid tumours are one of the most important and intriguing extracolonic manifestations of familial adenomatous polyposis (FAP). They have been studied only in small numbers of patients. METHODS Patients with FAP who also had desmoid tumour were identified from a polyposis registry database and their hospital notes were reviewed. RESULTS(More)