نتایج جستجو برای: familial adenomatous polyposis

تعداد نتایج: 64354  

Journal: :Australian and New Zealand Journal of Ophthalmology 1994

Journal: :Gastroenterology 2007
Miguel Abal Antonia Obrador-Hevia Klaus-Peter Janssen Laura Casadome Mireia Menendez Sabrina Carpentier Emmanuel Barillot Mechthild Wagner Wilhelm Ansorge Gabriela Moeslein Hafida Fsihi Vladimir Bezrookove Jaume Reventos Daniel Louvard Gabriel Capella Sylvie Robine

BACKGROUND & AIMS Chromosomal instability, a hallmark of most colorectal cancers, has been related to altered chromosome segregation and the consequent deficit in genetic integrity. A role for the tumor suppressor gene APC has been proposed in colorectal cancer that leads to compromised chromosome segregation even though the molecular mechanism is not yet understood. Here, we tackled the geneti...

2008
C. Palanivelu Kalpesh Jani K. Sendhilkumar R. Parthasarathi P. Senthilnathan G. Maheshkumar

BACKGROUND Familial adenomatous polyposis is a hereditary disease characterized by the presence of thousands of colonic adenomas, which, if untreated, invariably undergo malignant transformation. Because this disease manifests at a young age, the laparoscopic approach to perform surgery would be desirable due to its cosmetic benefits. We describe our experience with this procedure and review th...

Journal: :Cancer research 1999
B Romagnolo D Berrebi S Saadi-Keddoucci A Porteu A L Pichard M Peuchmaur A Vandewalle A Kahn C Perret

Mutations in the adenomatous polyposis coli gene or activating mutations in the beta-catenin gene itself are thought to be responsible for the excessive beta-catenin signaling involved in intestinal carcinogenesis. We generated transgenic mice that expressed large amounts of a NH2-terminally truncated mutant beta-catenin (deltaN131beta-catenin) in the intestine. These mice had multifocal dyspla...

Journal: :Anales del sistema sanitario de Navarra 2006
A Alonso S Moreno A Valiente M Artigas A Pérez-Juana M A Ramos Arroyo

A proportion of colorectal cancers shows some type of genetic predisposition that can be recognised in clinical practice. From the classical dominant inheritance pattern of familial adenomatous polyposis or hereditary non-polyposis colorectal cancer, through the recessive transmission of the MYH associated polyposis, to the new syndromes of the "serrated pathway" or low-penetrance alleles, the ...

Journal: :Hepato-gastroenterology 2005
Wiktor Bednarz Robert Olewinski Romualda Wojczys Krzysztof Sutkowski Pawel Domoslawski Waldemar Balcerzak

BACKGROUND/AIMS Restorative proctocolectomy is the "golden standard" in surgical treatment of ulcerative colitis and familial adenomatous polyposis. The two alternative techniques of ileal-pouch-anal anastomosis include hand-made suture and double line stapled suture. The aim of the study was the analysis of postoperative complications and functional results of the two types of anastomosis. M...

2009

Gardner=s syndrome refers to a group of children born with familial adenomatous (multiple) polyposis and significant extracolonic manifestations. Familial adenomatous polyposis is an autosomal dominant disorder originating from a germline alteration of the adenomatous polyposis coli gene in the long arm of chromosome 5. The most significant extracolonic manifestation of Gardner=s syndrome consi...

Journal: :Human mutation 2006
Sophie Lejeune François Guillemot Jean-Pierre Triboulet Stéphane Cattan Christine Mouton Nicole Porchet Sylvie Manouvrier Marie-Pierre Buisine

Familial adenomatous polyposis has been linked to germline mutations in the APC tumor suppressor gene. However, a number of patients with familial adenomatous polyposis (with either classical or attenuated phenotype) have no APC mutation. Recently, germline mutations in the Wnt pathway component gene AXIN2 have been associated with tooth agenesis-colorectal cancer syndrome. Moreover, biallelic ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2012
James M Amos-Landgraf Amy A Irving Cory Hartman Anthony Hunter Brianna Laube Xiaodi Chen Linda Clipson Michael A Newton William F Dove

Studies of tumors from human familial adenomatous polyposis, sporadic colon cancer, and mouse and rat models of intestinal cancer indicate that the majority of early adenomas develop through loss of normal function of the Adenomatous polyposis coli (APC) gene. In murine models of familial adenomatous polyposis, specifically the multiple intestinal neoplasia mouse (Min) and the polyposis in the ...

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