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Colorectal Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Jennie Grainger, Samson Tou, Steve Schlichtemeier, William Speake, Fung Joon Foo, Frank McDermott
What is FAP?Familial adenomatous polyposis.Characterised by the presence of more than 100 adenomatous polyps by the second decade.Most common adenomatous polyposis syndrome.Autosomal dominant inherited disorder characterised by early onset of hundreds to thousands of adenomatous polyps throughout the colon.Mutation in the adenomatous polyposis coli (APC) gene chromosome 5q.
Familial Adenomatous Polyposis
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Paul Kolarsick, Steven D. Wexner
Familial adenomatous polyposis (FAP) syndrome results from a mutation in the adenomatous polyposis coli (APC), a tumor suppressor gene located on chromosome 5q21. Familial adenomatous polyposis confers a nearly 100% lifetime risk of developing colorectal cancer, mostly by forty years of age. Autosomal dominant in its inheritance pattern, FAP affects 1:10,000 individuals but accounts for <1% of all colorectal cancer [1].
Familial adenomatous polyposis
Published in Alejandra Vilanova-Sánchez, Marc A. Levitt, Pediatric Colorectal and Pelvic Reconstructive Surgery, 2020
Alessandra C. Gasior, Mark Arnold
Familial adenomatous polyposis patients start to develop adenomas at the age of 12–14. There have been reports of polyps and even cancers occurring earlier, however this is rare. Genetic mutation testing should also be conducted at the same time the surveillance colonoscopy is performed. There is no need to perform this testing earlier as the disease usually does not manifest clinically before mid-teens. Additionally, the patient should be old enough to participate in the genetic counseling discussion. If the patient does not carry the FAP mutation, she/he can resume general population guidelines for surveillance.
Expression Levels of WNT Signaling Pathway Genes During Early Tooth Development
Published in Organogenesis, 2023
Yuhan Song, Fujie Song, Xuan Xiao, Zhifeng Song, Shangfeng Liu
Adenomatous polyposis coli (APC) gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in cell migration and adhesion, transcriptional activation, and apoptosis.61 Mutations in Apc may cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy.62 Besides, other diseases such as Gardner syndrome, which is characterized by the presence of multiple intracolonic polyps and extracolonic tumors, can also be caused by Apc mutation. Our previous study found that patients with Gardner syndrome also had multiple impacted and supernumerary teeth.16 We found that Apc was expressed at E14.5-P7 and there are up to 2037 different mutation forms in Apc, suggesting that Apc played an important role in all stages of early tooth development.
Impact of artificial intelligence on colorectal polyp detection for early-career endoscopists: an international comparative study
Published in Scandinavian Journal of Gastroenterology, 2022
Diba Ainechi, Masashi Misawa, Ishita Barua, Solveig Linnea Veen Larsen, Vemund Paulsen, Kjetil Kjeldstad Garborg, Lars Aabakken, Christer Julseth Tønnesen, Magnus Løberg, Mette Kalager, Shin-Ei Kudo, Kinichi Hotta, Kazuo Ohtsuka, Shoichi Saito, Hiroaki Ikematsu, Yutaka Saito, Takahisa Matsuda, Hayato Itoh, Kensaku Mori, Michael Bretthauer, Yuichi Mori
We selected 200 colonoscopy video sequences with a length of 5 s: 100 videos without polyps and 100 with one polyp. The videos were recorded in patients aged 18 years or older who underwent colonoscopy between October 2018 and January 2019 at Showa University Northern Yokohama Hospital, Yokohama, Japan. All patients provided informed consent for data provision for the study. Exclusion criteria were: Inflammatory bowel disease.Submucosal tumour or related disease (e.g., carcinoid, malignant lymphoma, etc.).Hereditary polyposis (e.g., familial adenomatous polyposis).Polyps which could not be identified because of artefacts (e.g., bubbles, residues, halation, etc.).Polyp consisting of fewer than 16 consecutive frames of white light image.Two or more polyps shown in a single frame.
Long term outcomes of sporadic large fundic gland polyps: a single-center experience
Published in Scandinavian Journal of Gastroenterology, 2021
Abdul Mohammed, Rajat Garg, Sushrut Trakroo, Amandeep Singh, Madhusudhan R. Sanaka
The Institutional Review Board approved this study at the Cleveland Clinic. A total of 4000 consecutive patients diagnosed with FGP undergoing EGD from April 2014 to December 2019 in a tertiary care hospital were retrospectively reviewed. Two investigators independently examined all EGD reports and associated histopathology reports. Of them, 132 patients were included only if they satisfied both inclusion criteria, gastric polyps ≥ 10 mm on EGD and a histopathologic diagnosis of FGP. We only included patients who had sporadic FGPs, defined as fundic gland polyps without dysplastic features, and are not a part of polyposis syndromes. Therefore, we excluded patients with any hereditary polyposis syndromes like familial adenomatous polyposis (FAP), dysplasia, adenoma, or carcinoma. The inclusion and exclusion criteria are depicted in the form of a flowsheet in Figure 1.