Download e-book for kindle: Intestinal Polyposis Syndromes: Diagnosis and Management by Lisa A. Boardman

By Lisa A. Boardman

This publication presents a entire, state-of-the paintings evaluate of intestinal polyposis syndromes. The booklet reports the main up to date scientific, administration, and genetic information about the constantly evolving colorectal that manifests as a polyposis . It offers a reference for clinicians and researchers in realizing the complexity of intestinal polyposis and the significance of using a number of modalities for the prognosis, administration and regulate of those stipulations. It additionally offers an outline of what should still alert a care supplier to the potential of a polyposis syndrome.

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Eur J Hum Genet. 2014;22(11):1334–7. 12. David SS, O’Shea VL, Kundu S. Base-excision repair of oxidative DNA damage. Nature. 2007;447(7147):941–50. Epub 2007/06/22. 13. Lipton L, Tomlinson I. The genetics of FAP and FAP-like syndromes. Fam Cancer. 2006;5(3):221–6. Epub 2006/09/26. 14. Hegde M, Ferber M, Mao R, Samowitz W, Ganguly A. Working Group of the American College of Medical G, et al. ACMG technical standards and guidelines for genetic testing for inherited colorectal cancer (Lynch syndrome, familial adenomatous polyposis, and MYHassociated polyposis).

Mork Clinical Cancer Genetics Program, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA E. D. A. E. Mork and E. Vilar Clinical Characteristics MAP is an autosomal recessive condition caused by biallelic mutations of MUTYH with a prevalence of 1:20,000 to 1:40,000 based on the estimated carrier frequency of 1–2 % in the general population [2]. MAP is typically characterized by the development of 10 to 100 adenomatous polyps in the colorectum, most frequently located in the proximal colon, and confers a life-time risk of CRC ranging from 43 % to nearly 100 %, being diagnosed at an average age of 48 [3].

1146/ annurev-med-050913-022545. Chapter 2 MUTYH-Associated Polyposis Maureen E. Mork and Eduardo Vilar Introduction Lynch syndrome and familial adenomatous polyposis (FAP) have long been identified as hereditary predisposition syndromes to colorectal cancer (CRC), most easily recognized on the basis of their autosomal dominant inheritance, young age of onset of CRC and other associated malignancies, and, in the case of FAP, the presence of adenomatous polyposis. However, in 2002 the first report of a novel hereditary predisposition to CRC describing a family with three siblings affected with CRC and polyposis who were negative for germline APC mutations was published [1].

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