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NCBI states that physicians must ensure they understand the "risks, benefits, and limitations" of any genetic test done, since in "for almost one third of individuals assessed for FAP, the physician misinterpreted the test results".

Once the diagnosis of FAP is made, close colonoscopic surveillance with polypectomy is required. Prenatal testing is possible if a disease-causing mutation is identified in an affected family member; however, prenatal testing for typically adult-onset disorders is uncommon and requires careful genetic counseling.

Ultrasound of the abdomen and blood tests evaluating liver function are often performed to rule out metastasis to the liver. Because of the way familial polyposis develops, it is possible to have the genetic condition, and therefore be at risk, but have no polyps or issues so far.

Therefore, an individual may be diagnosed "at risk of" FAP, and require routine monitoring, but not yet actually have FAP i.

Clinical management can cover several areas:. NCBI states that "Although most individuals diagnosed with an APC-associated polyposis condition have an affected parent, the family history may appear to be negative because of failure to recognize the disorder in family members, early death of the parent before the onset of symptoms, or late onset of the disease in the affected parent.

A small number of polyps can often be excised removed during the procedure, if found, but if there are more severe signs or numbers, inpatient surgery may be required.

NCBI states that when an individual is identified as having FAP, or the mutations resulting in FAP: "It is appropriate to evaluate the parents of an affected individual a with molecular genetic testing of APC if the disease-causing mutation is known in the proband [person first identified with the condition] or b for clinical manifestations of APC-associated polyposis conditions".

Treatment for FAP depends on the genotype. Most individuals with the APC mutation will develop colon cancer by the age of 40, although the less-common attenuated version typically manifests later in life 40— Accordingly, in many cases, prophylactic surgery may be recommended before the age of 25, or upon detection if actively monitored.

There are several surgical options that involve the removal of either the colon or both the colon and rectum. Treatment for the two milder forms of FAP may be substantially different from the more usual variant, as the number of polyps are far fewer, allowing more options.

Various medications are being investigated for slowing malignant degeneration of polyps, most prominently the non-steroidal anti-inflammatory drugs NSAIDs.

NSAIDS have been shown to significantly decrease the number of polyps but do not usually alter management since there are still too many polyps to be followed and treated endoscopically.

Prior to reaching the advanced stages of colorectal cancer, the polyps are confined to the inner wall and thickness of the intestinal tract and do not metastasize or 'spread'.

So provided FAP is detected and controlled either at the pre-cancerous stage or when any cancerous polyps are still internal to the intestinal tract, surgery has a very high success rate of preventing or removing cancer, without recurrence, since the locations giving rise to cancer are physically removed in toto by the surgery.

Following surgery, if a partial colectomy has been performed, colonoscopic surveillance of the remaining colon is necessary as the individual still has a risk of developing colon cancer.

However, if this happened, it would be a fresh incident from polyps developing anew in the unremoved part of the colon subsequent to surgery, rather than a return or metastasis of any cancer removed by the original surgery.

The incidence of the mutation is between 1 in 10, and 1 in 15, births. Without colectomy, colon cancer is virtually inevitable.

The mean age of colon cancer in untreated individuals is 39 years range 34—43 years. As a result, it retains part of its ability to suppress polyps.

This table compares the different subtypes of FAP: [2] [1]. Because of the genetic nature of FAP, polyposis registries have been developed around the world.

The purpose of these registries is to increase knowledge about the transmissibility of FAP, but also to document, track, and notify family members of affected individuals.

One study has shown that the use of a registry to notify family members call-ups significantly reduced mortality when compared with probands. Mark's polyposis registry is the oldest in the world, started in , and many other polyposis registries now exist.

Ankyrin : Long QT syndrome 4. From Wikipedia, the free encyclopedia. June Am J Hum Genet. Glandular and epithelial neoplasms ICD-O — Small-cell carcinoma Combined small-cell carcinoma Verrucous carcinoma Squamous cell carcinoma Basal-cell carcinoma Transitional cell carcinoma Inverted papilloma.

Renal cell carcinoma Endometrioid tumor Renal oncocytoma. Lobular carcinoma in situ Invasive lobular carcinoma. Medullary carcinoma of the breast Medullary thyroid cancer.

Acinic cell carcinoma. Warthin's tumor Thymoma Bartholin gland carcinoma. See also Template:Epithelium and epithelial tissue. Squamous cell carcinoma Adenocarcinoma.

Duodenal cancer Adenocarcinoma. Carcinoid Pseudomyxoma peritonei. Squamous cell carcinoma. Gastrointestinal stromal tumor Krukenberg tumor metastatic.

Primary peritoneal carcinoma Peritoneal mesothelioma Desmoplastic small round cell tumor. Cytoskeletal defects.

Hypertrophic cardiomyopathy 7, 2 Nemaline myopathy 4, 5. Hypertrophic cardiomyopathy 3 Nemaline myopathy 1. Hypertrophic cardiomyopathy 9.

Charcot—Marie—Tooth disease 2A Hereditary spastic paraplegia Primary ciliary dyskinesia Short rib-polydactyly syndrome 3 Asphyxiating thoracic dysplasia 3.

Tauopathy Cavernous venous malformation. Spectrin : Spinocerebellar ataxia 5 Hereditary spherocytosis 2, 3 Hereditary elliptocytosis 2, 3 Ankyrin : Long QT syndrome 4 Hereditary spherocytosis 1.

See also: cytoskeletal proteins. Categories : Benign neoplasms Gastrointestinal cancer Hereditary cancers. Hidden categories: CS1 Spanish-language sources es All articles with unsourced statements Articles with unsourced statements from January Namespaces Article Talk.

Views Read Edit View history. Help Community portal Recent changes Upload file. Download as PDF Printable version.

Wikimedia Commons. Endoscopic image of sigmoid colon of patient with familial adenomatous polyposis. Gastroenterology , Oncology.

Colonoscopy Polypectomy Upper endoscopy Colectomy. Under 0—, typ. Gastric fundic polyps and duodenal adenomas are also seen.

Therefore, polyps and cancers may manifest in the upper portion of the colon or upper gastrointestinal tract rather than the usual locations.

Not settled as yet. Colorectal cancer risk penetrance and age if untreated. Typical ages: 34—43 avg. The likelihood of detecting an APC mutation is highly dependent on the severity of colonic polyposis and on the family history..

Linkage testing is not possible for families with a single affected individual, a situation that often occurs when an individual has a de novo gene mutation and no affected offspring..

Most partial and whole APC deletions are associated with — colonic adenomas, although attenuated FAP has been seen.

Attenuated FAP is associated with mutations typically truncating in the 5' part of the gene codons 1— , exon 9, and the distal 3' end of the gene; interstitial deletions of chromosome 5q22 that include APC; partial and whole-gene deletions; and somatic mosaicism for APC mutations that are generally associated with classic FAP.

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