Meanings of adenomatous polyposis in English

Surgery has an important role in the management of familial adenomatous polyposis.

We conclude that desmoid tumors can precede gastrointestinal manifestations of familial adenomatous polyposis or Gardner's syndrome.

Conclusions: Indomethacin suppository treatment was effective in controlling rectal remnant polyps in the two patients with familial adenomatous polyposis.

This study investigates the natural history of adrenal incidentaloma in familial adenomatous polyposis, and suggests a schema for management.

The familial adenomatous polyposis is the most common analyzed syndrome that results from germline mutations in the APC gene.

In this paper a case of vast desmoid tumor of the abdominal wall associated with familial adenomatous polyposis is reported.

Although the natural history is similar to lesions occurring sporadically, these patients have concomitant familial adenomatous polyposis-associated manifestations under radiologic surveillance.

Ileorectal anastomosis is still an option in patients with familial adenomatous polyposis with rectal polyp sparing and good compliance for follow-up.

The molecular studies allow the clinician to have a new approach in the management and screening of families with familial adenomatous polyposis.

Although the majority of reported cases manifested attenuated adenomatous polyposis, hyperplastic polyps and serrated adenomas appear to be more common than expected.

PMID: 12908794 In this paper a case of vast desmoid tumor of the abdominal wall associated with familial adenomatous polyposis is reported.

Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene are linked to both familial and sporadic human colon cancer.

They are extremely rare in the sporadic form, while they are found in about 10% of patients affected by familial adenomatous polyposis.

These findings offer a novel option in the pharmacological treatment of desmoids, leading to medical therapy of these neoplastic lesions in familial adenomatous polyposis patients.

We believe that if there were a strong genetic predisposition or association with familial adenomatous polyposis, it should have been seen in this patient sample.

Most mutations found in familial adenomatous polyposis patients are of the truncation type, and the phenotype is affected by the mutation sites in the gene.