polyposis

(redirected from polyposis coli)
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pol·yp·o·sis

 (pŏl′ə-pō′sĭs)
n. pl. pol·yp·o·ses (-sēz)
The presence of several polyps in the body.

polyposis

(ˌpɒlɪˈpəʊsɪs)
n
(Medicine) med the formation of many polyps or a condition characterized by such
Translations

pol·y·po·sis

n. poliposis, formación numerosa de pólipos.

polyposis

n poliposis f; familial adenomatous — poliposis adenomatosa familiar
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References in periodicals archive ?
In particular, most colorectal cancers are due to hyperactive Wnt pathway activity in the intestinal epithelium, caused by mutational inactivation of the Adenomatous Polyposis Coli (APC) tumour suppressor or by mutational activation of beta-catenin.
Existen mutaciones que inactivan la [beta]-catenina y/o el gen APC (adenomatous polyposis coli); este ultimo es un supresor tumoral que codifica una proteina inhibidora del cancer colorrectal.
(13) In general, multiple genetic alterations involved in usual colorectal neoplasia may also function in adenomatous change in juvenile polyps, including alterations in APC (adenomatous polyposis coli), K-ras, p53 and DCC (deleted colorectal carcinoma).
The classic tumor suppressor gene adenomatosis polyposis coli (APC) has been well studied in many malignancies [6-8].
Sporadic desmoid tumors are commonly associated with somatic mutations of the beta-catenin gene while desmoids associated with familial adenomatous polyposis coli often contain mutations in the APC gene [11].
Mesenteric and abdominal wall desmoid tumors are usually associated with familial adenomatous polyposis, which is caused by germline mutations in the adenomatous polyposis coli gene.
Both FAP and AFAP are associated with inherited mutations to the adenomatous polyposis coli (APC) gene [1-3].
Adenomatous Polyposis Coli is an oncosuppressor gene, whose mutation in germ line is responsible for FAP, but it is also mutated in the majority of sporadic CRCs.
Rafferty, "Polyps and polyposis coli," Clinics in Colon and Rectal Surgery, vol.
In the absence of Wnt, the free cytosolic beta-catenin is phosphorylated and is tightly controlled by a destruction complex, consisting of AXIN, tumor suppressor adenomatous polyposis coli (APC), and glycogen synthase kinase-3 (GSK-3beta).
Genotype-phenotype correlations in attenuated adenomatous polyposis coli. Am.
[2] Gardner's syndrome is believed to occur owing to mutation in a gene located on chromosome 5 (5q21-22) known as adenomatous polyposis coli (APC) tumor suppressor gene, which is strongly linked to extracolonic manifestations.