RT-PCR was used to examine the expression of LAR (encoding the leukocyte-common antigen-related protein tyrosine phosphatase) in normal human colon mucosa, and colon polyps and tumors.
In the case of colon cancer, we were fortunate in identifying an inherited tumor suppressor gene, the APC gene, that plays a major etiologic role in both the inherited disease, familial adenomatous polyposis (FAP), and in sporadic colon polyps.
There were no significant differences between the TT and NTT groups in gender; age at first admission, colectomy, and last follow-up visit; number of colonic polyps; or in presence of colorectal cancers, gastroduodenal adenomas, gastric fundic gland polyposis, retinal pigmented lesions, or extraintestinal tumors.
We have previously suggested that the APC protein might modulate the frequency of mutations, such as loss of heterozygosity (LOH), necessary for colon polyp formation.
Clinical studies revealed that the GST activity of blood lymphocytes from individuals with either a personal or family history of colorectal cancer or a personal history of colon polyps was decreased significantly when compared to that of healthy controls.
Clinical studies revealed that the GST activity of blood lymphocytes from individuals with either a personal or family history of colorectal cancer or a personal history of colon polyps was decreased significantly when compared to that of healthy controls.
We conclude that it is important to analyze p53 mutations in colonic polyps, especially when the cut end of the polyp is difficult to evaluate histologically, in order to predict recurrence.
It was shown that the 3-month supplementation of patients having colon polyps with folic acid (5 mg/day) led to a 35% decrease in abnormally high ornithine decarboxylase activity in polyps that was accompanied by a 43% increase of S-adenosylmethionine content in polyps.
In conclusion, patients with active Acro have a reduced expression of PPARgamma in the colonic mucosa, which appears be related to the increased serum IGF-I levels and might lead to an increased prevalence of colonic polyps.
Inactivation of one Cdx2 allele predisposes mice to develop colon polyps, and loss of CDX2 expression is a feature of some poorly differentiated colon carcinomas in humans.
In conclusion, patients with active Acro have a reduced expression of PPARgamma in the colonic mucosa, which appears be related to the increased serum IGF-I levels and might lead to an increased prevalence of colonic polyps.
The HPP1 gene was initially discovered because of its frequent hypermethylation in hyperplastic colon polyps, but it is also hypermethylated in colorectal adenomas and carcinomas.
In this study we evaluated the expression of PPARgamma in the biopsy samples of the polyps and outside polyps colonic mucosa from seven patients with active, untreated acromegaly, 11 with cured disease, and 15 controls.
In this study the expression and mutations of the PPARgamma gene in the colonic polyps and mucosa outside polyps were investigated in 10 acromegalic and 17 non-acromegalic patients.
The proband's metastatic duodenal cancer and his sister's malignant colon polyps had high-frequency microsatellite instability but had detectable MLH1, MSH2, and MSH6 proteins by immunohistochemistry.
From this descriptive study, it seems that the short-term risk for colonic polyps in I1307KAPC mutation is low, primarily affecting patients with previously diagnosed colon tumors.