An extended study, involving adenomatous polyps and carcinomatous material in immunostaining, revealed detectable presence of the p185 protein in 20% of carcinomas, consistent with immunoprecipitation data derived using established cell lines.
Since some gastric cancers are considered to originate from the intestinal metaplasia, it is likely that the adenomatous polyposis coli (APC) gene, the mutation of which causes adenomatous polyps in the colon, is associated with carcinogenesis of gastric cancer.
In this study plasminogen activators and their type 1 inhibitor were evaluated in colonic tissue from 19 patients with familial adenomatous polyposis coli, an inherited disorder characterised by the presence of thousands of adenomatous polyps in the colorectum which predispose to colorectal cancer.
Desmoid tumors are usually a complication of familial adenomatous polyposis, a predisposition to the early development of premalignant adenomatous polyps in the colorectum due to chain-terminating mutations of the APC gene.
The expression of CD44-mRNA was examined in 90 specimens from 44 patients with colorectal cancer or colorectal adenomatous polyps and in the peripheral blood leukocytes from 7 healthy volunteers by reverse transcription-polymerase chain reaction and Southern blot hybridization.
In the present study, expression of alternatively spliced variants of CD44 and their cellular distribution have been investigated in human colonic tumours and in the corresponding normal mucosa, in addition to benign adenomatous polyps.
Expression of several members of the BCL-2 family of genes was investigated by immunohistochemical methods in 30 primary colorectal adenocarcinomas and 24 adenomatous polyps.
We conclude that enhanced immunoreactivity of MUC1, MUC2 and MUC3 mucin tandem repeats occurs in adenomatous polyps and is associated with an increased risk for malignant transformation.
We conclude that enhanced immunoreactivity of MUC1, MUC2 and MUC3 mucin tandem repeats occurs in adenomatous polyps and is associated with an increased risk for malignant transformation.
We conclude that enhanced immunoreactivity of MUC1, MUC2 and MUC3 mucin tandem repeats occurs in adenomatous polyps and is associated with an increased risk for malignant transformation.
We conclude that enhanced immunoreactivity of MUC1, MUC2 and MUC3 mucin tandem repeats occurs in adenomatous polyps and is associated with an increased risk for malignant transformation.
When compared to the intensity observed in adjacent normal mucosal epithelial cells, the intensity of Bcl-X immunostaining was elevated in 18 of 30 (60%) carcinomas (P = 0.0001) and 12 of 24 (50%) adenomatous polyps (P = 0.0001).
When compared to the intensity observed in adjacent normal mucosal epithelial cells, the intensity of Bcl-X immunostaining was elevated in 18 of 30 (60%) carcinomas (P = 0.0001) and 12 of 24 (50%) adenomatous polyps (P = 0.0001).
We conclude that enhanced immunoreactivity of MUC1, MUC2 and MUC3 mucin tandem repeats occurs in adenomatous polyps and is associated with an increased risk for malignant transformation.
Furthermore, the adenomatous polyposis coli (APC) gene on Chr 5, mutated somatically in adenomatous polyps and mutated in the germline of patients with familial adenomatous polyposis, is not linked to hereditary juvenile polyposis.
Serum levels of the mutant p53 protein in patients with colorectal cancer (mean=0.97+/-0.14 ng/ml, ranged from 0.7 ng/ml to 1.37 ng/ml, n=50) were significantly greater than those in patients with adenomatous polyp (mean=0.73+/-0.06 ng/ml, ranged from 0.69 ng/ml to 0.83 ng/ml) (p<0.001).
In this study, expression of DRA and its cellular distribution have been investigated in a series of benign adenomatous polyps and malignant colorectal tumors and in corresponding normal colonic mucosa.
Germline mutations (nonsense, frameshift) of APC are associated with familial adenomatous polyposis, an autosomal dominant syndrome, clinically characterized by young onset, hundreds of adenomatous polyps in the colon, and increased risk for extracolonic tumors.
The observation that the attenuated form of adenomatous polyposis coli (AAPC) has a different mutational spectrum in both the adenomatous polyp and the carcinoma than the classical form of APC has led to the hypothesis that AAPC alleles retain some residual APC activity associated with a greatly reduced number of polyps.
In the 4 adenomatous polyps with carcinomatous foci, BAT-26 positivity was detected in 2 cases (50%) in both (adenomatous and carcinomatous) components of the lesions. p53 immunoreactivity was observed in 6 adenomatous polyps, 2 of them with malignant transformation.