Intestinal Polyps
Mostrando 13-24 de 24 artigos, teses e dissertações.
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13. Immunolocalization of beta catenin in intestinal polyps of Peutz-Jeghers and juvenile polyposis syndromes.
AIM: To examine the membranous and nuclear distribution of beta catenin in the epithelial cells of gut polyps from Peutz-Jeghers syndrome and juvenile polyposis in comparison with other types of polyps and tumours. METHODS: Immunohistochemistry for beta catenin and proliferation markers was performed on conventional paraffin sections. Immunohistological stai
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14. Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesis
We used the hypomorphic Egfrwa2 allele to genetically examine the impact of impaired epidermal growth factor receptor (Egfr) signaling on the ApcMin mouse model of familial adenomatous polyposis. Transfer of the ApcMin allele onto a homozygous Egfrwa2 background results in a 90% reduction in intestinal polyp number relative to ApcMin mice carrying a wild-typ
The National Academy of Sciences.
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15. Juvenile polyposis of the stomach: clinicopathological features and its malignant potential.
AIMS: To clarify a clinical entity of juvenile polyposis of the stomach compared with generalised juvenile gastrointestinal polyposis. METHODS: The clinicopathological features of juvenile polyposis dominantly involving the stomach at initial presentation were reviewed in 12 patients (three new patients and nine from the literature). These were compared with
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16. A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors.
Germ-line mutations in the human adenomatous polyposis coli (APC) gene result in familial adenomatous polyposis, an autosomal dominant disorder characterized by the early onset of multiple adenomatous polyps in the large bowel with a high likelihood of developing colorectal carcinomas. To understand the role of APC in intestinal tumor formation, we have intr
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17. Mutations of PTEN in patients with Bannayan-Riley-Ruvalcaba phenotype.
We report three new mutations in PTEN, the gene responsible for Cowden disease in five patients with Bannayan-Riley-Ruvalcaba syndrome from three unrelated families. This finding confirms that Cowden disease, a dominant cancer predisposing syndrome, and Bannayan-Riley-Ruvalcaba syndrome, which includes macrocephaly, multiple lipomas, intestinal hamartomatous
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18. Opposing effects of DNA hypomethylation on intestinal and liver carcinogenesis
Genome-wide DNA hypomethylation and concomitant promoter-specific tumor suppressor gene hypermethylation are among the most common molecular alterations in human neoplasia. Consistent with the notion that both promoter hypermethylation and genome-wide hypomethylation are functionally important in tumorigenesis, genetic and/or pharmacologic reduction of DNA m
National Academy of Sciences.
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19. Concurrent suppression of hyperlipidemia and intestinal polyp formation by NO-1886, increasing lipoprotein lipase activity in Min mice
We have previously reported a hyperlipidemic state in two strains of Apc-deficient mice, Min and Apc1309, associated with low expression levels of lipoprotein lipase (LPL) in the liver and small intestine, and enforced induction of LPL mRNA by peroxisome proliferator-activated receptor (PPAR)α and PPARγ agonists clearly suppressed hyperlipidemia and intest
National Academy of Sciences.
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20. hP1.B, a human P-domain peptide homologous with rat intestinal trefoil factor, is expressed also in the ulcer-associated cell lineage and the uterus.
The six-cysteine P-domain motif forms the basic repeat unit of a growing family of mucin-associated peptides. A precursor for a human secretory polypeptide has been discovered by molecular cloning and deduced to have a single P-domain, termed hP1.B. The pre-pro-peptide has 67% amino acid identity with rat intestinal trefoil factor. We find, using the techniq
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21. Identification of the Modifier of Min 2 (Mom2) Locus, a New Mutation That Influences Apc-Induced Intestinal Neoplasia
Min (Multiple intestinal neoplasia) mice carry a dominant mutation in the adenomatous polyposis coli (Apc) gene and develop multiple adenomas throughout their intestinal tract (Moser et al. 1990; Su et al. 1992). Polyp multiplicity in Min mice is greatly influenced by genetic background. A modifier locus, Mom1 (Modifier of Min 1), was identified and localize
Cold Spring Harbor Laboratory Press.
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22. HER2 (c-erbB-2) oncoprotein expression in colorectal adenocarcinoma: an immunohistological study using three different antibodies.
Paraffin wax sections of 70 surgically resected colorectal adenocarcinomas were examined for the overexpression of HER2/c-erbB-2 oncoprotein using three different specific antibodies and the avidin-biotin immunoperoxidase technique. The patients included 38 men and 32 women aged between 47 and 80 years. The tumours were derived from various parts of the larg
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23. Sialic acid histochemistry and the adenoma-carcinoma sequence in colorectum.
A change in sialic acid, notably loss of O acetyl substitution, was studied histochemically in a series of 93 colorectal adenomas that included 14 malignant polyps. Changes in sialic acid were uncommon in adenomas showing mild dysplasia but became increasingly common in moderately and severely dysplastic adenomas and were always present in carcinomatous area
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24. A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates β-catenin but its zygotic expression is not essential for the regulation of Armadillo
Mutations in the adenomatous polyposis coli gene (which encodes a protein called APC) are associated with the formation of intestinal polyps and colon cancers. To facilitate the functional study of APC we have isolated its Drosophila homolog (D-APC) by screening an expression library with an antibody against human APC. The isolated cDNA encodes a predic
The National Academy of Sciences of the USA.