Mutations in adenomatous polyposis coli (APC) gene have not been previously characterized among Romanian patients with colorectal cancer (CRC). We initiate this study to detect the mutations in APC gene in blood and tumor samples collected from 16 patients (10 men and 6 women) and blood samples from 21 first and second degree relatives of the patients. For this the presence of mutations in exon...

The APC (adenomatous polyposis coli) gene is responsible for familial adenomatous polyposis and is also associated with the development of sporadic tumors of the colon and stomach. To investigate whether or not mutations of APC play any role in tumors arising in other organs, we examined somatic mutations of this gene in sporadic (nonfamilial) renal cell carcinomas, hepatocellular carcinomas, a...

Familial adenomatous polyposis is an autosomal dominantly inherited disorder. Mutation studies in the corresponding gene (APC) may provide information for predictive tests for persons at risk in affected families. We report here a new mutation in exon 6 (codon 233) of the APC gene and clinical data in a large family with late onset of the disease in most affected persons.

A poor anticoagulant response to activated protein C (APC r&stance) induced hy the ArglGln8g8 mutation of the Factor V gene is, in ssversl countries, the most oommon genetic defect sssootatsd with thmmbophilic disorders. Frequencies of APC resistance between 2050% have teen observed in pstients with deep venous thrombosis, SugQedinQ the importance of the Pmtein C System acttvity. Also, in other...

Inactivation of the adenomatous polyposis coli (APC) gene is a major initiating event in colorectal tumorigenesis. Most of the mutations in APC generate premature stop codons leading to truncated proteins that have lost beta-catenin binding sites. APC-free beta-catenin stimulates the Wnt signaling pathway, leading to active transcription of target genes. In the current study, we describe a nove...

A poor anticoagulant response to activated protein C (APC r&stance) induced hy the ArglGln8g8 mutation of the Factor V gene is, in ssversl countries, the most oommon genetic defect sssootatsd with thmmbophilic disorders. Frequencies of APC resistance between 2050% have teen observed in pstients with deep venous thrombosis, SugQedinQ the importance of the Pmtein C System acttvity. Also, in other...

Inherited colorectal cancer syndromes in humans exhibit regional specificity for tumor formation. By using mice with germline mutations in the adenomatous polyposis coli gene (Apc) and/or DNA mismatch repair genes, we have analyzed the genetic control of tumor regionality in the mouse small intestine. In C57BL/6 mice heterozygous for the Apc multiple intestinal neoplasia mutation (Apc(Min)), in...

A poor anticoagulant response to activated protein C (APC r&stance) induced hy the ArglGln8g8 mutation of the Factor V gene is, in ssversl countries, the most oommon genetic defect sssootatsd with thmmbophilic disorders. Frequencies of APC resistance between 2050% have teen observed in pstients with deep venous thrombosis, SugQedinQ the importance of the Pmtein C System acttvity. Also, in other...

Colon cancer frequently results from mutations that constitutively activate the Wnt signaling pathway, a major target being the tumor suppressor gene adenomatous polyposis coli (APC). We recently identified the transcription factor RIP140 as a new inducer of APC gene transcription that inhibits colon cancer cell growth and impedes the Wnt signaling pathway by reducing β-catenin activation.