This study suggests that immunohistochemistry is valuable for assessing p53 gene mutations in colorectal neoplasms, but further study is needed to elucidate the precise link between immunohistochemistry and molecular genetic alterations.
Telomerase activity in 100% of the tumors suggests telomerase activation is a universal event in colorectal tumor progression; however, telomerase activity appears to be independent of p53 mutations and clinical staging.
These results demonstrate an increased incidence of p53 mutations associated with secondary lesions of colorectal tumors suggestive of a role for p53 in the establishment of colorectal hepatic metastases.
We have analyzed the prevalence of MDM2 gene amplifications and SNP309 in 284 colorectal tumors using a relatively new highly sensitive PCR/ligase detection reaction method in relation to TP53 mutational status and genomic instability.
Human colorectal tumors with wild-type TP53 and high PBF expression also had low p53 protein levels (P < 0.05), further emphasizing a putative interaction between these genes in vivo.
Fifty-four archival formalin-fixed paraffin-embedded colorectal tumors were also stained with PAb1801. p53 was detectable, sometimes with a weaker intensity, in 50% of 18 adenocarcinomas and 22% of 36 adenomas, and most of these showed severe dysplasia.(ABSTRACT TRUNCATED AT 250 WORDS)
Distinct genetic abnormalities (loss-of-function mutations of APC and p53 and oncogenic activation of Ki-ras) are associated with specific stages of the sporadic, most common types of colorectal tumors.
In this study, 153 tumor tissues from colorectal cancer patients, including 63 smokers and 90 nonsmokers, were examined for p53 mutation and p53 protein expression by direct sequencing and immunohistochemistry (IHC), respectively. p53 mutations were detected in 77 of 153 (50.3%) colorectal tumors, and no difference was observed in the p53 mutation frequencies in tumors from smokers and nonsmokers (33 of 63, 50.8% for smokers vs. 44 of 90, 48.9% for nonsmokers, P = 0.743).
Patients with ulcerative colitis are at an increased risk for developing colorectal neoplasms. p53 mutations and the occurrence of DNA aneuploidies are common events in the development of sporadic colorectal neoplasias.
In this study, we investigated the clinicopathologic significance of TUFM and p53 expression for the normal-adenoma-carcinoma sequence in colorectal epithelia and evaluated the roles of TUFM during the progression of colorectal tumors.
Studies thus far involving colorectal tumors obtained from patients have focused predominantly on the predictive value of levels of TS expression and p53 mutations in determining response to 5-FU.
We suggest that the LST exhibited a characteristic pattern in terms of the Ki-ras as well as the p53 gene mutation pattern, thereby supporting the hypothesis that LST is a specific subtype of colorectal tumors.
Multiplex Ligation-dependent Probe Amplification, TP53 sequencing, real-time polymerase chain reaction (PCR) for MUC1 and SCGB2A2 and immunocytochemistry, together with senescence detection assay and real-time microscopic observations were used to analyze primary neoplastic cells isolated from prostate, breast and colorectal tumors, as well as stable cancer cell lines (MCF7, MDA-MB-468, SW962, SK-MEL28, NCI-H1975 and NCI-H469).