An immunohistochemical study using PAb1801, a monoclonal antibody specific to the human p53 protein (wild and mutant), was performed to detect over-expression of p53 protein in colorectal cancers and dysplasia complicating ulcerative colitis, compared with that in sporadic colorectal cancers and adenomas.
Using the polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) method, mutations within exons 5-8 of the p53 gene were examined in 108 colorectal cancers including 30 right-sided and 78 left-sided colorectal cancers.
We performed an epidemiological study to determine whether p53 protein overexpression, in tumours obtained at the time of resection, is associated with cigarette exposure in colorectal cancer.
Our results indicate that immunohistochemical analysis of p53 expression provides valuable information for the understanding of colorectal cancer biology and clinical behavior.
DNA was extracted from paraffin sections of 16 human mucinous colorectal carcinomas and the mutation frequency was determined by sequencing of p53 exons amplified in PCR.
Out of 11 patients with gastric cancer, 3 were treated with chemotherapeutic drugs before resection; 5 of 13 patients with colorectal cancer had 30 Gy radiation prior to surgery. p53 mutations were detected in 4 cases of gastric cancer (36.4%) and in 6 cases of colorectal cancer (46.2%) by immunohistochemical staining.
Fifteen synchronous colorectal cancers (30 tumors) were examined for histologic differences as well as genetic mutations. p53 gene abnormalities were detected by polymerase chain reaction (PCR) followed by single-strand conformation polymorphism analysis.
The aim of this work is to establish whether a relationship is found between p53 mutations and survival in patients undergoing adjuvant chemotherapy for advanced Dukes' D colorectal cancers.
To further investigate whether multiple genetic changes are involved in the development of colorectal cancer, we performed an immunohistochemical analysis of p53 and ras p21 protein expression in 139 specimens of colorectal adenoma with varying degrees of dysplasia, 57 specimens of early cancer with an adenomatous component, and 12 specimens of superficial early cancer without any adenomatous component.
The aims of the study were 1) to test whether numerical #17 aberrations are involved in functional TP53 loss in locally confined colorectal carcinomas; 2) to search for correlations between aberrant p53 expression and #17 aberrations with DNA ploidy and histopathology; and 3) to test the prognostic significance of these factors.
We conclude that c-myc might induce p53 expression in human colorectal cancer and that wild-type but not mutant p53 might be involved in a negative feedback regulation of c-myc expression.
Structural changes of the p53 gene are the most frequent observed mutations in colorectal carcinoma and are suspected to be involved in the carcinogenesis at a relatively early stage.
In this study, the clinico-pathological features and frequency of p53 overexpression in 17 left-sided RER+ CRCs were compared with 35 left-sided RER- CRCs.
This concept prompted us to search for possible mutations in the APC, k-ras, and p53 genes in an advanced cancer coexisting with a large villous adenoma of the rectum in a 54-year-old patient with no family history of colorectal cancer.