p53 nuclear overexpression: an independent predictor of survival in lymph node--positive colorectal cancer patients.

Abstract

In node-positive colorectal cancer patients with low preoperative CEA levels, nuclear p53 overexpression as determined by immunohistochemistry on archived tissue is an independent predictor for prognosis.

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

“…Disruption of p53 by gene targeting in human colon cancer cells results in cell resistance to different chemotherapeutic agents, as opposed to wild type cells (35). Hence, loss of p53 in human colorectal cancers may explain the inefficacy of chemotherapy and may be correlated with decreased survival in patients with colorectal adenocarcinomas (36)(37)(38)(39).…”

Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer

“…Mutations of the TP53 gene have been observed in the progression of colonic polyps to colon cancer (Vogelstein et al, 1988;Fearon and Vogelstein, 1990). We have previously found that p53 nuclear overexpression correlates well with poor survival in colorectal cancer (Zeng et al, 1994). Our hypothesis for the present study is that colorectal tumours with positive or negative p53 nuclear staining may be characterised by aetiological heterogeneity, which could reflect a difference in the causal pathway, or could be indicative of a difference in the magnitude of effect with the same mechanism.…”

“…We studied a total of 107 (59 males, 48 females) patients with primary colorectal carcinoma. This series was previously studied for the prognostic significance of p53 in colorectal carcinoma (Zeng et al, 1994 PAb 1801 at the concentration of 200 ng 14l-I at 4°C. Sections of a breast carcinoma known to contain mutant p53 protein were used as a positive control.…”

“…Epidemiological studies show that increased risk of colorectal cancer may be associated with both genetic and environmental factors (Potter et al, 1993). For the genetic component of CRC, two major types of CRC predisposition have been identified: familial adenomatous polyposis (FAP), which is believed to account for 1% of CRC cases, and hereditary non-polyposis colorectal cancer (HNPCC), which is considered to explain about 4-15% of CRC cases (Peltomaki et al, 1993 (Marks et al, 1991;Cunningham et al, 1992;Vahakangas et al, 1992;Dalbagni et al, 1993;Cordon-Cardo et al, 1994;Jacquemier et al, 1994). TP53 mutational spectra can point to particular leads in the aetiology and carcinogenesis of cancer (Harris, 1993 (Field et al, 1991;Brachman et al, 1992), oesophageal (Hollstein et al, 1991) and bladder cancers (Spruck et al, 1993;Zhang et al, 1994a).…”

“…Mutations at this locus are reported to be the most frequent molecular abnormalities in human cancer. The TP53 gene is associated with control of the cell cycle, DNA repair and synthesis, cell differentiation, genomic plasticity and programmed cell death (Harris, 1993;Wyllie, 1993 (Marks et al, 1991;Cunningham et al, 1992;Vahakangas et al, 1992;Dalbagni et al, 1993;Cordon-Cardo et al, 1994;Jacquemier et al, 1994). TP53 mutational spectra can point to particular leads in the aetiology and carcinogenesis of cancer (Harris, 1993 (Kondo et al, 1992;Miller et al, 1992;Suzuki et al, 1992), head and neck (Field et al, 1991;Brachman et al, 1992), oesophageal (Hollstein et al, 1991) and bladder cancers (Spruck et al, 1993;Zhang et al, 1994a).…”