Alterations of K-ras and p53 mutations in colorectal cancer patients in Central Europe.

Many molecular investigations of colorectal cancer (CRC) have suggested that the accumulation of specific mutations in proto-oncogenes and tumor suppressor genes regulating cell growth via signal transduction trigger the stagewise progression to malignancy. In this study, the frequency, location, and type of mutations of the K-ras proto-oncogene exon I and p53 tumor suppressor gene exons 5-8 were analyzed in colorectal carcinomas of 65 patients from Central Europe, using polymerase chain reaction (PCR)-cold single-strand conformation polymorphism (SSCP) screening and direct sequencing. The incidence of K-ras activating mutations in these Central European samples was lower (25%) compared to that obtained in American and western European populations (40-50% at least), while the incidence of p53 inactivating mutations was similar (58%). These results suggest that some other genetically linked mechanisms may play a role in CRC development and progression, and hence K-ras and p53 mutations cannot be considered to be universal genetic markers for CRC.

Nucleolar organizer regions (AgNORs) in intraepithelial neoplasia of the uterine cervix.

The authors have studied the AgNORs counts in intraepithelial lesions of the uterine cervix. The following values were obtained (mean +/- SD AgNORs/cell): normal specimens--2.11 +/- 0.98; mild dysplasia--2.83 +/- 1.12; moderate dysplasia--3.42 +/- 1.13; severe dysplasia--3.55 +/- 1.28; carcinoma in situ--4.63 +/- 1.34; glandular extensions of carcinoma in situ--4.64 +/- 0.98. The values in moderate and severe dysplasia were similar, an argument for grouping these categories in the high-grade lesions. AgNORs counts in carcinoma in situ were, however, higher than in severe dysplasia, suggesting a continuous evolution of the neoplastic process.