To investigate genetic heterogeneity during in vitro cultivation of human prostatic carcinomas following radical prostatectomy we performed DNA fingerprinting using the digoxygenin-labeled probes (GACA)4 and (GTG)5. DNA was isolated from fresh material stemming from different areas within one tumor and from cell cultures of the same material. The patterns which were obtained by the nucleolar organizer region (NOR)-specific probe (GACA)4 exhibit only a few prominent low molecular mass bands and no differences were observed between any of the tumors analyzed so far. Changes in the fingerprint pattern occurred between cell cultures derived from different areas within one tumor when the DNA was cleaved by HaeIII and signals detected with the (GTG)5 probe. The "area-specific" pattern was stable during several subcultivations of these cell lines, indicating genetic stability of these prostatic carcinoma cells in vitro. Thus individual cell lines derived from radical prostatectomy seem to represent a biological system very close to the situation in vivo.

Base Sequence↗

PubMedDate not supplied

Differential activity of two oncogenes from chromosome #7 in human glioblastoma cell lines.

Human glioblastoma cell lines are known to develop polysomy of cytogenetically intact chromosomes #7 and overexpression of the erbB oncogene (7p12-p14) at a level even higher than is to be expected from the number of #7 chromosomes. The met oncogene, however, which is also located on chromosome #7 (7q31-q32), was shown not to be overexpressed in a panel of 7-polysomic glioblastoma cell lines overexpressing erbB. Molecular analysis of the cell line HeRo gave proof that there is no detectable amplification or rearrangement of the erbB gene which could be responsible for its overexpression. These findings favor the assumption of differential regulation of the met and erbB oncogenes, e.g. by means of insufficient activity of a trans-acting erbB suppressor gene possibly located on a chromosome with a low copy number.

Chromosome Aberrations↗

PubMedDate not supplied

Characterization of intermediate type (WHO "atypical") meningiomas.

The intermediate type meningioma (formerly "meningioma variant with signs of increased proliferation activity"; WHO "atypical" meningioma) represents a meningioma group the mean Ki-67 index and the recurrence rate of which lie between those of the ordinary and the anaplastic type [Kolles et al. 1995]. In the study cited (n = 160) the percentage of recurrences was 9% in the common, 29% in the intermediate, and 50% in the anaplastic type. The present study focuses on 49 subsequently diagnosed meningiomas of the intermediate type. Apart from certain histopathological features, the most important independent factors associated with recurrence were Ki-67 indices covering the 95% confidence interval between 3.7% and 4.9%. At the light-microscopic level, however, meningiomas in general, and especially those supposed to belong to the intermediate type, are highly variable in tissue architecture and do, in contrast to the anaplastic type, not display frank histological features of anaplasia. Morphologically, the growth pattern of solid ("syncytial") sheets, micronecroses, and large distinct nucleoli are suspicious. Cytogenetically, independent of the loss of one chromosome 22, it has been shown that terminal loss of the short arm of one chromosome 1 (1p-) or complete loss of this chromosome were useful additional indicators of meningioma progression.

Adult↗