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Biomedical subjects

W Henn

Publications and source records attributed to W Henn.

At least 55 records · Page 3Linked to original sources
PubMed1993

Bilateral multicentric papillary renal tumors with heteroclonal origin based on tissue-specific karyotype instability.

BACKGROUND: Papillary chromophilic renal tumors were cytogenetically characterized by combined trisomies 7 and 17 along with other numeric chromosome aberrations. They occurred as bilateral multifocal lesions. METHODS: A patient was presented who simultaneously developed bilateral multicentric papillary renal tumors. Tissue specimens from six tumors and tumor-free kidneys were cytogenetically characterized. RESULTS: The tumors showed trisomy of chromosomes 7, 16, and 17 along with various other numeric abnormalities. In normal tissue from both kidneys, a wide variety of clonal and nonclonal numeric and structural chromosome aberrations were found. CONCLUSIONS: The cytogenetic heteroclonality of the tumors strongly favors the assumption that they arose as independent primaries. A tissue-specific karyotype instability may be the basic event of multiple tumorigenesis.

Adenoma↗
PubMed1993

Telomeric associations and loss of telomeric DNA repeats in renal tumors.

In a series of cytogenetically analyzed renal tumors of different histological types (chromophobe carcinoma, clear-cell carcinoma, chromophilic carcinoma, and oncocytoma) and normal renal tissue, the length of the telomeric DNA repeats was assessed using a (TTAGGG)3 oligonucleotide probe. A strong correlation was noted between pronounced telomere shortening and the appearance of telomeric associations of chromosomes. These data suggest an etiologic role of the loss of telomeric DNA repeats in the formation of telomeric associations and a possible involvement of this mechanism in the pathogenesis of chromosome aberrations in human tumors.

Adenocarcinoma↗
PubMed1993

Clonal chromosome aberrations in cell cultures of synovial tissue from patients with rheumatoid arthritis.

Cytogenetic analysis of primary cell cultures and/or passages 1-3 of synovial tissue from seven patients with rheumatoid arthritis was performed. As the only recurrent chromosome aberration, trisomy 7 was found in six of seven cultures. In four cultures, trisomy 7 occurred as a clonal change in up to 20% of the analyzed cells, with an increase of the proportion of cells with +7 with the duration of the in vitro culture. Apart from this recurrent change, a variety of partly clonal, partly nonclonal numerical and structural chromosome aberrations were observed in all cases. These findings support the view that clonal chromosome aberrations may play a role in the pathogenesis of invasive growth of the synovial tissue in rheumatoid arthritis although the localized synovial hyperproliferation is not a true neoplastic process.

Arthritis, Rheumatoid↗
PubMed1993

Immunophenotyping of mitotic cells from long-term cultures of chorionic villi.

Chromosomal mosaicism in chorionic villus samples (CVS) may arise from different sources, such as clonal diversity within the chorionic tissue or contamination with maternal cells. To determine the origin of karyotyped cells, we compared the immunocytochemical features of mitotic cells in CVS long-term cultures with histological sections of their tissue of origin, i.e. chorionic villi. Immunolabelling of intermediate filaments specific for epithelial cells (cytokeratin) and mesenchymal cells (vimentin) established that mitoses yielded from CVS long-term cultures indeed stem from independently growing clones derived from both the epithelial and mesenchymal parts of the chorionic villi. Thus, mosaicism in CVS cultures may reflect true genetic heterogeneity within the biopsy. However, epithelial chorionic cells undergo in vitro metaplasia leading to co-expression of cytokeratins and vimentin. Fetal-specific immune markers (beta-HCG and SP1-glycoprotein) are not reliably expressed in CVS cell culture.

Chorionic Gonadotropin↗
PubMed1993

Recurrent t(12;19)(q13;q13.3) in intracranial and extracranial hemangiopericytoma.

We report on a recurrent intracranial hemangiopericytoma cytogenetically studied after short-term culture. The tumor had a uniform karyotype 47,XX,add(7)(q21),t(12;19)(q13;q13.3),del(13)(q14q22), +21. Remarkably, one case with an identical reciprocal (12;19) translocation has been previously reported as the sole cytogenetic change in a recurrent retroperitoneal hemangiopericytoma. This nonrandom structural change may characterize a subentity of hemangiopericytoma and might be of diagnostic value.

Aneuploidy↗
PubMed1992

Search for putative suppressor genes in meningioma: significance of chromosome 22.

Cytogenetic and molecular studies of various solid tumors have indicated that a series of different chromosomal regions may be deleted in the tumor genome. Usually, losses of heterozygosity are observed and, from this finding, the presence of specific genes acting as tumor suppressors has been deduced. In particular tumors, however, only a single chromosome site appears to be affected. Therefore, we have carried out a study of human meningioma, investigating 7 such putative suppressor regions by applying twelve site-specific DNA markers. In 6 out of 19 tumors, we exclusively found loss of heterozygosity for markers of the long arm of chromosome 22; none of the tumors showed statistically significant additional allelic losses for the regions 1p, 3p, 5p, 5q, 11p, 13q, 17p. Our data support the long-standing observation that only losses of or within chromosome 22 are associated with the development of meningiomas. Other suppressor regions are apparently not involved.

Adult↗
PubMed1991

Large-scale physical mapping within the region 22q12.3-13.1 in meningioma.

The lack of physical mapping data strongly restricts the analysis of the meningioma chromosomal region that was assigned to the bands 22q12.3-qter. Recently, we reported a new marker D22S16 for chromosome 22 that was assigned to the region 22q13-qter by in situ hybridization. Utilizing somatic cell hybrids we now sublocalized the marker D22S16 within the band region 22q12-13.1, thus placing it in the vicinity of the gene for the platelet derived growth factor (PDGFB). A physical map was established for the regions surrounding the PDGFB gene and the D22S16 marker. By means of pulsed-field gel electrophoresis (PFGE) D22S16 and PDGFB were found to be physically linked within 900 kb. We also identified two CpG clusters bordering the PDGFB gene. For the enzyme NotI, a variation of the PDGFB restriction pattern was found between different individuals. PFGE analysis of the two loci (PDFGB and D22S16) failed to identify major rearrangements in meningioma.

Animals↗
PubMed1991

Mosaic tetraploidy in a liveborn infant with features of the DiGeorge anomaly.

We report on a liveborn male infant with mosaic tetraploidy who presented with multiple congenital anomalies including features of the DiGeorge anomaly (type I truncus arteriosus with other cardiovascular malformations, thymic hypoplasia, hypocalcemia). No structural chromosome aberrations, namely of chromosome 22, were detected. These findings contribute to the variability of symptoms of the polyploid phenotype. Additionally, the cytogenetic studies in our case emphasize the necessity of investigating fibroblasts in order to evaluate the relevant proportion of aberrant cells in mosaicism.

Abnormalities, Multiple↗
PubMed1991

Loss of heterozygosity on chromosome 3, bands q24----qter, in a diploid meningioma.

Cytogenetic analysis of a meningioma from a 46-year-old female patient exhibited as the sole cytogenetic aberration a deletion on the long arm of one chromosome 3 involving bands 3q24----qter. To verify this finding, RFLP analysis was performed with two polymorphic probes, MOX2 and D3S5. The patient was informative for both single copy probes and demonstrated loss of heterozygosity in the region above whereas chromosome 22 displayed no loss of heterozygosity as judged by a proximal and a distal probe.

Chromosome Banding↗
PubMed1990

The cellular myb oncogene is amplified, rearranged and activated in human glioblastoma cell lines.

The human c-myb gene which encodes a DNA binding protein and which is rarely amplified in neoplastic cells was found to be altered in four human glioblastoma cell lines. It exists in multiple copies in 2 out of 4 cases studied. The degree of amplification as determined by densitometry was about 10-fold, a rearrangement within the coding region and an enhanced gene activity of c-myb were noted. The observation of c-myb oncogene amplification and activity in glioblastoma cell lines presents the first report of this effect in human brain tumor cells.

Brain Neoplasms↗
PubMed1990

In situ chromosome preparation technique for simultaneous cytogenetic and immunocytochemical studies on cell cultures of solid tumors.

Immunophenotyping of cultured cancer cells requires intact antigenic structures; these are mostly destroyed by conventional chromosome preparation techniques. Thus, the simultaneous cytogenetic and immunocytochemical characterization of solid tumor cells appears unfeasible. Here, we describe a novel method that allows in situ chromosome preparation from monolayer cultures of solid tumor cells without affecting their immunological features. Using this technique, it is possible to achieve detailed cytogenetic data including chromosome banding together with the demonstration of cytoplasmic and nuclear antigens within the same tumor cells.

Antibodies, Monoclonal↗
PubMed1988

A human glioblastoma line with karyotypic nullisomy 13 containing several chromosome 13-specific sequences.

Using a biochemical approach (evaluation of esterase D activity) and recombinant DNA techniques (in situ and filter hybridization with specific DNA probes) a glioblastoma cell line with karyotypical nullisomy 13 was shown to contain several chromosome #13-specific sequences. They were assigned to a marker chromosome. This finding suggests that cytogenetic descriptions of deletions or chromosome losses will gain considerable power of the statement when supplemented by molecular analysis, particularly since, by now, DNA probes have been accumulated for all chromosomes and all their subfragments.

Chromosome Banding↗
PubMed1986

Polysomy of chromosome 7 is correlated with overexpression of the erbB oncogene in human glioblastoma cell lines.

Chromosome analysis in a series of human glioblastoma cell lines (HeRo, HeRo-SV1, A172, T406, T508, T705) has indicated characteristic changes in the karyotype, the most striking and consistent of which is a significant increase in the copy number of chromosome 7, with up to 8 copies per metaphase. As determined by Spurr et al., chromosome 7 represents the genomic locus for the oncogene erbB (7pter-q22). Therefore, we have compared the number of chromosomes 7 to the levels of expression of the erbB oncogene. Interestingly, in all of them erbB-specific mRNA was found to be increased at levels even higher than expected from the number of chromosomes 7 found. In contrast, in an astrocytoma of slightly lower grade of malignancy (cell line T567), neither polysomy 7 nor significant expression of the erbB oncogene was noted.

Astrocytoma↗
PubMedDate not supplied

Nuclear and DNA-binding proteins in human brain tumors.

Nuclear proteins obtained from human brain tumor cell lines by differential salt extraction were subjected to high-resolution two-dimensional electrophoresis. Several hundred spots were detectable in the low salt (0.4 M NaCl) extract using silver staining. These patterns exhibited remarkable differences between the different cell lines we analyzed. A less complex pattern occurred when nuclei were subsequently treated with high salt (2.5 M NaCl/5 M urea). We compared the electropherograms from various human glioblastoma cell lines and found them very similar and even a high degree of similarity occurs between glioblastomas and other human tumor cell lines. Beside these more general observations we detected several proteins at least enriched in human glioblastomas which were totally absent in low grade astrocytomas and nonglial tumors. They could be separated from the bulk of nonspecific proteins by simple modifications of the isoelectric focusing conditions. From these results we conclude that nuclear proteins obtained by sequential salt extraction and separated by two-dimensional techniques may provide tumor specific proteins suitable for antibody production.

Brain Neoplasms↗