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Biomedical subjects

G Thiel

Publications and source records attributed to G Thiel.

306 records · Page 17Linked to original sources
PubMedDate not supplied

Monitoring genomic alterations with a panel of oligonucleotide probes specific for various simple repeat motifs.

Germline and somatic instability of the human genome was studied, using synthetic oligonucleotides specific for simple repeat motifs. The following probes were used: (GTG)5, (GACA)4, (GATA)4, (CT)8, (TTAGGG)3, (GT)8, (GAA)6 and (GGAT)4. Each of them is unique with respect to the target regions recognized in the genome. Thus compilation of the various fingerprint data provides a complex map of the genome (and its deviations). While the fingerprints of differentiated somatic tissues never showed any alterations, in tumor tissues (namely gliomas) many changes could be detected. Most of the latter reflect secondary karyological aberrations. In nearly one third of the gliomas, drastically amplified and apparently monomorphic DNA fragments were identified. This marker should make it possible to deal with causal pathogenetic mechanisms as well as novel diagnostic strategies.

Base Sequence↗
PubMedDate not supplied

Giant mitochondria in "zero-hour" transplant biopsies.

Giant mitochondria in kidneys have increasingly been observed since the introduction of Cyclosporin A (CSA) as immunosuppressant in kidney transplants and in patients with autoimmune disorders. In animals treated with CSA, giant mitochondria were also described. In a study of "zero-hour" biopsies taken immediately before or after reperfusion of the renal transplant, giant mitochondria were often unexpectedly found. Retrospective analysis revealed that a significant increase in the number of giant mitochondria is more often associated with CSA therapy than ischemia. Giant mitochondria with sparse cristae seem to prevail in ischemia, whereas those with dense matrix and crystalloid structures predominate in CSA therapy.

Adolescent↗
PubMedDate not supplied

Chromosomal changes and correspondingly altered proto-oncogene expression in human gliomas. Value of combined cytogenetic and molecular genetic analysis.

A combined cytogenetic and molecular genetic study was performed to analyze seven primary brain tumors: one oligoastrocytoma WHO-grade II, one anaplastic astrocytoma grade III, one anaplastic astrocytoma grade III/IV and four glioblastomas by G-banding and RNA dot blotting. A normal karyotype was found in the oligoastrocytoma. One of the two anaplastic astrocytomas (male) contained cells with a normal karyotype and cells with a Y-chromosomal loss, and the other one showed structural abnormalities too complex for complete analysis in mostly polyploid cells. Two of the four glioblastomas had few and the other two multiple chromosomal changes such as +7, +20, -8, -9 del(9)(p21), -10, del(10)(q24), -13,14, del(17)(p21), -22, add(3)(q13), double minutes and marker chromosomes. Compared to normal brain, all tumors had an increased EGFr and both anaplastic astrocytomas as well as three glioblastomas a decreased H-ras expression. The two glioblastomas with multiple chromosomal changes showed increased EGFr, Ki-ras, myb, mos and myc, decreased H-ras and N-ras and unchanged levels of abl, src and sis. Both the cytogenetic and molecular genetic findings are compatible even in the case of chromosomal losses, where the genes on the remaining allele may be responsible for dominant gene regulation mechanisms which result in a protooncogene overexpression. Our findings indicate that, apart from proto-oncogene overexpression, other mechanisms, e.g. tumor suppressor gene inactivation, are important for glial tumorigenesis. Karyotypic analysis makes it possible to search specifically for genetic events still unknown but arising from particular chromosomal changes.

Adult↗
PubMedDate not supplied

Somatic mutations in the neurofibromatosis 1 gene in gliomas and primitive neuroectodermal tumours.

The increased frequency of glioma among neurofibromatosis 1 (NF1) patients suggests a general involvement of the NF1 gene in glioma tumourigenesis. Using the methodology of conventional Southern blotting with a complete panel of overlapping partial cDNAs covering the whole NF1 gene, we screened 31 gliomas of several different subtypes and 3 primitive neuroectodermal tumours (PNETs) from non-NF1 patients for aberrant restriction patterns in their tumour DNA samples. Clear evidence for somatic mutation events at the NF1 gene locus was found in 1 astrocytoma, 2 glioblastomas, 1 ependymoma and 1 PNET with an astrocytic component. These results suggest that the NF1 gene is important in suppressing tumours of neuroectodermal origin.

Aged↗