Search PubMed⌕ Search

Biomedical subjects

G Bittner

Publications and source records attributed to G Bittner.

33 records · Page 2Linked to original sources
PubMed1985

Thallium-201 scintigraphy in the diagnosis of pheochromocytoma.

6 patients were studied by 201Tl scintigraphy; 1 of them suffered from a benign, and another from a malignant adrenal pheochromocytoma. 1 patient had a hormonal inactive adrenal tumor, 3 others multiple organ metastases of malignant pheochromocytomas. At the same time, 3 of the patients were studied by 131I-metaiodobenzylguanidine (131I-MIBG) scintigraphy. Using different techniques like kinetic studies, whole-body scan or a 201Tl-99m-Tc difference scan, benign and malignant pheochromocytoma tissues could be localized by 201Tl scintigraphy. Benign and malignant pheochromocytomas showed different kinetics of 201Tl. In 2 patients with multiple organ metastases of malignant pheochromocytomas, the metastases were partly imaged by 131I-MIBG, the others by 201Tl.

3-Iodobenzylguanidine↗
PubMed1984

Antiproliferative activity of human interferons against ovarian cancer cells grown in human tumor stem cell assay.

Fresh biopsies from 14 of 22 (64%) ovarian carcinomas cultivated in the human tumor stem cell assay (HTSCA) were sensitive (greater than 70% inhibition in cell growth) to human interferons (HuIFNs). To achieve 70% inhibition of colony growth, 500 units/ml of a naturally produced IFN-alpha or IFN-alpha A were required in 71% of the sensitive specimens. The antiproliferative potencies of five IFNs were evaluated including two native alpha IFNs, two highly purified cloned subtypes of IFN-alpha, IFN-alpha D and IFN-alpha A, and one native fibroblast-derived beta interferon (IFN-beta). The antiviral activity of the IFN-alpha as determined by a human cell target correlated with their relative antiproliferative action. IFN-alpha D had minimal inhibitory effect at the highest concentration tested, while three IFN-alpha with high antiviral activities were equivalent with respect to growth inhibition in the HTSCA. Although instability could not be eliminated as a contributing factor, IFN-beta had significantly less growth inhibitory potency for cells from ovarian cancers when compared simultaneously with native IFN-alpha in the human tumor stem cell assay (HTSCA). Assuming direct antiproliferative effects are primary, future clinical trials evaluating IFN-alpha in ovarian cancer may require high titers of IFN.

Cell Division↗
PubMed1984

Enhancement of the sensitivity of human colon cancer cells to growth inhibition by acivicin achieved through inhibition of nucleic acid precursor salvage by dipyridamole.

This study was undertaken to determine if salvage of nucleic acid precursors might constitute a mechanism of resistance to acivicin in human colon cancer cells and, if so, to establish whether dipyridamole, an inhibitor of nucleoside and nucleobase transport, can block the salvage process and restore sensitivity to acivicin. Acivicin inhibited the replication of human colon cancer cells (VACO 5) in vitro in a dose- and time-dependent fashion. In addition, marked cell lysis was evident after a 24-hr exposure to acivicin at concentrations greater than 1 microgram/ml. The primary metabolic effect of acivicin was depletion of the cytidine triphosphate and guanosine triphosphate pools. Adenosine triphosphate levels were also reduced, but apparently as a consequence of the guanosine triphosphate depletion. VACO 5 cells exposed to acivicin (3 micrograms/ml) efficiently salvaged low levels (1 micron) of cytidine, guanosine, and guanine and could, therefore, restore the depleted nucleotide pools. The combination of cytidine and guanosine, but not either nucleoside alone, provided significant protection against the growth-inhibitory properties of acivicin. Dipyridamole, at a noncytotoxic concentration (5 microM), blocked repletion of the cytidine triphosphate and guanosine triphosphate pools in cells exposed to acivicin and the nucleic acid precursors. As a result, the growth-inhibitory effects of acivicin were maintained. The salvage of cytidine was particularly sensitive to inhibition by dipyridamole, and no restoration of cytidine triphosphate pools was evident. The cellular uptake of a variety of nucleic acid precursors was differentially sensitive to inhibition by dipyridamole. The 50% inhibitory dose values ranged from 0.01 to 2.5 microM for cytidine and uridine, respectively. The results of this study indicate that, although the replication of VACO 5 cells was inhibited by acivicin, low levels of nucleosides and nucleobases can circumvent the cytotoxicity. Dipyridamole effectively blocked the salvage pathways and restored the sensitivity of the cancer cells to the antiproliferative actions of acivicin.

Antibiotics, Antineoplastic↗
PubMedDate not supplied

Comparison of spontaneous and induced mutation rates in an immortalized human bronchial epithelial cell line and its tumorigenic derivative.

To determine the relationship between neoplastic transformation and increased genetic instability, spontaneous and induced mutation rates were compared in a nontumorigenic, immortalized human bronchial epithelial cell line (NL20) and a tumorigenic cell line (NL20T) spontaneously derived from the NL20 line. Using the hypoxanthine phosphoribosyltransferase (HPRT) locus as a marker for determining mutation rate, fluctuation analysis was utilized to evaluate the spontaneous mutation rate. Induced mutation rates were determined for each cell line after N-methyl-N'-nitro-N-nitrosoguanidine exposure. Both the spontaneous and induced mutation rates were noted to be significantly higher in the nontumorigenic NL20 cell line. These findings suggest that increasing genetic instability, as measured by spontaneous or induced mutation rate in the HPRT locus, does not correlate with tumorigenicity in these cells.

Adult↗