Biomedical subjects
L F Meisner
Publications and source records attributed to L F Meisner.
Establishment and characterization of a SV40 T-antigen immortalized human bronchial epithelial cell line.
Explore the source record for details and available documents.
Protective effect of vitamin E on genotoxicity of methylmercury.
The cytogenetic effects of methylmercury (MeHg) producing chromosomal breakages, C-mitosis, and sister chromatid exchange are well documented. The present investigation was to determine whether vitamin E, which has been shown to exert a certain protective measure on the nervous system of animals exposed to methylmercury, also will diminish the genotoxicity of MeHg. Adult hamsters were given a daily injection (ip) of methylmercury chloride at a dosage of 2.0 mg/kg body weight (kg b.w.) and/or with 2.0 mg/kg b.w. vitamin E for 3 wk. All animals were sacrificed 5 d after the last day of MeHg exposure. Fibroblast cultures were established with cells obtained from skins of these animals. Chromosome preparations were made from these cultures and evaluated, using a double-blind system, for incidences of chromosomal breakage. It was found that all the fibroblast cultures grew well except from those animals treated with MeHg. Furthermore, while the saline control and vitamin E alone cultures showed no significant number of chromosomal breakages, cells from animals treated with only MeHg showed a high incidence of chromosomal damage (50% with 1 break and 15% with 2 or more breaks). Such chromosomal damage, however, was totally eliminated by vitamin E treatment (no chromosomal breakage was observed in cultures from MeHg/vitamin E animals). Our present study represents the first report on in vitro chromosomal damages as a result of in vivo MeHg exposure. Furthermore, our investigation also demonstrated the protective potential of vitamin E against genotoxicity of methylmercury.
Acute granulocytic leukemia in Hodgkin's disease.
Two cases of acute myeloblastic leukemia were observed in Hodgkin's disease patients two and five years following intensive radiation therapy. Sixteen additional cases of acute granulocytic leukemia occurring in radiation-treated Hodgkin's disease patients have been reported in the literature and are reviewed. It is suggested that the development of acute leukemia was related to irradiation in these patients, and that additional such cases could be expected with the use of intensive radiation and chemotherapy, a risk probably justified in view of the improved control of Hodgkin's disease achieved by these programs.
Emergence of acute non-lymphocytic leukemia in breast cancer patients.
The appearance of acute non-lymphocytic leukemia (ANLL) in patients with other hematologic and non-hematologic malignancies is now a well recognized syndrome. These patients have an unusual form of leukemia with distinct clinical and morphological features. With improved therapy many cancer patients have experienced prolonged survival and cure. Some of these patients will develop ANLL as a consequence of their previous therapy, or for reasons associated with their primary tumor (host factors or common oncogenic virus). It is also possible that a fraction of these patients will develop the usual form of leukemia (de novo ANLL) that is unrelated to the underlying malignancy. Indeed, a statistical analysis assuming ANLL incidence rates to be unaffected by breast cancer or cancer therapy, predicted the occurrence of three new ANLL cases with a history of breast cancer in Wisconsin per year. Eleven patients with ANLL and a history of breast cancer were seen at the University Hospitals over a ten-year span (1969-1978). Clinical, morphological and cytogenetic features were examined and it was found that five of the eleven patients had features atypical for therapy related leukemia. Indeed, two of the patients had not received breast cancer therapy. The distinction between de novo and therapy related leukemia is important because remission and prolonged survival are more likely in the former and morbidity and mortality associated with therapy are more likely in the latter. We suggest that if features of de novo leukemia exist, despite previous therapy for underlying malignancy, intensive antileukemia therapy should be considered.
Mechanisms of chromatid breakage in human lymphocyte cultures.
G2 banding of human peripheral blood cultures with actinomycin D and tetracycline produced chromatid breakage in lightly stained Giemsa bands, and the number of such breaks tended to increase with fixation time. Chromatid breakage due to 3H-thymidine incorporation into DNA was also localized in light bands, but the number of these breaks did not increase with fixation time. These findings suggest that modification of chromosomal protein as a result of exposure to AMD or other chemicals following DNA synthesis can result in fixative-dependent chromatid breakage of susceptible chromosomal regions, unlike breakage due to 3H-thymidine which primarily affects DNA and is not affected by fixation. Thus, chromatid breakage observed in short-term lymphocyte cultures is not necessarily evidence of mutagenicity involving DNA, but rather may be due to toxic effects on synthesis or attachment of chromosomal proteins.
Chemically-induced chromosome changes in human cells in vitro.
Explore the source record for details and available documents.