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Biomedical subjects

F Mitelman

Publications and source records attributed to F Mitelman.

At least 469 records · Page 26Linked to original sources
PubMed1978

Interindividual variation in the responses of cultured human lymphocytes to exposure from DNA damaging chemical agents: interindividual variation to carcinogen exposure.

Human population variability to standardized doses of N-acetoxy-2-acetylaminofluorene (NA-AAF) and 7, 12-dimethylbenz(a) anthracene (DMBA) was determined in cultured lymphocytes by measuring (a) differential stimulation of unscheduled DNA synthesis after 1 h induction of DNA damage by 10 micrometer NA-AAF, (b) the level of NA-AAF induced chromosome aberrations remaining after 8 h of DNA-repair synthesis, and (c) the level of [3H]DMBA bound to DNA after 18 h incubation of resting lymphocytes in 5 micrometer DMBA. All 3 parameters indicated individual variation to carcinogen exposure and were correlated to the population differences in age, sex, blood pressure and mortality rates. Males always had a greater potential to accumulate DNA-damage than did females regardless of the sampled population. DNA-damage potentials increased with increasing age, blood pressure or mortality rates. There was always proportionally greater DNA-damage potentials in the males than in females. The in vitro response of mature granulocytes to a 10 micrometer NA-AAF dose, as estimated by [3H] thymidine incorporation from unscheduled DNA synthesis, was much lower than lymphocyte response. Nevertheless, individual variations in granulocyte NA-AAF induced unscheduled DNA synthesis paralleled the inter-individual fluctuations observed in the lymphocyte responses to NA-AAF.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Normal chromosome banding pattern in Alzheimer's disease.

Lymphocyte chromosomes were studied in 10 female patients with Alzheimer's disease, including 5 cases with positive heredity for organic dementia. The chromosomes were analyzed by means of the Giesma banding technique. All patients had a normal karyotype with a completely normal banding pattern in all metaphases analyzed. It may be concluded that chromosomal changes demonstrable with methods available today are not involved in the causation of Alzheimer's disease, whether sporadic or with positive heredity for organic dementia starting in the presenile or senile periods.

Aged↗
PubMed1977

Pronounced deficiency in T-cells and lymphocyte chromosomal aberrations in a patient with sarcoidosis, myelofibrosis and acute leukaemia following thorotrast angiography.

A patient exposed to thorotrast angiography developed sarcoidosis 21 years after the injection and myelofibrosis 13 years later. On the latter occasion an extreme deficiency in circulating lymphocytes forming rosettes with sheep erythrocytes (T-cells) was observed and a large fraction of the cells had chromosomal aberrations. Acute leukaemia developed 1 year later. The multiple clinical symptoms may be related to radiation-induced destruction of bone marrow tissue, mutations in haemopoietic cells and depression of cell-mediated immunity.

Autoradiography↗
PubMed1977

Acute myeloid leukaemia with the Philadelphia chromosome.

A case report of serial chromosome studies on a 26-year-old male with acute myeloid leukaemia (AML) is presented. The classic Philadelphia chromosome (Ph1) translocation, t (9;22) was found in 77% of the metaphases at diagnosis and in 100% in relapse; during a 3-month remission period the cytogenetic picture was normal or the Ph1 was present in a minor cell population only. The clinical and morphologic features of this case indicated that it was really a case of AML and less likely chronic myeloid leukaemia (CML) presenting in blast crisis. It is suggested that the oncogen producing the 9;22-translocation and CML may also induce AML in rare instances.

Adult↗
PubMed1977

Hodgkin's disease and acute leukaemia. A clinical and cytogenetic study.

Three patients developing acute myeloid leukaemia after treatment for Hodgkin's disease are reported. They appeared among 153 patients treated since 1971. All three patients were treated with high-voltage radiation of large target volumes as well as multiple-drug chemotherapy. In two of the patients chromosomal analyses of the leukaemic bone marrow cells were performed by modern banding technique. Chromosome abnormalities were found in both patients. The value of cytogenetic analysis with the new staining techniques for elucidating the mechanism of leukaemogenesis in Hodgkin's disease is discussed.

Adult↗
PubMed1976

Non-random karyotypic evolution in chronic myeloid leukemia.

The chromosome banding pattern was analyzed in bone-marrow cells and/or spleen cells of 10 patients in the blastic phase of chronic myeloid leukemia (CML). It was obvious from the karyotype analysis that the chromosome aberrations occurring addition to the Philadelphia chromosome (Ph1) were strictly non-random. An extra Ph1, trisomy 8 and/or trisomy for the long arm of chromosome 17 were observed in all cases. This consistent pattern of chromosome involvement in CML was confirmed in 57 cases from the literature studied with banding techniques. In 88% of the total number of cases with further changes at least one of the three main chromosomal aberrations was found ("major route" of karyotypic evolution).

Adult↗
PubMed1976

Non-random chromosome changes in acute myeloid leukemia. Chromosome banding examination of 30 cases at diagnosis.

Bone-marrow chromosomes were examined with the G-banding technique in 30 patients with acute myeloid leukemia at the time of diagnosis. In 13 of the 30 patients (43%) only normal diploid bone-marrow cells were found, and no deviations from the normal banding pattern could be detected in these cells. In bone-marrow cells of 17 patients (57%), distinct chromosome abnormalities were found; in 10 of the patients only abnormal cells were observed, whereas in 7 of the patients the abnormal cells coexisted with normal diploid cells without any visible chromosome banding abnormality. The results of the detailed analysis of the karyotypic aberrations demonstrated that when chromosome aberrations occurred they were clearly non-random. All patients except two displayed trisomy 8,9 or 21 or monosomy 7. Analysis of cases of acute leukemia from other laboratories indicated that the same consistent pattern of chromosome involvement prevailed in them.

Adolescent↗
PubMed1976

Deoxyribonucleic acid repair synthesis: a new factor for defining high blood pressure.

1. The level of DNA repair synthesis has been compared in males diagnosed as having hypertension (diastolic blood pressure greater than or equal to 100 mmHg), males with slightly elevated blood pressure (greater than 95th percentile corrected for age) and males with normal or subnormal blood pressure (less than or equal to 30th percentile corrected for age). 2. The hypertensive males and the males with elevated blood pressure could not be distinguished from each other with respect to the levels of chemically induced repair synthesis, but both were significantly increased over the induced repair synthesis values of individuals with normal or low blood pressure. Since it has been shown previously that lymphocytes with high repair synthesis values also have increased levels of both carcinogen-DNA binding and chromosomal aberrations (Nordén, Scherstén, Thulin, Pero, Bryngelsson & Mitelman, 1975), the biological significance of this variable appears to be of value in discriminating between normal and high blood pressure groups.

Adolescent↗
PubMed1976

High blood pressure related to carcinogen-induced unscheduled DNA synthesis, DNA carcinogen binding, and chromosomal aberrations in human lymphocytes.

Unscheduled DNA synthesis (excision-repair) of N-acetoxy-2-acetylaminofluorene (NA-AAF) damage to the DNA of human lymphocytes was determined quantitatively for 92 individuals with diastolic blood pressures ranging from 65 to 120 mm of Hg (8,7 to 16 kPa). Measurements of NA-AAF-induced repair synthesis (incorporation of[3H]thymidine in the presence of 10 mM hydroxyurea) showed linear increase with the blood pressure in the individuals under study. Concurrent determinations for the levels of 3H-labeled 7,12-dimethyl-benz[a]anthracene bound to the DNAs of lymphocytes after 18 hr of culturing have shown that increased amounts of DNA bound carcinogen were linearly proportional to increased NA-AAF-induced repair synthesis values, and therefore were correlated to high blood pressure. The number of NA-AAF-induced chromosomal abberations in lymphocytes increased linearly with the diastolic blood pressures of the individuals. High NA-AAF-induced repair synthesis values also tended to be associated with increased NA-AAF-induced chromosomal damage. Together, these results suggest that individuals with elevated blood pressures have a greater potential for accumulating DNA damage, because of an increased chemical reactivity of lymphocytes to carcinogen exposure, than do individuals with normal blood pressure.

9,10-Dimethyl-1,2-benzanthracene↗