Cytogenetic data

Example 4. The conclusion by Sarich10 11 in the early 1970s that the giant panda is allied with bears rather than with the lesser panda can be regarded as statistically robust. This view was consistent with a comprehensive anatomical study1,-13 and with fossil evidence13 and was afterward reinforced by more molecular and cytogenetic data.14... 

The cytogenetic data obtained showed that there was a positive correlation (p < 0.05) between the percentage of binucleated cells with MN (F)... 

Ikemura T. and Wada K. (1991). Evident diversity of codon usage patterns of human genes with respect to chromosome banding patterns and chromosome numbers relation between nucleotide sequence data and cytogenetic data. Nucleic Acid Res. 16 4333-4339. 

Richardson, C., Williams, D.A., Allen, J.A., Amphlett, G., Changer, D.O. and Phillips, B. (1989). Analysis of data from in vitro cytogenetic assays. In UKEMS Sub-committee on Guidelines for Mutagenicity Testing. Report. Part III. Statistical Evaluation of Mutagenicity Test Data. (Kirkland, D.J., Ed.). Cambridge University Press, pp. 141-154. 

Hazleton Labs. 1988a. Mutagenicity tests on o-, m-, and p-cresol in an ivitro cytogenetic assay measuring chromosomal aberration frequencies in CHOcells. Unpublished data submitted to EPA/OTS. Fiche no. OTS0517691. 

Hazleton Labs. 1989c. Mutagenicity test on cresol program panel sample 2 meta-cresol in the mouse bone marrow cytogenetic assay. HLA study no. 10002-0- 451. Unpublished data submitted to Chemical Manufacturers Association,Washington, DC. 

Larson RA, Druker B, Guilhot F et al. Correlation of pharmacokinetic data with cytogenetic and molecular response in newly diagnosed patients with chronic myeloid leukemia in chronic phase (CML-CP) treated with imatinib-An analysis of IRIS study data (Abstract 429). B/oorf 2006 108 131a. 

The relationships between nilotinib plasma concentration and clinical efficacy (or toxicity) have not been studied yet. Irrespective of nilotinib PK-PD per se, Saglio et al. [72] showed that nilotinib at a dose of either 300 or 400 mg twice daily was superior to imatinib in patients with newly diagnosed chronic-phase Philadelphia chromosome-positive CML. At 12 months, the rates of major molecular response for nilotinib were nearly twice that observed for imatinib. The rates of complete cytogenetic response by 12 months were also significantly higher for nilotinib than for imatinib [72], No data have been published for nilotinib concentration-toxicity relationships nor plasma target values to be achieved for optimal clinical response. 

There is extensive information on the effects of chemicals on the genetic systems of vascular plants. Genetic studies cover both cytogenetic effects and gene mutations, include data on more than 100 plant species, and span the history of chemical mutagenesis. In fact, one of the earliest reports of mutagenic effects of chemicals was on the induction of chromosomal aberrations in pi tints. 328 Since then, several hundred chemical and physical mutagens have been studied in plants. 

T.S.S. Dikshith, Cytogenetic effects of pesticides in the bone marrow system of male rats, (unpublished data 1982, Scientific report ITRC, Lucknow, India 1981-1984), in Toxicology of Pesticides in Animals, Ed., T.S.S. Dikshith, CRC Press, Boca Raton, FL, 194, 1999 (Update) PB/99/166662. 

Genotoxicity. No studies were located regarding acrolein genotoxicity in humans. Dominant lethality of acrolein observed in mice indicated a genotoxic potential in mammals. The result is supported by in vitro data that showed mutagenic potential of acrolein in bacterial and mammalian cells without metabolic activation. Further studies in animals would be useful to determine the ability of acrolein to induce chromosomal aberrations after exposure. Cytogenetic analysis of peripheral lymphocytes of workers exposed to acrolein would provide an opportunity to assess its genotoxicity in humans. 

An evaluation of occupational chemical exposure, histological subtype, and cytogenetics was conducted on case studies of newly diagnosed AML or CML, or myelodysplastic syndromes (MDS) treated in the Main Hospital of Torino, Northern Italy, between October 1, 1989 and December 31, 1990 (Ciccone et al. 1993). There was a nonstatistically significant increased relative risk for exposure to benzene. Data show 3 AML, 2 CML, and 4 MDS cases with regard to benzene exposures. No excess of clonal chromosome abnormalities was detected among occupationally exposed AML patients. 

Negative results have been reported in vitro from Ames, cytogenetics, and gene mutation tests reported in the secondary literature. There are no in vivo data available. These data do not support classification. 

There is experimental evidence that several anticancer drugs can cause abnormalities of sperm chromosomes. Preliminary data have suggested that after platinum-containing chemotherapy for testicular cancer, penetration of oocytes can be severely impaired. Cytogenetic... 

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