Radiation-induced g2 delay and spontaneous chromosome aberrations in ataxia-telangiectasia homozygotes and heterozygotes

International Journal of Radiation Biology

Volumn 66, Issue 6, 1994, Pages

  Scott, D ^a   Spreadborough, A R ^a   Roberts, S A ^a  

^a CHRISTIE HOSPITAL   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ADOLESCENT; ADULT; AGED; ARTICLE; ATAXIA TELANGIECTASIA; BLOOD; CELL CYCLE G2 PHASE; CHILD; CHROMOSOME ABERRATION; COMPARATIVE STUDY; CYTOLOGY; FEMALE; GENETICS; HETEROZYGOTE; HOMOZYGOTE; HUMAN; LYMPHOCYTE; MALE; MITOSIS; MITOSIS INDEX; PATHOLOGY; PHYSIOLOGY; PRESCHOOL CHILD; RADIATION EXPOSURE; X RAY; CONFERENCE PAPER; CONTROLLED STUDY; HETEROZYGOSITY; HOMOZYGOSITY; HUMAN CELL; MAJOR CLINICAL STUDY; MITOSIS INHIBITION; PRIORITY JOURNAL; X IRRADIATION;

ADOLESCENT; ADULT; AGED; ATAXIA TELANGIECTASIA; CHILD; CHILD, PRESCHOOL; CHROMOSOME ABERRATIONS; COMPARATIVE STUDY; FEMALE; G2 PHASE; HETEROZYGOTE; HOMOZYGOTE; HUMAN; LYMPHOCYTES; MALE; MIDDLE AGE; MITOSIS; MITOTIC INDEX; SUPPORT, NON-U.S. GOV'T; X-RAYS;

EID: 0028556476     PISSN: 09553002     EISSN: None     Source Type: Journal    
DOI: 10.1080/09553009414551991     Document Type: Article

References (30)

1. Comparison of γ-irradiation-induced accumulation of ataxia-telangiectasia and control cells in G2 phase
2. Radiosensitivity in ataxia-telangiectasia: anomalies in radiation-induced cell cycle delay
3. G2 chromosomal radiosensitivity in ataxia-telangiectasia lymphocytes
4. Chromosomal aberration and sister-chromatid exchange frequencies in peripheral blood lymphocytes of a large human population sample. II. Extension of age range
5. The effects of ionizing radiation on cell cycle progression in ataxia-telangiectasia
6. Effect of caffeine in G2 on X-ray-induced chromosomal aberrations and mitotic inhibition in ataxia-telangiectasia fibroblast and lymphoblastoid cells
7. Effect of ionizing radiation on DNA synthesis in ataxia-telangiectasia cells
8. Participation of p53 protein in the cellular response to DNA damage
9. Ionizing radiation and UV induce p53 protein in ataxia-telangectasia cells by different pathways
10. p53, guardian of the genome
11. Enhanced levels of radiation-induced G2 phase delay in ataxia-telangiectasia heterozygotes
12. Differential induction of transcriptionally active p53 following UV or ionising radiation: defects in chromosome instability syndromes?
13. Comparative study of G2 delay and survival after 241Americium and 60Cobalt-γ-irradiation
14. Impaired lymphocyte transformation in ataxia-telangiectasia in part due to a plasma inhibitory factor
15. Kinetics of chromatid aberrations in G2 ataxia-telangiectasia cells exposed to X-rays and ara A
16. Comparison of kinetics of X-ray induced cell killing in normal, ataxia-telangiectasia and hereditary retinoblastoma fibroblasts
17. Mitogen receptor redistribution defects and concomitant absence of blastogenesis in ataxia-telangiectasia T lymphocytes
18. Radiobiology of ataxia-telangiectasia
19. Radiosensitivity in ataxia-telangiectasia. A new explanation
20. Carrier detection in xeroderma pigmentosum
21. The molecular basis of drug-induced G2 arrest in mammalian cells
22. Flow cytometric analysis of X-ray sensitivity in ataxia-telangiectasia
23. Identification of ataxia-telangiectasia heterozygotes by flow cytometric analysis of X-ray damage
24. Identification of A-T heterozygotes
25. Cell cycle dependence of mitotic delay in X-irradiated normal and ataxia-telangiectasia fibroblasts
26. Comparative studies on ataxia-telangiectasia and radiation-sensitive mouse lymphoma cells
27. Abnormal retention of x-irradiated ataxia-telangiectasia fibroblasts in G2 phase of the cell cycle, cellular RNA content, chromatin stability and the effects of 3-aminobenzamide
28. Cytogenetics of ataxia-telangiectasia
29. Cell death, chromosome damage and mitotic delay in normal human, ataxia-telangiectasia and retinoblastoma fibroblasts after X-irradiation
30. The response of normal and ataxia-telangiectasia cells to bleomycin: relationships between chromosome damage, cell cycle delay and cell killing