Endogenous blockage and delay of the chromosome cycle despite normal recruitment and growth phase explain poor proliferation and frequent edomitosis in Fanconi anemia cells.
- 1 September 1985
- journal article
- Vol. 37 (5) , 1022-30
Abstract
BrdU-Hoechst flow cytometry was employed to study the proliferation kinetics of blood lymphocytes from patients with Fanconi anemia (FA). Compared to controls, untreated FA lymphocytes show normal response to PHA stimulation, normal G0/G1 exit rates, and normal first S-phase durations. The G2 phase of the first cell cycle, however, is severely prolonged, and 24% of the recruited population become arrested during the first chromosome cycle (S, G2/M phases). The delay suffered during G2 appears to be compensated in part by a subsequent G1 phase duration that is unusually short for postnatal human cells (3.7 +/- 0.5 hrs). In analogy to what has been observed in other cell systems after experimental delays of the chromosome cycle, we therefore postulate that at least some FA cells enter their second growth phase without prior completion of the delayed chromosome cycle. Renewed replication would ensue in such cells without prior passing through mitosis and cytokinesis, leading to endoreduplication, which is a frequent finding in the FA syndrome.This publication has 19 references indexed in Scilit:
- Growth and the cell cycle of the yeast Saccharomyces cerevisiaeExperimental Cell Research, 1983
- Flow cytometric analysis of factors which influence the BrdUrd‐Hoechst quenching effect in cultivated human fibroblasts and lymphocytesCytometry, 1983
- Abnormal NAD+ levels in cells from patients with Fanconi's anaemiaNature, 1982
- Cytogenetic and flow cytometric studies of cells from patients with Fanconi’s anemiaCytogenetic and Genome Research, 1982
- Introduction to Cell Growth: Growth in Size and DNA ReplicationPublished by Springer Nature ,1981
- Specific cellular defects in patients with Fanconi anemiaJournal of Cellular Physiology, 1979
- Cell size, cell cycle and transition probability in mouse fibroblastsCell, 1978
- Deficiency of DNA ligase activity in Fanconi's anemiaHuman Genetics, 1978
- Cross-link repair in human cells and its possible defect in Fanconi's anemia cellsJournal of Molecular Biology, 1977
- Is Fanconi's anaemia defective in a process essential to the repair of DNA cross links?Nature, 1975