TRISOMY 8 MOSAICISM: CELL CYCLE KINETICS AND ...

46,XX cells (Verp et al.1988). Cell generation times were significantly different between
the two cell lines, resulting in abnormal cells with a longer turnover time (Verp et
al.1988). However, the results from our cell cycle kinetics analysis (Table 4) show
normal and trisomy 8 cells in the cord blood, transformed blood, and amnion do not have
a significant difference in growth rates. Therefore, these results exclude the growth rate
difference as a causal mechanism for the decrease in trisomy 8 cells.
Another mechanism proposed for the loss of trisomy 8 cells is apoptosis or
programmed cell death. Apoptosis occurs when a cell has sustained DNA damage or
been subjected to an injury or viral infection. This ingrained defense mechanism
recognizes errors and deters cellular division, resulting in cellular arrest. Chromosome 8
houses an oncogene, c-myc, directly related to checkpoint cyclins and the cell cycle.
Overexpression of c-myc has been known to result in the arresting of cells at the G2 phase
checkpoint, and therefore causing cells to undergo apoptosis before reaching metaphase
(Felsher et al. 2000). The apoptotic mechanism is assumed possible due to the additional
8 chromosome in the aneuploid cells, and may be involved in the complete disappearance
of trisomic cells over time. Studies on our patient were not performed to examine cell
death.
Finally, we suggested the entry of trisomy 8 cells into the GO phase of the cell
cycle would cause a decrease in trisomic metaphases. The GO phase, usually associated
with non-dividing cells and resting cells, occurs after mitosis and during the G1 phase of
interphase. This phase may last a short length of time, extended period of time, or
indefinitely. A passage into the GO phase would inhibit the procession into mitosis,
therefore resulting in a decrease of metaphase cells. This has been seen in mosaic
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