TRISOMY 8 MOSAICISM: CELL CYCLE KINETICS AND ...

T-lymphocytes and B-lymphoblasts in G-banded metaphases may be due to cell lineage
separation or perhaps T-lymphocytes are more tolerant of an extra 8 chromosome.
The extra-embryonic samples, which included amnion, chorion, and villi, each
contained fewer than 50% trisomy 8 cells, with chorion and villi having less than 10%
trisomy 8 cells (Table 1). The presence of trisomic cells in the embryonic and extra-
embryonic tissues confirms the early timing of the non-disjunction mitotic event; before
the embryonic and placental lineages separated. Had the non-disjunction occurred later,
after late blastocyst, the resulting levels of mosaicism would have been either confined to
the fetus, therefore having a normal placenta, or CPM with a normal fetus. The lower
level of trisomy 8 cells in the placental tissues could provide an explanation for the
pregnancy progressing to full term, with normal birth weight, despite the severity of the
patient’s phenotype. Once again this supports the concept of a normal placenta
supporting the growth and development of an aneuploid fetus to full term (Farra et al.
2000).
Growth disadvantage of Trisomy 8 cells
Selective growth advantage of normal cells in mosaic tissues was described by La
Marche et al. in 1967, while studying mosaic trisomy 18. La Marche et al. found an
individual’s mosaicism significantly changed from 90% trisomy cells/10% normal cells
at birth to 100% normal cells at ten months of age. They described this event as
disappearing mosaicism and concluded, “the normal population of cells exercised a
growth advantage, with eventual replacement of the abnormal cells” (La Marche et al.
1967). More recently, Mark and Bier (1997) and Jordan (1998) each concurred with the
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