TRISOMY 8 MOSAICISM: CELL CYCLE KINETICS AND ...

proliferates and thus mosaicism results. Other possible mechanisms for mosaicism
include anaphase lag or spindle fiber attachment failure (Kalousek 1999).
The presence of trisomic cells throughout various tissues, both embryonic and
extra-embryonic, depends upon the timing of the non-disjunction or error event (Webb et
al. 1998). The earlier the error, the more likely both the fetus and placental tissues will
be affected. T8m may occur in the fetus, placenta, or both simultaneously. When only
the placental tissues are affected, it is referred to as Confined Placental Mosaicism
(CPM). CPM occurs in 1-2% of all viable pregnancies analyzed by chorionic villi
sampling. Also CPM is estimated to occur in over 2-5% of spontaneous abortions (Griffin
et al. 1997). CPM has been associated with a broad range of outcomes such as normal
pregnancy, intrauterine growth retardation, and even intrauterine fetal death (Lestou et al.
1998, Kalousek 1999).
CPM can result from both meiotic and mitotic non-disjunction. Meiotic error
results in complete trisomic placental tissue, which can form a normal cell line and
mosaicism by going through trisomic rescue. Trisomic rescue occurs when a
chromosome is lost from either the trisomic trophoblast lineage or true embryonic
progenitors (Kalousek 1999). Whether there is CPM or fetal mosaicism, it has been
documented that chromosomally abnormal placental tissues are correlated with abnormal
fetal development (Farra et al. 2000). Also, as the proportion of trisomic cells in
placental tissue increases, so does the likelihood of intrauterine growth retardation or
fetal death. Compared to chromosomally abnormal placentas, normal placentas enhance
the survival and likelihood of abnormal fetuses going to term (Farra et al. 2000).
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