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The presence of monotypism in thick atherosclerotic lesions of
black females with G-6-PD mosaicism first reported by the Benditts
(1973) has been confirmed in two other laboratories. However, we
believe that it is premature to conclude that the finding of
monotypism necessarily indicates monoclonal origin of athero
sclerotic lesions. We have suggested two alternative explanations
for the obser vation of monotypism which we believe must be shown
to be invalid before accept ing monoclonal origin as the only
plausible way to account for the observed G-6-PD monotypism. One of
these two alternatives relates to clonal heterogeneity of cell
growth potential, i. e., during the course of progressive growth of
a le sion, progeny of one cell may overgrow all others in a portion
of the lesion. The other alternative is that one of the G-6-PD
alleles may be linked to genes that afford a preferential survival
characteristic in the abnormal environment present in
atheroscerotic lesions. Thus, cells with one allele may be able to
grow better than cells with the other allele, and this
characteristic may be unrelated to "A-ness" or "B-ness." We have
studied initiation of lesions in He diet-fed swine and demonstrated
that all active lesions that were studied were of multiple cell
origin (not monoclo nal). We have studied cell growth patterns in
developing atherosclerotic lesions in He diet-fed swine and found
evidence consistent with clonal heterogeneity in growth potential
of lesion cells."
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