The aptitude for organogenesis from normal hormone-dependent cultures very
commonly decreases as the tissues are serially subcultured. The reasons for
the loss of regenerative ability may vary under different circumstances: g
enetic variation in the cell population, epigenetic changes, disappearance
of an organogenesis-promoting substance, etc. The same reasons may be evoke
d for the progressive and eventually irreversible loss of organogenic totip
otency in the course of neoplastic progressions from hormone-independent tu
mors and hyperhydric teratomas to cancers. As in animal cells, plant cells
at the end of a neoplastic progression have probably undergone several inde
pendent genetic accidents with cumulative effects. They indeed are characte
rized by atypical biochemical cycles from which they are apparently unable
to escape. The metabolic changes are probably not the primary defects that
cause cancer, rather they may allow the cells to survive. How these changes
, namely an oxidative stress, affect organogenesis is not known. The litera
ture focuses on somatic mutations and epigenetic changes that cause aberran
t regulation of cell cycle genes and their machinery.