Polyploid somatic cells have 'programmed' roles in normal development and stress responses. Transient
polyploidy states have been observed in several
tumor types at early stages of
tumorigenesis. They can give rise to the
aneuploidy state which is a common feature of human
cancer cells. Similarly, to
cancer development,
cancer treatment can lead to transient
polyploidy.
Polyploid giant cells (PGCCs) in
cancer are often associated with poor prognosis and disease relapse.
Cancer cell senescence- a proliferation arrest accompanied by a set of characteristic markers- induced by
therapy is also associated with transient
polyploidy formation and
cancer relapse. The question is whether
therapy-induced senescence (TIS) and
therapy induced
polyploidy (TIP) are mechanistically or coincidentally connected. This problem needs to be solved rather urgently, because TIS appears to be more common phenomena than originally believed. Another arising question concerns reversibility of
cancer cell senescence as a consequence of atypical divisions of
polyploid cells. In our review we will try to answer this fundamental question by referring to published literature and to our own studies.