Cellular senescence is the state of permanent proliferation cessation. There are two types of
cell senescence. One is replicative senescence, which relies on telomere length-dependent limit of cell
divisions. The second is stress-induced premature senescence (SIPS) which is telomere- independent.
Cell senescence is a barrier to cancer. Paradoxically senescent cells, which are metabolically active secrete
factors which can be procancerogenic. The main culprit of cell senescence is DNA damage and
DNA damage response. Although cancer cells frequently possess mutations in two main signalling
pathways involved in cell senescence, namely p53/p21 and p16/Rb, they still preserve the ability to
undergo DNA damage-induced senescence. Cancer cell senescence is a new promising target for anticancer therapy. It
was shown that many types of cancer cells can undergo SIPS. Senescent cancer cells have generally the same features as
normal cells, such as enlarged size, accumulation of DNA damage foci and increased activity of Senescence-Associated β-
galactosidase. Moreover senescent cancer cells are frequently polyploid and it was shown that polyploidy might be connected
with abnormal cell division, which leads to the appearance of small descendants. In this review we will focus on
morphological hallmarks of senescent cancer cells as well as their functional capabilities, such as secretion, polyploidization,
and stemness. We will also discuss links with autophagy, mitotic catastrophe and the propensity of senescent cells to
regain proliferative activities. We would like to show the complexity of cancer cell phenotype arising after anticancer
treatment and difficulties in interpretation of the experimental data.