Commentary Volume 1, Issue 5 pp 438—441

Figure 1. Different cellular stresses can induce senescence including telomere shortening, DNA damage, and oncogene activation. Senescence of tumor cells represents a cell intrinsic tumor suppressor mechanism. In contrast senescence of non-transformed cells in aging organs may lead to loss of proliferative competition and selection of malignant clones. The senescence associated secretory phenotype (SASP) could have different effects on aging and cancer: (i) it could contribute to the induction and maintenance of senescence via a feedback loop, (ii) it could activate immune response leading to improved clearance of senescent tumor cells, (iii) it could stimulate proliferation of neighbouring tumor cells, (iv) it could impair the function of non-transformed tissue stem cells.