Several studies have shown that the induction of cellular senescence can inhibit particular cancers. Among these is astrocytoma, a tumor that occurs in the brain. Normal brain cells produce a protein that has been designated p57. Pathologic studies of astrocytomas demonstrate that they do not produce p57, although the gene that should produce p57 does not contain mutations. Canadian researchers have stimulated astrocytoma cells in laboratory cultures to begin expressing p57. They noted that the p57-induced astrocytoma cells enlarged and flattened. Within one week, they began to accumulate an enzyme called beta-galactosidase, which is associated with senescence. Thus, p57 induction is a stimulus for cellular senescence in astrocytoma cells and may be a potential therapeutic intervention for this disease.

Epstein-Barr virus is typically a benign infection, but in some cases, it serves as a stimulus for the development of cancer, particularly Burkitt's lymphoma. It has also been implicated in the lymphomas seen in AIDS patients, rare tumors of the nose and throat, and some breast cancers. Chinese researchers have discovered that a protein on the surface membrane of the Epstein-Barr virus prevents mouse cells from becoming senescent, allowing them to become immortal (that is, reproduce indefinitely) instead. They have also done work that demonstrates that this same Epstein-Barr membrane protein prevents senescence in human fibroblast cells. They speculate that this protein contributes to the development of cancer by somehow inducing cancer-causing genes to become active and by bypassing the normal senescence triggers.

Finally, investigators in Korea have published studies documenting that at least some of the cancer-fighting effects of the chemotherapeutic drug hydroxyurea occur by inducing cellular senescence. Erythroleukemia is an unusual form of leukemia featuring cancerous red blood cells rather than white blood cells. Cultures of erythroleukemic cells treated with hydroxyurea for seven days were noted to have modified into a senescent form. The treated cells began to produce beta-galactosidase and other enzymes associated with senescence. The DNA of the cells did not become fragmented, as is common with cell death. The researchers concluded that long-term treatment of cancer cells with hydroxyurea seems to work by inducing cellular senescence.