Selective destruction of senescent cells in old tissues offers the promise of some degree of rejuvenation, coupled with effective therapies for a range of age-related diseases that currently cannot be controlled. In the past few years, a number of companies have raised venture funding for the development of senolytic therapies, those capable of removing some portion of senescent cells with an acceptable side-effect profile. The potential market is enormous, and thus despite the many potential competitors, any new mechanism by which senescent cells can be destroyed might be the pathway to success and revenue for the individuals and organizations involved in that research. A great deal more attention and funding is being devoted to the biochemistry of senescent cells than was the case even five years ago.

Cellular senescence is also of great interest to cancer researchers. Senescence in response to DNA damage is a way in which our biochemistry removes the riskiest cells from circulation. Senescence irreversibly shuts down the ability to replicate, senescent cells secrete signals to attract the immune system to the vicinity, so that problem cells can be destroyed, and in any case most senescent cells self-destruct shortly after entering this state. This works quite well at the outset, but not all senescent cells are destroyed. Eventually, there are enough of them that their signaling results in significant inflammation and disarray in the surrounding tissue - and that actually helps the development of cancer.

Nonetheless, at the front line of cancer research, any reliable approach that can force cancer cells into senescence is a win. Today's paper describes the possible foundation for such a treatment. While this isn't good for the patient in the long term - much of the shortened life expectancy of chemotherapy patients is most likely due to their high burden of senescent cells - it is a much better option than the outcome of uncontrolled cancer. It seems quite plausible that one of the results of the present raised level of interest in senescent cell biochemistry will be a range of more selective, more reliable, better ways to force cancer cells into senescence; approaches that rely on cellular biochemistry that is common to many or all cancers. That can then be coupled with senolytic therapies: turn the cancerous cells senescent and immediately destroy them. Might there be a practical end to cancer somewhere in the senescence research of the next decade or two? Maybe so.

Inhibitors of histone acetyltransferases KAT6A/B induce senescence and arrest tumour growth