The authors of today's open access research offer an interesting viewpoint on cellular senescence in the context of cancer, presenting it as an aspect of the innate immune response to the signs of cancer-inducing mutational damage, or to the signs of cancer suppression programs operating in cells. The objective of the body's numerous, layered defenses against cancer is to destroy all cells that show the signs of becoming cancerous. The first line of defense is the state of cellular senescence, in which cells shut down their ability to replicate, prime themselves to self-destruct via the programmed cell death path of apoptosis, and alert the immune system via a mix of inflammatory secretions known as the senescence-associated secretory phenotype (SASP). These secretions also raise the odds of other surrounding cells becoming senescent, which in theory helps to stay ahead of the replication of an early cancer.

Cellular senescence in this context of cancer is likely an adaptation of an existing tool. Transient cellular senescence occurs during embryonic growth and wound healing, a way to help guide structure and regeneration. That it can also help to shut down early stage cancer has the look of a later development. Unfortunately cellular senescence is an imperfect tool: senescent cells are not reliably removed by the immune system, and they do not reliably self-destruct. Some tiny fraction linger, and their continued inflammatory secretions are an important contributing cause of aging and age-related disease.

In recent years, the research community has found ways to selectively destroy a fraction of the senescent cells present in old tissues. This approach to the treatment of aging reliably extends life span and reverses numerous age-related diseases in mice. Numerous companies are working on ways to destroy senescent cells, and the first therapies are entering human trials. Meanwhile, ever more funding is flowing towards fundamental research into the biochemistry of senescence, as there are likely many more potential approaches to the destruction or management of senescent cells yet to be discovered. This point is illustrated well in the open access paper here, as the authors propose a new point of intervention based on their research.

The innate immune sensor Toll-like receptor 2 controls the senescence-associated secretory phenotype