Cancer Is A Cheater Before It Kills

Her work employs nontraditional approaches of applying models of animal and plants relationships to one another ecologically to systems in the human body. In a recent Harvard lecture she focused on the relation of cancer cells to healthy cells, stating that cancer cells can be seen as cheaters within working cell systems.

The rare crested cactus is one of the reasons why she started looking at the disease from an evolutionary perspective, being that it displays clustered cells that are cancer like in appearance, which is an example of fasciation, that led to 2 observations: Humans aren’t the only ones to struggle with cancer; and that plants are able to grow and survive even with abnormal growths. She goes on to say these observations have profound implications for human research.

The disease is a byproduct of cell cooperation; with about 30 trillion cell within the body cooperating and coordinating gene expression. Unfortunately the possibility of cheater cells appearing to exploit the system increases as multicellular organisms evolve and systems grow. This is what cheating cancer cells do: Proliferate without limit, monopolize resources, destroy the surrounding environment, co-opt other cell labor, and avoid cell death. If cancer is present rules of intercellular cooperation break down. When there are cells taking advantage of other cells around them that are following rules, cellular cheating really isn’t a metaphor.

Using this model one might think larger organisms would have more gene mutations and be more cancer prone, but that is not true, says Aktipis. She traced cancer incidence across different multicellular species which included melanoma and blood cancers in mollusks and claims during 12 months residence at Berlin Institute for Advanced Study, she discovered as multicellular life evolves so does the ability of organisms to restrict incidence of cellular cheating, life solved the problem of cellular cheating.

Cancer cells evolve to exploit body ecology while the body evolves to suppress invasions, such as TP53 gene evolution to regulate and suppress tumors. Larger organisms have more copies of TP53, such as elephants which have 20 times as many as humans to support and deal with their body size. The human body has an amazing multilayer of cellular detection, think of these mechanisms as cellular conscience, the cells moderating itself, with the upshot being that bodies have a collective cellular intelligence which has evolved to keep incidence of cancer lower than it would be otherwise. These defenses, much like the disease itself, are fundamental consequences of multicellularity, according to Aktipis.

Possible future paths for research could be to allow that cancer is genetically inevitable and concentrate on its management. The disease isn’t very likely to be eradicated completely, but new treatments can bolster cheater detection systems to increase the ability of the body to fight off invasions and infections. As an example researchers are finding non-steroidal inflammatory drugs can slow mutations rates and decrease progressions of esophageal cancer; or a new form of adaptive therapy had been found to control cancers in mice models and is showing promise in human trials, in this case tumors are treated with drugs only when actively growing otherwise they are left alone which keeps drug resistant cells from taking over. She says evolutionary informed treatments such as these may offer the greatest hopes for cancer treatments.