Multi-cellular organisms have solved a special problem that single celled organisms don’t have: how to make cells cooperate together and restrain themselves from reproduction. In single cell organisms, there is no (little) cost to replication. Every division and replication = higher fitness. Not so for multi cell organisms. Multi-cell organisms benefit because cells can differentiate and perform different jobs. This division of labor allows increased flexibility and potential for adaptation. But, flexibility comes with a cost: specialized cells must cease or slow their own cell division. This reduction in cell division is altruistic but potentially evolutionarily unstable. How? Rogue cells that prioritize replication are favored by short term selection. These traits benefit the cell, but not the organism as a whole. This conflict is inherent in multicellularity. When cooperation breaks down, cancer happens.
In cancer, clonal cells evolve ways to escape restraints on growth and motility. These evolved traits favor the fitness of the clones (in the short term anyway) usually to the detriment of the organism that gave rise to the cancer. However, cancer lineages are usually dead ends, so that adaptations that allow cancer are not passed on from generation to generation. New cancers have to start from scratch, evolving de novo mechanisms to evade controls on growth and reproduction in each lineage. At the same time, anti-cancer adaptations have evolved in multicellular organisms that control and remove proto-cancerous cells. Multi-generational selection thus permits ongoing evolution of adaptations against outlaw cells, keeping cancer at bay, at least most of the time.
What happens when cancer lineages don’t die with their host? Those cancers would not require de novo mutations to escape control. One might suppose that a cancer that can jump from host to host would evolve to be a formidable parasite with efficient means of evading host control. A transmissible leukemia found in clams seems to support this view. Transmissible cancer in clams joins only two other contagious cancers, the facial tumors of Tasmanian devils and a venereal cancer of dogs. In these unfortunate cases, the cancers is apparently passed from generation to generation. These cancers do not have the handicap of starting from scratch in carcinogenic evolution. They behave more like pathogens, in a never ending evolutionary arms race with the host organism.
- Aktipis and Nesse Evolutionary foundations for cancer biology
- A second transmissible cancer in Tasmanian Devils
- Cancer across the tree of life.
Writing project (pick one)
- If cancer is an inevitable part of life, and starts with a single cell, it makes sense that early detection should allow doctors to start treatment early, and save lives. However, aggressive widespread early screening and treatment of many cancers can be counterproductive: Screening for breast cancer in young women and widespread melanoma screening have each failed to reduce death rates. If screening really does not save lives, why do you suppose this is so?
- Doctors often biopsy tumors to figure out how dangerous a cancer is. High genetic diversity of the tumor predicts a bad outcome, carrying an increased rate of death. From an evolutionary perspective, why is high genetic diversity in cancers bad for mortality?
Emergency Physician, Educator, Researcher, interested in the microbiome, evolution, and medicine
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