I. Whales and elephants have many more cells than humans. You might think that they would get more cancer since each cell has an opportunity to accumulate somatic mutations that could lead to cancer. In fact whales and elephants, despite their larger size have lower cancer rates compared to humans. This phenomenon is called Peto’s paradox, the lack of association between larger body size and cancer incidence.
Why do elephants have little cancer? My friends Carlo Maley and Josh Schiffman set out to figure out why. Their answer that has to do with DNA repair mechanisms and apoptosis, the process whereby damaged cells kill themselves. They published their results in JAMA this month:
Abegglen Maley Schiffman Potential Mechanisms
(Students scroll to the bottom for assignments for 11/3/15)
II. Clam cancer
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 neoplasm. However, cancer lineages are usually dead ends, so that adaptations that allow neoplasia 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-neoplastic 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. Recently 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.
In soft shell clams found in the Northeastern US and Canada, a leukemic cancer is genetically identical and widespread, suggesting it has evolved a parasite-like capacity for infection and transmission.
Skim Metzger et al’s article: Horizontal Transmission of Clonal Cancer Cells Causes Leukemia in Soft-Shell Clams
For an in depth article on Tasmanian Devil facial cancer, read David Quamman’s 2008 article
III. Why does cancer evolve in the first place?
Read: Aktipis and Nesse Evolutionary foundations for cancer biology
IV. Maternal fetal conflicts and the evolution of cancer.
Read: Maternal-fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer
Assignment for Tuesday 11/3/15: There will be no writing assignment due. Instead come prepared to talk about these readings. Read all of them, but specific assignments will depend on your birthday month: If your birthday is January, February or March, you will discuss elephants and Peto’s paradox. If your birthday is April, May or June you will discuss cancer in clams and Tasmanisn devils. If your birthday is July, August or September, Evolutionary foundations of cancer. If your birthday is October, November, or December you will discuss Maternal-fetal conflict imprinting and cancer.
Emergency Physician, Educator, Researcher, interested in the microbiome, evolution, and medicine
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