Cancer modeling and writing project

Some take away points from the cancer lecture:

Cancer evolution that Dr. Forrest described is different from evolution of other traits.

Cell level evolution:

Evolution in the computer modeling of Dr. Forrest is selection on the human cell level. It is not evolution on the individual or population level. For breast cancer, a mutation happens within a human life span.  Subsequent cell evolution lasts until the patient dies. This is different from most other evolution by natural selection.  As an example, natural selection for intelligence (probably) changed human gene frequencies.  Homo sapiens’ large cerebral cortex evolved by this process over many thousands of years.

The evolution of a cancer lineage has a short time span. Evolution of that cancer is essentially reset with each death.  This makes it attractive from a modeling standpoint. Each computer run is similar to the course of a malignant cells’ reproduction. Modelers can then try to figure out which features are most important in the growth and appearance of cancerous cells.

Complexity and function.

Presumably, individuals with larger brains did better that their competitors with small brains. If so, they left more offspring, and over time human populations developed large brains with additional brainpower. Natural selection, acting on individual differences, led to changes in gene frequencies that were associated with more complex brains. In this instance and others, natural selection results in traits that are complex and have apparent function.

The evolution of cell lineages in a cancer cell, by contrast, can result in diminished complexity and reduced function. A tumor may consist of what appear to be developmentally immature cells. Their growth interferes with the function of the organs that they grow in or around.

Special cases:

In some cancers, evolution is not reset with each death of the patient. One example is cancer caused by HPV viruses. These viruses promote cell replication and inhibit human cell apoptosis. Those features prevent the immune system from eliminating the virus, and they help spread the virus to other people. Thus a wart is  a little tumor that is produced by the virus in order to enhance its virulence. Sometimes that tumor becomes malignant and results in cervical, or oral cancer. Gardasil is a vaccine that has been developed to reduce the incidence of cervical cancer by preventing infection by certain HPV strains.

In another nonhuman example, Tasmanian devils (a real animal, cartoon fans!) carry an infection that results in a disfiguring tumor of the face. This tumor is spread by direct contact between the animals and might end up contributing to the extinction of this animal.

Infectious causes of cancer can affect generation after generation. Evolution of at least the precancerous stages does not end with the death of the patient, because they have a transmissable component. Some of these traits do not benefit the human sufferer, but benefit the pathogen. But does the virus benefit by causing full blown cancer? Or does it only benefit from causing a cervical wart (which is a precancerous lesion).

So here are some questions for you to write about for next week:

1) Does the HPV virus that causes cervical cancer benefit when it causes cancer? What are the virulence factors of HPV viruses that might predispose cervical cells to cancer?

2) How are computer viruses like human viruses? How are they different? (Deep stuff!)

3) Many cancers seem to affect the reproductive system. Why do you suppose that might be?

Have fun and see you next week!

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