Category Archives: evolution

Quora activity for January 2015 – August 2016

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!


Would it be possible to avoid cancer by modifying our DNA?

Is whole genome sequencing of any use in cancer diagnostics?

If our body can detect cancerous cells, why do people still get cancer? Does it mean that we can improve our body’s defenses against cancer before even getting sick?

If 2/3 of cancers are caused by chance mutations, why should I work to help prevent cancer?

Is it possible that cancer is not actually a disease to be “cured”, but it is actually an inherent defect of genetics?

Is cancer an intrinsic feature of life?

Is worrying about cancer the biggest cause of cancer?

What are the chances (if any), that a blind person getting cancer in the eye would allow them to see again?

What cure would be most beneficial to discover: HIV/AIDS or cancer?

Can Ebola be treated with cancer drugs?


If two people have identical DNA fingerprints, what other molecular evidence does forensics use to distinguish between biological samples?

Can a methylation pattern be sequenced?

What could potentially be the most exciting application of epigenetic research?

Why hasn’t Lamarck been acknowledged in the face of the burgeoning advances made in the science of epigenetics?

In what way does histone methylation prevent transcription?

Is the epigenetic system of a person heritable?

Is there a meaningful way to diagnostically test a patient for epigenetic changes caused by long term use of medications?

Other Scientific Subjects

Is it a possibility that parents of genotype AA have an offspring with AS?

What is the reason that viruses are inactive when not inside any organism? What is the mechanism?

Will the final solution to HIV be to just accept it as part of the human genome?

What can you tell about a gene based on its tissue expression patterns?

What are some interesting examples of people becoming infected with typically fatal diseases (e.g. Ebola, HIV/AIDS, rabies, anthrax) through unusual means or at long odds?

Could cellular environment (pH, temperature, molecular crowding, redox state) affect a cell’s interactome?

What causes mutation in viruses?

Which (multicellular) animal is most deadly to humans?

What would happen if all the DNA in my body suddenly disappeared?

What are the most useful lab hacks, tips and tricks for molecular biology/biochemistry?

Do viruses have nutritional value for any organism?

What will next-generation sequencing be called a generation from now?

When will we be able to sequence the genome of every living vertebrate on Earth?

What are the oddest organisms?

Biochemistry: Why does the yeast two-hybrid system system have low specificity?

About Scientific Research and Careers

What does a principal investigator at a molecular biology lab spend time doing during the day?

How common is it for scientists to hire people to write their grant proposals?

How do I improve my grant writing?

I want to apply for a grant for a project, but I have no idea how to write a proper grant proposal. How can I go about this?

What is your favorite annual scientific conference?

Does a biochemist/biologist have to know all the reactions of cellular respiration or other general topics by heart after graduating?


Is there racism in Canada? Why?

What’s the best story about “fighting fire with fire”?

What are some of the best moments while taking exams?

Why do people believe in the ancient aliens theory?

If cloning of people was legal, whom would you choose and why?

What are some great optical illusions?

Which is the best way to pass the PMP exam?

Why do some people choose to use Quora over writing a blog?


On the Origin of Tumours by Means of Natural Selection

[This was one of the first blog posts I ever wrote, back in June 2007. Originally posted on my old Blogspot site]

I had an interesting conversation with a medical doctor this week. Granted, I’d much rather he’d chosen not to discuss cancer stem cells while removing a suspicious mole from my arm, but these things often seem to happen to me when a physician asks what I do for a living.

Our conversation got me thinking about how the development of cancer mirrors the process of evolution. This comparison first occurred to me during my undergraduate degree in genetics. To understand the molecular nature of cancer, we had to learn to see things from a tumour cell’s point of view.

Cell growth and division are usually very tightly regulated processes; various mechanisms have evolved to ensure that a cell can only divide into two daughter cells if the conditions are right. The correct growth factor chemicals must be present, DNA replication must have been successfully completed, the cell must have reached a certain minimum size, and be in an appropriate position with respect to other cells and tissues.

A tumour develops when these inhibitory mechanisms fail. DNA replication is not 100% accurate, and some daughter cells will receive mutations in genes that usually help to regulate cell division. Most mutant cells will be weeded out and marked for destruction when they fail to meet other cell division criteria, but the occasional gene mutation escapes notice and survives.

Imagine a mutant cell that no longer requires growth factors in order to grow and divide. The cell will divide regardless of its chemical environment, passing on its mutation to both daughter cells, each of which will then divide into two more mutated cells. In this way the mutation is passed down through successive generations of cells. If there are no growth factors present, the mutant cells will continue to divide while normal cells are inhibited. The mutant cells will rapidly come to outnumber the normal cell population. You might say that they have a selective advantage, and therefore produce more offspring.

Eventually, one of the rapidly dividing, growth-factor independent cells will acquire a second mutation in another inhibitory gene. Suddenly, we have a growth-factor independent cell that will divide when it reaches a smaller size than normal. This cell will be able to divide before its merely growth-factor independent relatives are ready. Again, this mutation confers a selective advantage, and subsequent daughter cells will outcompete and outnumber the original population of mutant cells. As cells grow and divide faster and faster, more DNA copying errors creep in. Some of these errors even increase the frequency of further mutations. The end result of this evolutionary process is a clonal population of aggressively growing cells that can move to other locations in the body to produce secondary tumours.

This process is obviously disastrous for the host. But you can not deny that the tumour cells themselves are immensely successful. Their ability to divide more rapidly than the body’s normal cells lets them produce more offspring, and increase the frequency of their beneficial mutations within the total cell population.

The gradual evolution from normal to malignant cells illustrates a very simple natural law. If an individual produces a number of offspring via an imperfect copying mechanism, the result will be a mixed population of individuals with slightly different characteristics. If one of the variants is able to produce offspring faster than its peers, then those offspring will be over-represented in subsequent generations. In this way, characteristics that increase reproductive success are inherited by more individuals and continue to increase in frequency, gradually changing the overall demographics of the population.

This really should be self-evident, and I have a very hard time understanding why evolution deniers find the concept so difficult to grasp. The gradual accumulation of mutations during cancer development is well documented, but I don’t think I’ve ever seen these data used to teach the principles of evolutionary theory. I fear that I would not make a very good teacher myself as I would become too easily frustrated with those who just can’t seem to get it. But if anyone reading this is involved in science education, please let me know what you think.

Oh, the suspicious mole turned out to be only slightly dodgy. No matter how cool evolution is, I’m happy to avoid observing the survival of the fittest within my own puny Celtic skin.

Leave a comment

Posted by on 2014/02/23 in cancer, evolution, stem cells