Darwin's Drugs: My Article in Today's New York Times

By Carl Zimmer | August 21, 2012 12:24 am

Two years ago, I wrote in the New York Times about scientists exploring evolution to discover the function of our genes. We share a 1.2 billion-year-old common ancestor with fungi, for example, and it turns out that fungi (yeast in particular) have networks of genes remarkably similar to our own.

Back in 2010, the scientists I interviewed told me they hoped to use this method to find new drugs. In today’s New York Times, I write about how they’ve delivered on that promise. It turns out that a drug that doctors have used for over 40 years to kill fungi can slow the growth of tumors. It’s a striking illustration of how evolution provides a map that allows medical research to find their way to promising new treatments. Check it out.

CATEGORIZED UNDER: Evolution, Medicine, Writing Elsewhere

Comments (5)

  1. This goes to the larger theme of a research establishment desperately trying to accelerate drug discovery. Along with using evolutionary biology to find drugs more efficiently, I have seen efforts to create an artificial “body” (interconnected system of fake organs) that would accurately mimic the real thing to speed drug trials. Another thrust is to create virtual drugs and test them in virtual trials before you take the time and money to make and test the real compound.

  2. Great article, Carl. As someone who has suffered through cancer treatment, and someone who has written about evolution, I really appreciate you bringing this approach to research to the general public. My big question, as politicians on national and local stages continue to claim that the theory of evolution is “just a theory”–that is, just scientific speculation–is this: Will evolution denialists put their bodies, and their families’ bodies, where their mouths are and refuse such treatments when they eventually become available? Somehow I doubt it.

  3. I had the honor to have worked with exactly this subject, not cancer but yeast genetics. Evolution and genetics are really beautiful after you start to realize how the mechanism work in real life. For over 150 years scientist tried to disprove evolution, fortunately without success
    I bet that in the next decade hospitals will pay more attention and use concepts of evolution on every day problem. The control of pathogens is one of them, such as tuberculose. Cancer evolution is using concepts of evolution for a while. Now medical students got to have and study more about this wonderful world of evolution …

  4. John Kwok

    Carl, this is yet another exceptional essay of yours which illustrates the power of evolutionary medicine via the application of phylogenetic analysis in searching for homologous sets of genes in humans and yeast for the development of new drugs to fight cancer. I regret I’m over a week behind in reading this, but I am most appreciative.

  5. Tomas Linder

    Hi Carl,
    Maybe I missed something in you NY times article or in the PLoS Biology paper but wouldn’t it make sense that thiabendazole would inhibit tumor growth? After all thiabendazole affects microtubule stability just like Taxol does (a fairly well-known anti-cancer drug), which in turn would target rapidly dividing cells i.e. tumors. Secondly, I think the “68 genes that work together to build cell walls” are probably nothing of the sort. The reference to lovastatin (a cholesterol-lowering compound) in the start of the PLoS Biol paper leads me to suspect that they were actually looking for drug-interaction profiles that match the early part of the steroid synthesis pathway (also known as the mevalonate pathway) and not cell wall synthesis. Steroids are of course not components of the cell wall but of the cell MEMBRANE. Yet for some reason people who do these types of gene-drug interaction studies love to mix up cell wall synthesis with steroid (and cell membrane) synthesis. Still, as a yeast scientist myself I salute your article that brings yeast research to a wider audience!

    [CZ: It couldn’t have made too much sense, since no one had looked into the possibility of using this anti-fungal drug against tumors before. What’s more, when Marcotte and his colleagues tested the drug out on embryos, it targeted growing blood vessels, not the many other rapidly dividing cells in the embryo. If you want more details on the pathway that the genes are in, I’d suggest reading Marcotte’ previous paper on this strategy for drug discover in PNAS, cited in the PLOS paper.]


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The Loom

A blog about life, past and future. Written by DISCOVER contributing editor and columnist Carl Zimmer.

About Carl Zimmer

Carl Zimmer writes about science regularly for The New York Times and magazines such as DISCOVER, which also hosts his blog, The LoomHe is the author of 12 books, the most recent of which is Science Ink: Tattoos of the Science Obsessed.


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