If a group of genes cause a certain phenotype in yeast (say, sensitivity to a compound called lovastatin) and a similar group of genes causes some other phenotype in mammals (say, promoting angiogenesis, the creation of new blood vessels), then drugs that affect the one phenotype in yeast may affect the other phenotype in mammals. Since many cancers rely on angiogenesis to grow, compounds that affect that affect lovastatin sensitivity in yeast could identify novel anti-cancer drugs for use in humans (which are mammals, after all).

That’s a pretty simple observation that makes intuitive sense, but does it actually work? Apparently it does. The researchers identified a bunch of compounds that affect the group of genes that regulates lovastatin sensitivity in yeast, then chose one, thiabendazole, for further investigation. The results are promising: thiabendazole inhibited and even reversed angiogenesis in models and cultured human tissue.

As a proof-of-concept for a way to find human drug targets using data on yeast, it’s interesting. Thiabendazole’s usefulness as an anti-cancer drug is still far from certain, but it’s nice to see a new approach to identifying drugs and drug targets from that mess of genomic data that we’ve accumulated over the past decade or two.

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Published on 25 August 2012 and tagged as
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