Chromosome ends are like the plastic tips on shoelaces: they shield DNA from fraying with every cell division. Ordinary cells lose these tips over time and stop dividing. Cancer cells have found a way around this. They either switch on an enzyme that rebuilds the ends, or they take a backup route that works a bit like mending a rope with a neighboring strand. The key helper on that backup route is the PIF1 protein.
PIF1 does two things at once. First, it untangles the knots that form in DNA and get in the way of copying it. These knots show up especially often at chromosome ends. Second, PIF1 itself kicks off DNA copying, starting from the site of a break. Thanks to this, cancer cells lengthen their chromosomes and produce extra ring-shaped scraps of DNA.
This finding matters for cancer treatment. Roughly one in ten tumors uses the backup route for lengthening chromosomes, and such tumors often resist standard drugs. Create a drug that switches PIF1 off, and you can strip these cells of their ability to repair their chromosomes. So far the drug has only been tested in the lab, but it has already shown that it kills both types of cancer cells: those that use the usual enzyme and those that rely on the backup route.
The PIF1i inhibitor (Compound 1) was checked in the lab by HPLC, mass spectrometry, and NMR, and its purity came out close to 99%. It is a rare case of a small molecule against a helicase being so thoroughly characterized before use in cell experiments.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.