This year's Nobel Prize for Physiology and Medicine was awarded to Leland Hartwell, Tim Hunt and Paul Nurse for “discoveries of key regulators of the cell cycle”, and a recurring theme in press coverage of the award is that their work will lead to new therapies for cancer. Indeed, two of the winners — Leland Hartwell and Paul Nurse — are directors of large cancer research institutes. They also both work on yeast — single-celled organisms that are incapable of getting cancer. So, how can basic research translate to the development of new anticancer drugs?

Cancer has long been considered to be a disease of the cell cycle. Many genes that are involved in the control of cell division — some of which were discovered by the Nobel laureates — have altered expression patterns in tumour cells, and a class of mutant that regulates mitosis is believed to contribute to tumorigenesis, as discussed by Prasad Jallepalli and Christoph Lengauer in this issue.

At mitosis, sister chromatids attach to the spindle via their kinetochore. A checkpoint monitors this process to ensure that each sister chromatid is attached and aligned correctly, which prevents premature segregation of the sisters. So what happens if the checkpoint fails? A defective checkpoint can mean that a cell receives neither or both copies of a sister chromatid, resulting in chromosomal instability — a hallmark of cancer.

Several genes involved in sister-chromatid separation, or in the checkpoint that regulates it, have been implicated in cancer. And, excitingly, new technologies are now allowing drug developers to use this defect against cancer cells. It's early days yet, but perhaps this will be one of many leaps that takes basic research on cell division to a place where it directly benefits patients with cancer.