IT IS usually impossible to tell whether someone鈥檚 cancer will respond to therapy. That could change with the discovery of a genetic signature that predicts whether a variety of cancers will respond to the most common treatments. This could help identify which patients need drugs and radiotherapy, and which can be treated less aggressively.
at the University of Chicago and his colleagues discovered that many cancers show abnormalities in 49 genes, collectively known as the IFN-related DNA damage resistance signature (IRDS).
They then analysed 34 different cancer cell lines and several hundred primary human cancers. The IRDS was associated with resistance to radiotherapy among the cell lines from certain cancers, while in breast cancer patients it correctly predicted which cancers would be resistant to radiotherapy and drugs that work by causing DNA damage in dividing cells 鈥� although not other cancer drugs (Proceedings of the National Academy of Sciences, ).
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鈥淎mong breast cancer patients, the signature correctly predicted which cancers would be resistant to chemotherapy鈥�
鈥淭his moves us one step closer to personalising cancer treatment, and points towards ways to improve the effectiveness of chemotherapy and radiotherapy,鈥� says a spokeswoman for Cancer Research UK (CRUK).
In a separate study, at CRUK鈥檚 Cambridge Research Institute and his colleagues discovered how breast cancers become resistant to the drug tamoxifen. This could lead to the discovery of new drugs and ways of screening patients who are unlikely to respond to tamoxifen.
Around 75 per cent of breast cancers are fuelled by the hormone oestrogen. Tamoxifen works by blocking oestrogen receptors, but cancers can get around this problem by expressing an alternative receptor called Her2. Carroll discovered that a cancer cell鈥檚 ability to express Her2 receptors is dependent on the relative amounts of two proteins called Pax-2 and AIB-1. If Pax-2 is missing, or AIB-1 is present in large quantities, the cancer cell will activate Her2 and become resistant to tamoxifen (Nature, ).
Drugs designed to target these proteins could prevent the expression of Her2 and allow further treatment with tamoxifen.
