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Scientists at Trinity College Dublin have made a breakthrough in understanding how cancer cells can evade the cell-killing effects of chemotherapy and enter a "zombie-like state," called premature senescence, that can attract the wound-healing properties of the immune system.

Although our immune system protects us from infection, it also plays a critical role in coordinating repair and replacement of damaged tissue, which is a process called wound healing. The wound-healing capabilities of the immune system stimulate cell division within damaged tissue to replace cells that have been lost through injury and bring extra nutrients and oxygen into the injured tissue by triggering the growth of new blood vessels. This is a complex and highly coordinated process, which ensures that new cells are only produced where and when they are needed.

However, cancers can exploit these wound-healing capabilities for their own ends by masquerading as damaged tissue and tricking the immune system into helping malignant cells to divide and acquire extra oxygen and nutrients rather than killing them. For these reasons, cancers have been described as "wounds that do not heal," but how they switch on the wound-healing capabilities of the immune system is still poorly understood.

In research published in the journal Science Advances , scientists from the Smurfit Institute of Genetics at Trinity College Dublin have found that molecules called inhibitor of apoptosis proteins (IAPs) can enable tumors to escape the cell-killing effects of commonly used chemotherapeutic drugs.

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