What happens if the artful criminal is so well disguised they completely give the police the slip? Like many a criminal character, cancer cells are intrinsically unstable. Over time their appearance and personality changes. Their chromosomes go haywire and stop faithfully copying the normal cargo of 23 pairs when the cell divides. Some are copied in threes. Bits fall off. Two or three might join up. Some disappear altogether. What remains on the wonky chromosomes is a very disturbed set of genes.

Loss of tumour suppressor genes will allow cancers to grow. Loss of genes that tell cells where they can and can’t go in the community can lead to metastasis (moving from the primary site of cancer). Another common finding is the loss of genes involved in the MHC and antigen processing. By not displaying the right identity tag, cancer cells can go unrecognised by the immune system. In effect they become invisible, free to go whereever they like and do whatever they like.

An organised workforce of proteins ensures that the correct ID (the unique MHC) is properly assembled on the surface of our cells. Proteins are each encoded by distinct genes and each is potentially affected in cancer. Perhaps the best understood is a protein called TAP (Transporter associated with Antigen Processing). Researchers have noticed in many different types of cancer, particularly in more advanced stages, that the amount of TAP is reduced or even absent prompting a reduction or loss of MHC and hence a fraudulent ID. This defect can be used to predict cancer progression and survival rates in humans.

Research from British Columbia by Professor Wilfred Jefferies and his team has now shown that the TAP gene itself isn’t at fault. Faulty TAP protein results from changes in the epigenome of cancer cells. This is the first demonstration of an epigenetic way for cancers to dodge the immune system.