The discovery was made using a model of B-progenitor acute lymphoblastic leukemia (B-ALL), the most common cancer affecting children. Researchers from the Walter and Eliza Hall Institute showed that switching off a gene called Pax5 could cause cancer in a model of B-ALL, while restoring its function could 'cure' the disease. "Along with other genetic changes, deactivating Pax5 drives normal blood cells to turn into leukemia cells, which has been shown before," Ms Liu said. "However we showed for the first time that reactivating Pax5 enabled the cells to resume their normal development and lose their cancer-like qualities, effectively curing the leukemia. What was intriguing for us was that simply restoring Pax5 was enough to normalise these cancer cells, despite the other genetic changes." "This work shows how inactivating the tumour suppressor gene Pax5 contributes to B-ALL development and how leukemia cells become 'addicted' to low Pax5 levels to continue proliferating. Even though the B-ALL cells have multiple genetic mutations, simply reactivating Pax5 causes tumour cells to resume normal development and lose their cancerous properties." However Dr Dickins said that genes that are lost in tumour cells are not traditionally drug targets. "It is very difficult to develop drugs that restore the function of genes that are lost during cancer development," Dr Dickins said. "However by understanding the mechanisms by which Pax5 loss causes leukemia, we can begin to look at ways of developing drugs that could have the same effect as restoring Pax5 function."