Experts have discovered how some forms of children's cancers can change to make them harder to treat. Nine out of 10 children with the most common form of blood cancer - acute lymphoblastic leukaemia (ALL) will currently survive the disease after leaps in the available treatment.
For those whose cancer does not respond to the usual treatments hope is pinned on new antibody and immune cell-based treatments such as CAR-T-cells. These target the surface of the cancer cells.
But medics say these cells sometimes change to evade the treatment. This can see them changing the proteins which cover the surface of the cancer cell - or even switch to a different type of cancer to stop the therapies working.
Now researchers say they have discovered the mechanism behind the so-called "chameleon cancers", reports Chronicle Live. And it means fresh hope for those fighting the disease.
Dr Simon Bomken, a clinical scientist and honorary consultant based at Newcastle University and the Newcastle Hospitals NHS Trust, has been part of an international team investigating how the cancer cells work to fight off treatments. Dr Bomken - along with experts at the Princess Maxima Center in Utrecht in the Netherlands, and at the University of Birmingham - has now identified the gene which allows ALL to resist potentially life-saving treatments.
The scientists have now published a paper in the journal Blood which explains how this relapse happens - and provides hope for treating the patients concerned. Dr Bomken said: "ALL cells carrying this chromosomal rearrangement have long been known to be able to relapse as a different type of blood cancer, acute myeloid leukaemia (AML). When this switch occurs, the leukaemia becomes extremely difficult to treat."
The top medic explained that the study had found how the "switch" can happen in blood cells throughout their development in bone marrow, and added: "Importantly, the switch can be a result of additional genetic changes that can be caused by chemotherapy itself. As a consequence, some leukaemias completely ‘re-programme’ themselves and switch identity from one cell type to another."
This "re-progamming" is driven by genetic changes - and Dr Bomken said identifying this had "important implications" for understanding the diseases and how to treat them. He added: "[The results] begin to enable us to identify which patients are at greatest risk of relapse, thereby informing the choice of which treatments to use and when.
"In time specific therapies may become available to help prevent or overcome leukaemic switching and prevent the chameleon from changing its colours." The research was funded by Cancer Research UK, Blood Cancer UK and the Kay Kendall Leukaemia Fund.
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