Scientists have reported progress on the use of immune therapy for recurring acute myeloid leukaemia.
This therapy uses antibodies and inhibitors to eliminate cancer cells that are outside the scope of regular therapies, say Dr Philipp Greif of Munich University Hospital, Germany, and his colleagues in the German Cancer Consortium.
The team explain that, for about a third of acute myeloid leukaemia patients, their cancer is caused by uncontrolled cell division due to a mutation in the growth receptor FLT3.
A new antibody that attacks FLT3 has been developed by the research team and is currently undergoing clinical trials. It works my marking leukaemia cells which remain chemotherapy, so that these cells are recognised and destroyed by the immune system.
Dr Greif says: 'Immune therapy solely with the FLT3 antibody, however, is not always successful. In some cases the FLT3 receptor has mutated so much that it has largely disappeared from the surface of the leukaemia cell and is therefore no longer accessible to the antibody.'
The team set out to treat acute myeloid leukaemia with FLT3 antibody plus special inhibitors called kinase inhibitors, to bring the mutated FLT3 receptor back to the cell surface to make it vulnerable to immune therapy again.
Co-author Katrin Reiter says that this technique eliminates more acute myeloid leukaemia cells.
'The combination of both treatments worked much better in our pre-clinical trials than just one active substance', she says. Full details were published last week in Leukemia.
The team state that both FLT3 inhibitors and FLT3 antibodies are 'quite advanced in clinical trials'.
For example, the FLT3 inhibitor midostaurin has recently been approved for use in combination with standard chemotherapy.
Source: Reiter, K. et al. Tyrosine kinase inhibition increases the cell surface localization of FLT3-ITD and enhances FLT3-directed immunotherapy of acute myeloid leukemia. 12 September 2017 Leukemia doi: 10.1038/leu.2017.257
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