Events such as changes in DNA can cause leukaemia. Healthy cells sense the presence of cancer genes and, as an intrinsic anti-tumour response, immediately undergo suicide or stop cell division to prevent the occurrence of cancer.
Unfortunately, some cells are able to de-activate this intrinsic anti-tumour response, which leads to the development of leukaemia and lymphoma. In addition to this malfunction, leukaemia cells also acquire additional defects that support the cancer’s progression. Little is currently known about the cause of these additional defects or how their development helps activate cancer genes.
With our funding, Dr Feldhahn’s laboratory is analysing this earliest stage of leukaemia development: the moment at which a healthy cell becomes a leukaemia cell. They are currently investigating at what stages of leukaemia key defects occur, and to what extent the activation of cancer genes promotes the development of cancer cells.
They will further compare genomic instability during the onset of leukaemia between different leukaemia progenitor cell types. The team will also perform a genome-wide search for further unrecognised defects that occur after the cancer genes activate, which could be targeted as a treatment for leukaemia.