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While the first study, described above, provides a cellular population-level understanding of how leukaemia outcompetes healthy blood cell production, to get a grasp on why stem cells manage to resist ousting from bone marrow required distinct techniques.
There is an unmet clinical need for more effective therapies as the cure rate of AML is only 5-15% in patients older than 60, and the mainstay of treatment has not changed significantly in the last 30 years.
As the drug in question, Deferoxamine (which is commonly found in Irish clinics as a treatment for hemochromatosis), is approved for human use for a different condition, it is known to be safe.
Thus, as it is already in use, it should, in principle, be possible to progress to clinical trials much quicker (~5 years) than one could with a brand new drug (~10-15 years). Mouse bone marrow showing cancerous cells in red interacting with healthy bloods cells in yellow, and blood vessels in cyan. Person identification from DNA is, by now, a standard tool used for parentage determination, to evaluate chimerism after haematopoietic stem cell transplantation, and in criminal forensics.
As determining how the cancer arrests healthy blood production could have significant ramifications for the design and development of treatments for leukaemia, a multi-disciplinary international team undertook two related, experimentally sophisticated, studies to address this question by studying an aggressive AML model in mice that mimics the disease found in humans. Hawkins), in collaboration with myself and my ex-postdoc Tom Weber who is now at WEHI.
The first study was undertaken by members of Cristina Lo Celso's wet lab at Imperial College London (Olufolake Akinduro, Heather Ang, Myriam Haltalli, Nicola Ruvio, Delfim Duarte, N. To accurately determine the proliferation dynamics of both healthy blood cell production and cancer growth, as well as careful measurements of cell numbers, we implemented a method to measure the rate of cell division in vivo.