Acute Myeloid Leukemia is a type of cancer that is incredibly resistant to treatment. My research uses confocal imaging and staining to investigate whether or not mesenchymal stromal cells are transferring their functional mitochondria in vivo to AML cells.
Acute Myeloid Leukemia (AML) is exceptionally resistant to common cancer treatments due to its genetic profile variety. To effectively eradicate AML, treatments that target specific gene markers, or interactions within the bone marrow microenvironment are necessary. One interaction happening in the bone marrow microenvironment that has been observed in vitro is the transfer of functional mitochondria from mesenchymal stromal cells (MSCs) to AML cell lines, which are then transferring their dysfunctional mitochondria back to MSCs. This allows for the AML to proliferate and progress, eventually leading to fatality. The goal of this research is to determine both if the bidirectional mitochondrial transfer between MSCs and AML cells is happening in vivo and if so, whether or not it can be inhibited. To determine this, mice were then injected with AML and then stained so that their mitochondria would express green fluorescent protein (GFP). Cells were then extracted and isolated, and went under immunofluorescence microscopy to investigate whether or not the transfer was happening. To inhibit the transfer, Jasplakinolide was given to mice with AML. In mice models, the bidirectional transfer of mitochondria was seen, confirming the results. Jasplakinolide was seen to prolong the survival of mice and suppress AML development in vivo. These results point towards the potential therapeutic use of Jasplakinolide in treating AML, as well as the development of more treatments targeting and stopping this mitochondrial transfer. This could apply to a variety of cases of AML, and thus be used as a more consistent treatment, saving countless lives.
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