Scientists at The University of Texas at Austin have made a significant discovery in the fight against acute myeloid leukemia (AML), an aggressive cancer that starts in the bone marrow’s blood-forming cells.
This cancer rapidly spreads and is particularly deadly, claiming about 11,000 lives in the United States each year.
The research, led by Xiaolu Cambronne and conducted with collaborators from Dell Medical School and elsewhere, has been published in Cell Metabolism and offers new hope for treating this challenging disease.
AML primarily affects adults over the age of 65, who often have a poor response to aggressive treatments, leaving them with few options.
The research team’s breakthrough lies in identifying a key factor that fuels the cancer’s growth: elevated levels of a cellular transporter known as SLC25A51.
In healthy cells, SLC25A51 is responsible for moving cellular fuel into mitochondria, the cell’s powerhouse, supporting normal cell functions.
However, in AML cells, this transporter is overexpressed, akin to installing a larger fuel line that accelerates cellular replication and cancer growth.
The team found that by reducing the levels of SLC25A51, they could effectively starve the cancer cells without affecting healthy cells.
This intervention slowed down the disease’s progression, led to the death of cancer cells, and extended survival in animal models.
Cambronne highlighted the significance of this finding, pointing out the potential of targeting SLC25A51 as a new therapeutic approach for a disease known for its rapid spread and resistance to treatment.
One of the most promising aspects of this research is the targeted nature of the potential therapy.
Lowering SLC25A51 to a normal or slightly below-normal level did not adversely affect healthy bone marrow cells, suggesting a highly focused approach to killing cancer cells while sparing healthy ones.
Moreover, combining reduced transporter levels with 5-azacytidine, a chemotherapy drug already used in treating AML, showed increased effectiveness in shrinking tumors and enhancing survivability.
This suggests that lowering SLC25A51 could make cancer cells more susceptible to existing treatments, offering a two-pronged approach to battling this leukemia.
The next steps involve developing a drug capable of safely reducing SLC25A51 levels in humans.
Although no such drugs exist currently, the research team’s innovative use of gene editing to manipulate transporter levels in animal models provides a solid foundation for future drug development.
This discovery opens a new avenue for combating acute myeloid leukemia, offering hope to those affected by this aggressive cancer.
By pinpointing a specific target for therapy, researchers are paving the way for more effective, less harmful treatments that could significantly improve outcomes for patients with limited options.
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The research findings can be found in Cell Metabolism.
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