Over 4,700 Texans will be diagnosed with leukemia in 2024. Despite treatment availability, over 1,600 Texans die from leukemia each year. Although treatments for acute myeloid leukemia (AML) have improved dramatically, first-line options are still aggressive chemotherapy and bone marrow transplantation. These treatments have debilitating side effects that drastically reduce patients’ quality of life. Treatment resistance is also a frequent problem, particularly due to a small population of cancerous cells that are generally resistant to conventional treatments. Treatment improvements, particularly those that reduce side effects and increase effectiveness, are desperately needed. We aim to de...
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Over 4,700 Texans will be diagnosed with leukemia in 2024. Despite treatment availability, over 1,600 Texans die from leukemia each year. Although treatments for acute myeloid leukemia (AML) have improved dramatically, first-line options are still aggressive chemotherapy and bone marrow transplantation. These treatments have debilitating side effects that drastically reduce patients’ quality of life. Treatment resistance is also a frequent problem, particularly due to a small population of cancerous cells that are generally resistant to conventional treatments. Treatment improvements, particularly those that reduce side effects and increase effectiveness, are desperately needed. We aim to develop new, more effective therapies to address these issues. The increased cell division in cancer cells places extreme demands on them, causing severe redox imbalance and damage to mitochondria, which are more than just the powerhouse of the cell. Normally, damaged mitochondria are recycled to produce healthy mitochondria. But cancer disrupts this quality control process. Instead, dysfunctional mitochondria accumulate. We show that interfering with mitochondrial biochemistry can effectively trigger programmed cell death in AML cells. In contrast, healthy blood cells survive this treatment. We propose to elaborate on this discovery in several ways. First, we will optimize novel AML treatments we recently discovered. We will examine how patient-specific mutations impact drug function and optimize combinations of new drugs and current treatments for better, more personalized therapy. Finally, we will test our treatments in a pre-clinical model using mice injected with human AML cells to better predict how they will work in people. Ultimately, we will identify new, improved treatment combinations with fewer side effects. Our research will yield fundamental and innovative advances for cancer treatment and support CPRIT's mission to find new cancer remedies for Texans.
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