The cancer stem cell (CSC) concept derives from the fact that cancers are dysregulated tissue clones whose continued propagation is vested in a biologically distinct subset of cells that are typically rare. Rare CSCs have been isolated from a number of human tumors, including hematopoietic, brain, colon, and breast cancer. With the growing evidence that CSCs exist in a wide array of tumors, it is becoming increasingly important to understand the molecular mechanisms that regulate self-renewal and differentiation because corruption of genes involved in these pathways likely participates in tumor growth. Understanding the biology of CSCs will contribute to the identification of molecular targets important for future therapies.
Mitochondria play an important role in various metabolic pathways like oxidative phosphorylation free radical generation and apoptosis. Defects in mitochondrial function are responsible for a number of heterogenous clinical presentations along with development and progression of cancer. Decrease in cellular energy (ATP) production because of impaired oxidative phosphorylation is the most important cause for these underlying disorders. The present review article aims to provide current understanding of mitochondrial genetics and biology and relates the mt-DNA alterations in leukemia patients.
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