作者: Catriona H. M. Jamieson , Emmanuelle Passegué , Irving L. Weissman
DOI: 10.1007/978-3-642-18883-1_12
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摘要: Leukemias are cancers of the hematopoietic system. Like all cancers, several genetic and epigenetic events aid in transition from normal to malignant cell. These usually, if not always, include at least: 1) avoidance programmed cell death intrinsic signals; 2) acquisition poorly regulated or unregulated self-renewal capacity; 3) prevention critical telomere shortening; 4) inhibition differentiation an increasing degree as malignancy progresses; 5) innate adaptive immune responses that cause and/or phagocytosis tumor cells. Many these processes properties stem (HSC) highly regulated, yet hallmark populations most advanced leukemias, e.g., expanded population leukemic blasts, HSC. The phenotypic identity cells (LSC), i.e., only within leukemia capable propagating disease, has been clearly elucidated. In this speculative review, we have two goals: discuss stage which LSC reside, begin understand how recurrent changes, including translocations inversions, resulting increased decreased expression selected genes, play roles above described behaviors