Apoptosis in mieolodisplazic syndrome

"Programmed cell death called apoptosis is a normal physiological phenomenon that characterizes cell turnover. Apoptosis mechanisms, stages, initiation and adjustment module, the genes involved, modulators, apoptotic processes involved in disease pathogenesis and therapeutic strategies addressed according to the need to reduce or enhance apoptosis continues to be the subject of intense research is currently being one of the most studied physiological processes.
Myelodysplastic syndrome (MDS) is a model to study apoptotic processes in different diseases, because diseases grouped under this name presents different intensities of apoptosis and requires a special therapeutic approach.
SMD include: refractory anemia, refractory anemia with ring sideroblasti, sideroblastica anemia with excess blasts, sideroblastica anemia with excess blasts in transformation and chronic myelomonocytic leukemia.
MDS consists in the gradual accumulation of genomic damage in hematopoietic stem cells, reflected in the disruption of apoptotic process. This disorder apoptotic process occurs differently in diseases classified in MDS. In early forms - those with low risk of transformation to acute myeloid leukemia (AML) - genomic events cause excessive apoptosis of haematopoietic precursors with peripheral cytopenia consecutive, while advanced forms - increased risk of transformation to AML - Note hematopoietic precursor cells block apoptosis and accumulation of blast cells. This is why there is currently no standard treatment in MDS, and the results obtained by different groups of rapporteurs are often contradictory.
By modulating apoptosis to determine whether an appropriate therapy in various entities of MDS: blocking apoptosis and promoting excessive clonal differentiation in early forms, while for advanced forms of treatment is that by increasing the apoptotic process to eliminate neoplastic clones.
This volume presents various ultrastructural aspects of a comprehensive study on the apoptotic process in the evolution of myelodysplastic syndrome [68]. The work may provide useful information for a correct approach to therapy targeted to modulate pathways regulating apoptosis. "


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