Abstract

Cellular senescence's role in the course and prognosis of Myelodysplastic syndrome CD34+ or bone marrow mononuclear cells from MDS, acute myeloid leukaemia, and healthy controls were examined for p16INK4a expression. Quantitative senescence-associated -galactosidase staining of MDS and AML patients' bone marrow mononuclear cells, the leukaemia cell lines HL60 and SHI-1, and healthy control cells was also examined. When contrasted with solid people, the declaration of the senescence-related hereditary marker p16INK4a was demonstrated to be raised in MDS, while it was viewed as down regulated in AML. Our current investigation revealed that MDS accelerated cellular senescence, which may play a role in the disease's progression and prognosis.