“A study on the expression pattern of key apoptotic regulators in Acute Myeloid Leukemia patients from the North-East Indian regions”
Journal Title: IOSR Journal of Pharmacy and Biological Sciences (IOSR-JPBS) - Year 2017, Vol 12, Issue 5
Abstract
Cancer is the result of succession of genetic changes during which a normal cell is transformed into a malignant one. Evasion of cell death is one of the essential changes in a cell that causes this malignant transformation. Acute Myeloid Leukemia is a cancer of the hematopoietic cells which occurs due to mutational inactivation of some important genes or due to genome rearrangement. It is a malignant disease characterized by an accumulation of immature myeloid blast cells in the bone marrow and most often in the peripheral blood. Apoptosis in cancer occurs due to disrupted balance of pro-apoptotic and anti-apoptotic proteins, reduced caspase function and impaired death receptor signaling. In this study, we studied the role of apoptosis and activation of apoptosis signaling molecules in of AML. 20 blood samples were collected from which RNA was isolated and then cDNA was synthesized. Three apoptotic genes i.e. Bcl-2, Apaf-1 and P53 were used to analyze the samples in AML along with a reference gene (β-actin) for comparative purpose. The results showed a low expression pattern for all the three genes in the studied samples. Bcl-2 is an anti-apoptotic factor which helps in blocking apoptosis action, but in our samples it clearly shows down regulation. Apaf-1 is down regulated and it may disrupt the formation of apoptosomes. P53 helps in blocking the other apoptotic regulators like Bcl-2 but again, in our samples it shows low expression while Β-actin has been used as the normal reference gene for comparitive studies since it is a house-keeping gene. Usually, for apoptosis to occur we need high expression of the genes Apaf-1 and P53 but the unavailability of these genes could project towards error in apoptosis.
Authors and Affiliations
*Nistha Kashyap, Dr. Kandarpa Kumar Saikia2
Keywords
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- EP ID EP390941
- DOI 10.9790/3008-1205023239
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