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Molecule
of H2AX is a member of H2A histone which plays a role in chromatin formation.
H2AX will be phosphorylated at the serine-139 as a response of DNA damage.γH2AX
itself will induce apoptosis through 2 mechanisms, i.e., induce p53 suppressor
gene and activation of natural killer (NK) cells. Activated NK cells will
release perforin and granzyme B then lead to apoptosis of cell target.
Meanwhile, the result of apoptosis is breakdown of DNA repair enzyme, including
poly ADP-ribose polymerase (PARP). The aim of this study is to investigate the
role of γH2AX and activated NK cells to PARP as a product of apoptosis in adult
acute leukemia.
This study
was conducted on 21 adult patients with diagnosis of acute leukemia in Dr.
Soetomo General Academic Hospital in Surabaya, Indonesia. Bone marrow aspirate
and peripheral blood were collected at diagnosis. Peripheral bloods from 10
healthy donors were used as a control group. Phosphorylated H2AX and 89 kDa
fragment of PARP were tested from peripheral blood mononuclear cells (PBMC)
specimens. Activated NK cells were determined using antibody of CD56
FITC/CD69PE/CD45PerCP from whole blood-EDTA specimens. All of these tests were
performed by flow cytometry. Statistical analysis was used independent sample
t-test and linear regression analysis
The level
of γH2AX, activated NK cells and PARP of leukemic patients revealed significant
higher than control with p=0.013, p=0.000 and p=0.000, respectively. The γH2AX
and activated NK cell did not have an influence on PARP with p=0.591 and
p=0.181, respectively.
In
conclusion, γH2AX, activated NK cells and PARP increase in leukemic patients,
however H2AX and activated NK cells independently do not cause increasing of
PARP as an apoptosis product.
Keywords: γH2AX, Activated NK, PARP, Leukemia
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