Genomics and Applied Biology 2016, Vol.7, No.2, 1-7
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fixed in acetic acidemethanol (1: 3 vol/vol). Airdried preparations were stained with 4% Giemsa. Under 100°C
magnification, a minimum of 1 000 binucleate cells with well-preserved cytoplasm was scored from each patient
and the MN frequency was determined by the total number of MN in all the binucleate cells divided by the total
number of binucleate cells counted (Aristei et al., 2009).
2 Results
A significant difference emerged in SCE (p=0.008) and MN (p=0.004) between RT-a and control groups. No
statistical difference observed in BNC frequencies in breast cancer patients compared to control group. Compared
to the control group there was a significant increase in SCE frequencies in RT-b (p=0.008) and RT-c (p=0.005).
There was also a significant increase in SCE frequencies in RT-b (p=0.001) and RT-c (p=0.001) values compared
to RT-a measurements. There was not any statistically significant difference in the SCE frequencies between RT-b
and RT-c measurements.
The frequencies of MN were also significantly higher in RT-b (p=0.005) and RT-c (p=0.005) than in control group.
The MN frequencies were significantly increased in the RT-b compared to RT-a (p=0.001). However, there was
not any statistically significant difference in MN frequency between RT-a and RT-c measurements. MN levels
decreased to pre-RT levels three months after completion of treatment. MN decreased significantly at RT-c
compared to RT-b (p=0.001). No significant difference in BNC was observed between control group and any
study group values (Table 1).
Table 1 Frequency of the SCE, MN and BNC
SCE
MN
BNC
Control
274.50±122.37
4.60±2.36
489.80±84.71
Pre-RT
565.86±132.36
a
10.86±6.10
a
504.00±48.947
Completion of RT
742.41±187.37
a,b
22.64±7.32
a,b
525.70±72.58
3 months after RT
732.55±178.05
a,b
13.59±5.63
a,c
571.40±49.44
Note:
a
p<0.05 Compared to Control group;
b
p<0.05 Compared to pre-R;
c
p<0.05 Compared to completion of RT
3 Discussion
The damages caused by various carcinogenic, cytotoxic, anogenic and genotoxic agents that induce damage in
DNA chromosomes were identified by Fenech as biomarkers indicating that a damage has occurred in the DNA
(Fenech, 1999). DNA breakages, chromosome aberrations, micronuclei, aneuploidy and telomere shrinkage are
some of them (Fell et al., 2000). Anogenic and clastogenic agents are by far the best stimulators known in the
formation of MN and apoptosis. Both agents cause genomic instability characterized by direct DNA breakages in
dividing cells, acentric fragments, kinetochore anomalies, translocations and in vivo DNA amplification (Gül,
2005).
In a study they conducted, Barret 1993 and Bishop 1991 pointed out that chromosomal breakages, reorganizations
among chromozomes and induced DNA damages were fundamental mechanisms that led to the occurrence of
various cancer types (Gül, 2005).
In our study, we aimed to determine whether or not RT had a genotoxic effect after RT application for medicinal
purposes in patients with breast cancer, and whether or not there were increases in sister chromatid exchange
(SCE), micronucleus (MN) and binucleus in human peripheral lymphocytes.
In this study, human peripheral lymphocytes taken from patients with breast cancer who had received RT were
treated with Cyt-B at the 72
nd
hour and the results obtained from the study were compared with the results of other
researchers.
Natarajan and Obe reported in 1980 that 72-hour cultures allowed cells to undergo two cell cycles and that the
changes that occurred in the first cycle might undergo cellular repair in the second cycle (Seligmann et al., 2003).