%0 Journal Article
%T X-Ray Induced Mutation Frequency at the <i>Hypoxanthine Phosphoribosyltransferase</i> Locus in Clinically Relevant Radioresistant Cells
%A Yoshikazu Kuwahara
%A Mehryar Habibi Roudkenar
%A Yusuke Urushihara
%A Yohei Saito
%A Kazuo Tomita
%A Amaneh Mohammadi Roushandeh
%A Tomoaki Sato
%A Akihiro Kurimasa
%A Manabu Fukumoto
%J International Journal of Medical Physics,Clinical Engineering and Radiation Oncology
%P 377-391
%@ 2168-5444
%D 2017
%I Scientific Research Publishing
%R 10.4236/ijmpcero.2017.64034
%X To elucidate the molecular
mechanisms underlying cellular radioresistance, clinically relevant
radioresistant cell lines were established via long-term exposure to X-rays
with stepwise dose escalation. Established cells continue to proliferate
despite exposure to 2 Gy X-rays/day for more than 30 days, a standard protocol
in cancer radiotherapy. DNA repair fidelity in radioresistant and the parental
cells by evaluating the mutation frequency at the <i>hypoxanthine phosphoribosyltransferase</i> (<i>HPRT</i>) locus after exposure to X-rays was determined. Mutation spectrum at the <i>HPRT</i> locus
was examined by multiplex polymerase chain reaction. Rejoining kinetics of
X-ray-induced DNA double strand breaks (dsbs) was evaluated by the detection of
phosphorylated histone H2AX (¦ÃH2AX)
after X-irradiation. The fold increase in the <i>HPRT</i> mutation frequency due to acute radiation
was similar between radioresistant and the parental cell lines. However, fractionated radiation (FR) consisting of 2
Gy X-rays/day increased the mutation frequency at the <i>HPRT</i> locus
in parental but not in
%K Clinically Relevant Radioresistant (CRR) Cell
%K Hypoxanthine Phosphoribosyltransferase (HPRT)
%K Mutation Frequency
%K Phosphorylated Histone H2AX (¦ÃH2AX)
%K X-Rays
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=80133