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Article ; Online: G1 Premature Chromosome Condensation (PCC) Assay.

Okayasu, Ryuichi / Liu, Cuihua

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1984, Page(s) 31–38

Abstract: Premature chromosome condensation (PCC) is a sensitive and unique way to detect interphase chromosome damage and its recovery in mammalian cells irradiated with ionizing radiation. In this chapter, we describe G1 PCC assay with which one can measure ... ...

Abstract	Premature chromosome condensation (PCC) is a sensitive and unique way to detect interphase chromosome damage and its recovery in mammalian cells irradiated with ionizing radiation. In this chapter, we describe G1 PCC assay with which one can measure immediate chromosome breaks in G1 type chromosomes and their repair/rejoining. In order to induce G1 PCC, one needs to fuse mitotic cells with G1 cells to be tested. There are two methods to fuse cells; one is to use Sendai virus or its equivalent, and another method needs polyethylene glycol (PEG) as a fusing agent. The date obtained with PCC assay can bridge the gap between radiation-induced DNA damage (mainly double strand breaks) and chromosome aberrations observable at metaphase stage.
MeSH term(s)	Animals ; Biological Assay/methods ; CHO Cells ; Chromosomes/genetics ; Chromosomes/radiation effects ; Cricetinae ; Cricetulus ; G1 Phase ; HeLa Cells ; Humans ; Lymphocytes/metabolism ; Lymphocytes/radiation effects ; Polyethylene Glycols/chemistry ; Sendai virus/physiology ; X-Rays
Chemical Substances	Polyethylene Glycols (3WJQ0SDW1A)
Language	English
Publishing date	2019-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9432-8_4
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Article ; Online: Repair of DNA damage induced by accelerated heavy ions--a mini review.

Okayasu, Ryuichi

International journal of cancer

2012 Volume 130, Issue 5, Page(s) 991–1000

Abstract: Increasing use of heavy ions for cancer therapy and concerns from exposure to heavy charged particles in space necessitate the study of the basic biological mechanisms associated with exposure to heavy ions. As the most critical damage induced by ... ...

Abstract	Increasing use of heavy ions for cancer therapy and concerns from exposure to heavy charged particles in space necessitate the study of the basic biological mechanisms associated with exposure to heavy ions. As the most critical damage induced by ionizing radiation is DNA double strand break (DSB), this review focuses on DSBs induced by heavy ions and their repair processes. Compared with X- or gamma-rays, high-linear energy transfer (LET) heavy ion radiation induces more complex DNA damage, categorized into DSBs and non-DSB oxidative clustered DNA lesions (OCDL). This complexity makes the DNA repair process more difficult, partially due to retarded enzymatic activities, leading to increased chromosome aberrations and cell death. In general, the repair process following heavy ion exposure is LET-dependent, but with nonhomologous end joining defective cells, this trend is less emphasized. The variation in cell survival levels throughout the cell cycle is less prominent in cells exposed to high-LET heavy ions when compared with low LET, but this mechanism has not been well understood until recently. Involvement of several DSB repair proteins is suggested to underlie this interesting phenomenon. Recent improvements in radiation-induced foci studies combined with high-LET heavy ion exposure could provide a useful opportunity for more in depth study of DSB repair processes. Accelerated heavy ions have become valuable tools to investigate the molecular mechanisms underlying repair of DNA DSBs, the most crucial form of DNA damage induced by radiation and various chemotherapeutic agents.
MeSH term(s)	Cell Cycle/radiation effects ; Cell Survival/radiation effects ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA Repair ; Heavy Ions/adverse effects ; Humans ; Linear Energy Transfer ; Radiation, Ionizing
Language	English
Publishing date	2012-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.26445
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Article ; Online: Strategies to Enhance Radiosensitivity to Heavy Ion Radiation Therapy.

Lee, Younghyun / Okayasu, Ryuichi

International journal of particle therapy

2018 Volume 5, Issue 1, Page(s) 114–121

Abstract: Heavy ion radiation therapy has been increasingly used due to several advantages over low linear energy transfer (LET) photon therapy, but further improvement of its therapeutic efficacy would be necessary. In this review, we summarize effective ... ...

Abstract	Heavy ion radiation therapy has been increasingly used due to several advantages over low linear energy transfer (LET) photon therapy, but further improvement of its therapeutic efficacy would be necessary. In this review, we summarize effective radiosensitizers for heavy ion radiation therapy and mechanisms associated with the radiosensitization. High LET heavy ions induce more complex and clustered DNA damage than low LET radiation. Inhibition of homologous recombimation repair or nonhomologous end rejoining and dysfunctional cell cycle checkpoint have been reported to sensitize cancer cells to heavy ions. Radiosenstizing agents, including DNA damage response inhibitors, Hsp90 inhibitors, histone acetylase inhibitors, and nanomaterials have been found to enhance cell killing by heavy ion irradiation through disrupted DNA damage response, cell cycle arrest, or other cellular processes. The use of these radiosensitizers could be a promising strategy to enhance the efficacy of heavy ion radiation therapy.
Language	English
Publishing date	2018-09-21
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2331-5180
ISSN (online)	2331-5180
DOI	10.14338/IJPT-18-00014.1
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Article ; Online: Oxygen Enhancement Ratio in Radiation-Induced Initial DSBs by an Optimized Flow Cytometry-based Gamma-H2AX Analysis in A549 Human Cancer Cells.

Sunada, Shigeaki / Hirakawa, Hirokazu / Fujimori, Akira / Uesaka, Mitsuru / Okayasu, Ryuichi

Radiation research

2017 Volume 188, Issue 5, Page(s) 591–594

Abstract: High-linear energy transfer (LET) heavy ions cause higher therapeutic effects than low-LET radiation due to lower dependency on oxygen concentration in tumor cell killing. The lethality after irradiation largely depends on DNA double-strand breaks (DSBs), ...

Abstract	High-linear energy transfer (LET) heavy ions cause higher therapeutic effects than low-LET radiation due to lower dependency on oxygen concentration in tumor cell killing. The lethality after irradiation largely depends on DNA double-strand breaks (DSBs), however the detailed LET dependency for DSB induction under oxic and hypoxic conditions has not been reported. Therefore, we evaluated the oxygen enhancement ratio (OER) of heavy ion-induced DSB induction using a highly-optimized flow cytometry-based method of γ-H2AX detection. Non-small cell lung cancer (NSCLC) A549 cells were exposed to X-ray, carbon-ion and iron-ion radiations under oxic or hypoxic condition. As a DSB marker, the γ-H2AX signal was measured 1 h postirradiation and analyzed by flow cytometry. DSB slope values were calculated as DSB induction per Gy. Our method was able to detect high-LET radiation-induced DSBs even from clustered DNA damage sites. We also showed a decrease in OER value in an LET-dependent manner regardless of radiation type. In summary, we demonstrated a simple, quick and highly-optimized flow cytometry-based method of DSB analysis that detects DSBs induced by heavy-ion radiation for hypoxic and nonhypoxic cancer cells. Our study may provide a useful biological basis for heavy-ion radiotherapy.
MeSH term(s)	DNA Breaks, Double-Stranded/radiation effects ; Dose-Response Relationship, Radiation ; Flow Cytometry ; Histones/metabolism ; Humans ; Linear Energy Transfer/radiation effects ; Oxygen/metabolism
Chemical Substances	H2AX protein, human ; Histones ; Oxygen (S88TT14065)
Language	English
Publishing date	2017-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RR14824.1
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Article ; Online: Heterochromatin domain number correlates with X-ray and carbon-ion radiation resistance in cancer cells.

Sato, Katsutoshi / Imai, Takashi / Okayasu, Ryuichi / Shimokawa, Takashi

Radiation research

2014 Volume 182, Issue 4, Page(s) 408–419

Abstract: Although it is known that cancer cells can develop radiation resistance after repeated exposures to X rays, the underlying mechanisms and characteristics of this radiation-induced resistance of cancer cells are not well understood. Additionally, it is ... ...

Abstract	Although it is known that cancer cells can develop radiation resistance after repeated exposures to X rays, the underlying mechanisms and characteristics of this radiation-induced resistance of cancer cells are not well understood. Additionally, it is not known whether cells that develop X-ray resistance also would develop resistance to other types of radiation such as heavy-ions including carbon ions (C-ion). In this study, we established X-ray resistant cancer cell lines by delivering repeated exposures to X rays, and then assessed whether the cells were resistant to carbon ions. The mouse squamous cell carcinoma cell line, NR-S1, was X irradiated six times with 10 Gy, and the X-ray resistant cancer cells named X60 and ten subclones were established. Significant X-ray resistance was induced in four of the subclones (X60, X60-H2, X60-A3 and X60-B12). The X60 cells and all of the subclones were resistant to carbon ions. The correlation analysis between radioresistance and morphological characteristics of these cells showed that X-ray (R=0.74) and C-ion (R=0.79) resistance correlated strongly with the number of heterochromatin domains. Moreover, the numbers of γ-H2AX foci remaining in irradiated X60 cells and radioresistant subclones X60-A3 and X60-H2 were lower than in the NR-S1 cells after X-ray or C-ion irradiation, indicating that X60 cells and the radioresistant subclones rapidly repaired the DNA double-strand breaks compared with NR-S1 cells. Our findings suggest that the underlying causal mechanisms of X-ray and C-ion radiation resistance may overlap, and that an increase in heterochromatin domain number may be an indicator of X-ray and C-ion resistance.
MeSH term(s)	Animals ; Carbon/therapeutic use ; Cell Line, Tumor ; Heterochromatin/chemistry ; Heterochromatin/metabolism ; Histones/metabolism ; Mice ; Neoplasms/genetics ; Neoplasms/pathology ; Protein Structure, Tertiary ; Radiation Tolerance ; X-Rays
Chemical Substances	H2AX protein, mouse ; Heterochromatin ; Histones ; Carbon (7440-44-0)
Language	English
Publishing date	2014-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RR13492.1
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Article ; Online: Lethal DNA Lesions Caused by Direct and Indirect Actions of X rays are Repaired via Different DSB Repair Pathways under Aerobic and Anoxic Conditions.

Hirayama, Ryoichi / Ito, Atsushi / Uzawa, Akiko / Matsumoto, Yoshitaka / Noguchi, Miho / Li, Huizi / Suzuki, Motofumi / Ando, Koichi / Okayasu, Ryuichi / Hasegawa, Sumitaka / Furusawa, Yoshiya

Radiation research

2021 Volume 195, Issue 5, Page(s) 441–451

Abstract: We examined lethal damages of X rays induced by direct and indirect actions, in terms of double-strand break (DSB) repair susceptibility using two kinds of repair-deficient Chinese hamster ovary (CHO) cell lines. These CHO mutants (51D1 and xrs6) are ... ...

Abstract	We examined lethal damages of X rays induced by direct and indirect actions, in terms of double-strand break (DSB) repair susceptibility using two kinds of repair-deficient Chinese hamster ovary (CHO) cell lines. These CHO mutants (51D1 and xrs6) are genetically deficient in one of the two important DNA repair pathways after genotoxic injury [homologous recombination (HR) and non-homologous end binding (NHEJ) pathways, respectively]. The contribution of indirect action on cell killing can be estimated by applying the maximum level of dimethylsulfoxide (DMSO) to get rid of OH radicals. To control the proportion of direct and indirect actions in lethal damage, we irradiated CHO mutant cells under aerobic and anoxic conditions. The contributions of indirect action on HR-defective 51D1 cells were 76% and 57% under aerobic and anoxic conditions, respectively. Interestingly, these percentages were similar to those of the wild-type cells even if the radiosensitivity was different. However, the contributions of indirect action to cell killing on NHEJ-defective xrs6 cells were 52% and 33% under aerobic and anoxic conditions, respectively. Cell killing by indirect action was significantly affected by the oxygen concentration and the DSB repair pathways but was not correlated with radiosensitivity. These results suggest that the lethal damage induced by direct action is mostly repaired by NHEJ repair pathway since killing of NHEJ-defective cells has significantly higher contribution by the direct action. In other words, the HR repair pathway may not effectively repair the DSB by direct action in place of the NHEJ repair pathway. We conclude that the type of DSB produced by direct action is different from that of DSB induced by indirect action.
MeSH term(s)	Aerobiosis/genetics ; Aerobiosis/radiation effects ; Animals ; CHO Cells ; Cell Death/genetics ; Cell Death/radiation effects ; Cricetulus ; DNA Damage ; DNA End-Joining Repair/radiation effects ; Homologous Recombination/radiation effects ; Oxygen/metabolism ; X-Rays/adverse effects
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2021-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80322-4
ISSN	1938-5404 ; 0033-7587
ISSN (online)	1938-5404
ISSN	0033-7587
DOI	10.1667/RADE-20-00235.1
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Article: Arsenic accumulation, elimination, and interaction with copper, zinc and manganese in liver and kidney of rats.

Cui, Xing / Okayasu, Ryuichi

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2008 Volume 46, Issue 12, Page(s) 3646–3650

Abstract: The arsenic accumulation, distribution and influences on metallothionein-1 (MT-1) expression and other trace elements in various organs were examined in rats orally exposed to sodium arsenate (iAs(V)). Rats received a dose of 0, 1, 10 and 100ppm of iAs(V) ...

Abstract	The arsenic accumulation, distribution and influences on metallothionein-1 (MT-1) expression and other trace elements in various organs were examined in rats orally exposed to sodium arsenate (iAs(V)). Rats received a dose of 0, 1, 10 and 100ppm of iAs(V) in drinking water daily for 4- and 16-weeks. Arsenic seems to be distributed in all of the tissues, and was accumulated relatively higher in the spleen, lung and kidney compared to the liver, and much lower in skin and cerebrum. High dose of iAs(V)-exposure significantly increased the concentration of copper in the kidney, but did not influence other trace elements such as zinc and manganese in the liver. The mRNA expression of MT-1 was dose-dependently increased by iAs(V)-exposure in the liver whereas it was decreased in the kidney. These data indicate that arsenic is widely distributed and significantly accumulated in various organs and influences on other trace elements, and also modulates MT-1 expression in the liver and kidney.
MeSH term(s)	Animals ; Arsenic/pharmacokinetics ; Copper/pharmacology ; Feces/chemistry ; Kidney/drug effects ; Kidney/metabolism ; Liver/drug effects ; Liver/metabolism ; Male ; Manganese/pharmacology ; Metallothionein/biosynthesis ; Poisons/pharmacokinetics ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Distribution ; Zinc/pharmacology
Chemical Substances	Poisons ; RNA, Messenger ; Manganese (42Z2K6ZL8P) ; Copper (789U1901C5) ; Metallothionein (9038-94-2) ; Zinc (J41CSQ7QDS) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2008-12
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2008.09.040
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Zs.A 529: Show issues

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Article ; Online: Novel characteristics of CtIP at damage-induced foci following the initiation of DNA end resection.

Fujisawa, Hiroshi / Fujimori, Akira / Okayasu, Ryuichi / Uesaka, Mitsuru / Yajima, Hirohiko

Mutation research

2014 Volume 771, Page(s) 36–44

Abstract: Homologous recombination (HR) is a major repair pathway for DNA double strand breaks (DSBs), and end resection, which generates a 3'-single strand DNA tail at the DSB, is an early step in the process. Resection is initiated by the Mre11 nuclease together ...

Abstract	Homologous recombination (HR) is a major repair pathway for DNA double strand breaks (DSBs), and end resection, which generates a 3'-single strand DNA tail at the DSB, is an early step in the process. Resection is initiated by the Mre11 nuclease together with CtIP. Here, we describe novel characteristics of CtIP at DSBs. At early times following exposure of human cells to ionizing radiation, CtIP localized to the DSB, became hyperphosphorylated and formed foci in an ATM-dependent manner. At later times, when the initiation of resection had occurred, CtIP foci persist but CtIP is maintained in a hypophosphorylated state, which is dependent on ATM and ATR. Exposure to cycloheximide revealed that CtIP turns over at DSB sites downstream of resection. Our findings provide strong evidence that CtIP is continuously recruited to DSBs downstream of both the initiation and extension step of resection, strongly suggesting that CtIP has functions in addition to promoting the initiation of resection during HR.
MeSH term(s)	Adenosine Triphosphate/genetics ; Adenosine Triphosphate/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cycloheximide/pharmacology ; DNA Breaks, Double-Stranded/drug effects ; DNA Breaks, Double-Stranded/radiation effects ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; HeLa Cells ; Humans ; MRE11 Homologue Protein ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphorylation/drug effects ; Phosphorylation/genetics ; Phosphorylation/radiation effects ; Protein Synthesis Inhibitors/pharmacology ; Protein Transport/drug effects ; Protein Transport/genetics ; Protein Transport/radiation effects ; Recombinational DNA Repair/drug effects ; Recombinational DNA Repair/genetics ; Recombinational DNA Repair/radiation effects ; X-Rays/adverse effects
Chemical Substances	Carrier Proteins ; DNA-Binding Proteins ; MRE11 protein, human ; Nuclear Proteins ; Protein Synthesis Inhibitors ; Adenosine Triphosphate (8L70Q75FXE) ; Cycloheximide (98600C0908) ; MRE11 Homologue Protein (EC 3.1.-) ; RBBP8 protein, human (EC 3.1.-)
Language	English
Publishing date	2014-12-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206607-5
ISSN	1873-135X ; 1383-5718 ; 0027-5107 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
ISSN (online)	1873-135X
ISSN	1383-5718 ; 0027-5107 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
DOI	10.1016/j.mrfmmm.2014.12.001
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Article ; Online: TAS-116, a Novel Hsp90 Inhibitor, Selectively Enhances Radiosensitivity of Human Cancer Cells to X-rays and Carbon Ion Radiation.

Lee, Younghyun / Sunada, Shigeaki / Hirakawa, Hirokazu / Fujimori, Akira / Nickoloff, Jac A / Okayasu, Ryuichi

Molecular cancer therapeutics

2016 Volume 16, Issue 1, Page(s) 16–24

Abstract: Hsp90 inhibitors have been investigated as cancer therapeutics in monotherapy and to augment radiotherapy; however, serious adverse effects of early-generation Hsp90 inhibitors limited their development. TAS-116 is a novel Hsp90 inhibitor with lower ... ...

Abstract	Hsp90 inhibitors have been investigated as cancer therapeutics in monotherapy and to augment radiotherapy; however, serious adverse effects of early-generation Hsp90 inhibitors limited their development. TAS-116 is a novel Hsp90 inhibitor with lower adverse effects than other Hsp90 inhibitors, and here, we investigated the radiosensitizing effects of TAS-116 in low linear energy transfer (LET) X-ray and high LET carbon ion-irradiated human cancer cells and mouse tumor xenografts. TAS-116 decreased cell survival of both X-ray and carbon ion-irradiated human cancer cell lines (HeLa and H1299 cells), and similar to other Hsp90 inhibitors, it did not affect radiosensitivity of noncancerous human fibroblasts. TAS-116 increased the number of radiation-induced γ-H2AX foci and delayed the repair of DNA double-strand breaks (DSB). TAS-116 reduced the expression of proteins that mediate repair of DSBs by homologous recombination (RAD51) and nonhomologous end joining (Ku, DNA-PKcs), and suppressed formation of RAD51 foci and phosphorylation/activation of DNA-PKcs. TAS-116 also decreased expression of the cdc25 cell-cycle progression marker, markedly increasing G
MeSH term(s)	Animals ; Benzamides/pharmacology ; Carbon Radioisotopes ; Cell Line, Tumor ; DNA ; DNA End-Joining Repair ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Gene Expression Regulation, Neoplastic ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; HeLa Cells ; Histones/metabolism ; Humans ; Ku Autoantigen/metabolism ; Mice ; Protein Kinase C/metabolism ; Pyrazoles/pharmacology ; Rad51 Recombinase/genetics ; Rad51 Recombinase/metabolism ; Radiation Tolerance/drug effects ; Radiation, Ionizing ; Radiation-Sensitizing Agents/pharmacology ; X-Rays ; Xenograft Model Antitumor Assays
Chemical Substances	Benzamides ; Carbon Radioisotopes ; HSP90 Heat-Shock Proteins ; Histones ; Pyrazoles ; Radiation-Sensitizing Agents ; TAS-116 ; DNA (9007-49-2) ; Protein Kinase C (EC 2.7.11.13) ; Rad51 Recombinase (EC 2.7.7.-) ; Ku Autoantigen (EC 4.2.99.-)
Language	English
Publishing date	2016-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-16-0573
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Article ; Online: Radiosensitization by PARP inhibition to proton beam irradiation in cancer cells.

Hirai, Takahisa / Saito, Soichiro / Fujimori, Hiroaki / Matsushita, Keiichiro / Nishio, Teiji / Okayasu, Ryuichi / Masutani, Mitsuko

Biochemical and biophysical research communications

2016 Volume 478, Issue 1, Page(s) 234–240

Abstract: The poly(ADP-ribose) polymerase (PARP)-1 regulates DNA damage responses and promotes base excision repair. PARP inhibitors have been shown to enhance the cytotoxicity of ionizing radiation in various cancer cells and animal models. We have demonstrated ... ...

Abstract	The poly(ADP-ribose) polymerase (PARP)-1 regulates DNA damage responses and promotes base excision repair. PARP inhibitors have been shown to enhance the cytotoxicity of ionizing radiation in various cancer cells and animal models. We have demonstrated that the PARP inhibitor (PARPi) AZD2281 is also an effective radiosensitizer for carbon-ion radiation; thus, we speculated that the PARPi could be applied to a wide therapeutic range of linear energy transfer (LET) radiation as a radiosensitizer. Institutes for biological experiments using proton beam are limited worldwide. This study was performed as a cooperative research at heavy ion medical accelerator in Chiba (HIMAC) in National Institute of Radiological Sciences. HIMAC can generate various ion beams; this enabled us to compare the radiosensitization effect of the PARPi on cells subjected to proton and carbon-ion beams from the same beam line. After physical optimization of proton beam irradiation, the radiosensitization effect of the PARPi was assessed in the human lung cancer cell line, A549, and the pancreatic cancer cell line, MIA PaCa-2. The effect of the PARPi, AZD2281, on radiosensitization to Bragg peak was more significant than that to entrance region. The PARPi increased the number of phosphorylated H2AX (γ-H2AX) foci and enhanced G2/M arrest after proton beam irradiation. This result supports our hypothesis that a PARPi could be applied to a wide therapeutic range of LET radiation by blocking the DNA repair response.
MeSH term(s)	A549 Cells ; Apoptosis/drug effects ; Apoptosis/radiation effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/radiation effects ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Humans ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Neoplasms, Experimental/radiotherapy ; Phthalazines/administration & dosage ; Piperazines/administration & dosage ; Poly(ADP-ribose) Polymerase Inhibitors/administration & dosage ; Proton Therapy/methods ; Radiation Tolerance/drug effects ; Radiation-Sensitizing Agents/administration & dosage ; Radiotherapy Dosage ; Treatment Outcome
Chemical Substances	Phthalazines ; Piperazines ; Poly(ADP-ribose) Polymerase Inhibitors ; Radiation-Sensitizing Agents ; olaparib (WOH1JD9AR8)
Language	English
Publishing date	2016--09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2016.07.062
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