open access

Vol 21, No 2 (2016)
Special Issue Papers
Published online: 2016-03-01
Submitted: 2014-03-09
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Detection of γH2AX foci in mouse normal brain and brain tumor after boron neutron capture therapy

Natsuko Kondo, Hiroyuki Michiue, Yoshinori Sakurai, Hiroki Tanaka, Yosuke Nakagawa, Tsubasa Watanabe, Masaru Narabayashi, Yuko Kinashi, Minoru Suzuki, Shin-ichiro Masunaga, Koji Ono
DOI: 10.1016/j.rpor.2014.10.005
·
Rep Pract Oncol Radiother 2016;21(2):108-112.

open access

Vol 21, No 2 (2016)
Special Issue Papers
Published online: 2016-03-01
Submitted: 2014-03-09

Abstract

Aim

In this study, we investigated γH2AX foci as markers of DSBs in normal brain and brain tumor tissue in mouse after BNCT.

Background

Boron neutron capture therapy (BNCT) is a particle radiation therapy in combination of thermal neutron irradiation and boron compound that specifically accumulates in the tumor. 10B captures neutrons and produces an alpha (4He) particle and a recoiled lithium nucleus (7Li). These particles have the characteristics of extremely high linear energy transfer (LET) radiation and therefore have marked biological effects. High LET radiation causes severe DNA damage, DNA DSBs. As the high LET radiation induces complex DNA double strand breaks (DSBs), large proportions of DSBs are considered to remain unrepaired in comparison with exposure to sparsely ionizing radiation.

Materials and methods

We analyzed the number of γH2AX foci by immunohistochemistry 30[[ce:hsp sp="0.25"/]]min or 24[[ce:hsp sp="0.25"/]]h after neutron irradiation.

Results

In both normal brain and brain tumor, γH2AX foci induced by 10B(n,α)7Li reaction remained 24[[ce:hsp sp="0.25"/]]h after neutron beam irradiation. In contrast, γH2AX foci produced by γ-ray irradiation at contaminated dose in BNCT disappeared 24[[ce:hsp sp="0.25"/]]h after irradiation in these tissues.

Conclusion

DSBs produced by 10B(n,α)7Li reaction are supposed to be too complex to repair for cells in normal brain and brain tumor tissue within 24[[ce:hsp sp="0.25"/]]h. These DSBs would be more difficult to repair than those by γ-ray. Excellent anti-tumor effect of BNCT may result from these unrepaired DSBs induced by 10B(n,α)7Li reaction.

Abstract

Aim

In this study, we investigated γH2AX foci as markers of DSBs in normal brain and brain tumor tissue in mouse after BNCT.

Background

Boron neutron capture therapy (BNCT) is a particle radiation therapy in combination of thermal neutron irradiation and boron compound that specifically accumulates in the tumor. 10B captures neutrons and produces an alpha (4He) particle and a recoiled lithium nucleus (7Li). These particles have the characteristics of extremely high linear energy transfer (LET) radiation and therefore have marked biological effects. High LET radiation causes severe DNA damage, DNA DSBs. As the high LET radiation induces complex DNA double strand breaks (DSBs), large proportions of DSBs are considered to remain unrepaired in comparison with exposure to sparsely ionizing radiation.

Materials and methods

We analyzed the number of γH2AX foci by immunohistochemistry 30[[ce:hsp sp="0.25"/]]min or 24[[ce:hsp sp="0.25"/]]h after neutron irradiation.

Results

In both normal brain and brain tumor, γH2AX foci induced by 10B(n,α)7Li reaction remained 24[[ce:hsp sp="0.25"/]]h after neutron beam irradiation. In contrast, γH2AX foci produced by γ-ray irradiation at contaminated dose in BNCT disappeared 24[[ce:hsp sp="0.25"/]]h after irradiation in these tissues.

Conclusion

DSBs produced by 10B(n,α)7Li reaction are supposed to be too complex to repair for cells in normal brain and brain tumor tissue within 24[[ce:hsp sp="0.25"/]]h. These DSBs would be more difficult to repair than those by γ-ray. Excellent anti-tumor effect of BNCT may result from these unrepaired DSBs induced by 10B(n,α)7Li reaction.

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Keywords

Boron neutron capture therapy; High LET radiation; DSBs; γH2AX foci

About this article
Title

Detection of γH2AX foci in mouse normal brain and brain tumor after boron neutron capture therapy

Journal

Reports of Practical Oncology and Radiotherapy

Issue

Vol 21, No 2 (2016)

Pages

108-112

Published online

2016-03-01

DOI

10.1016/j.rpor.2014.10.005

Bibliographic record

Rep Pract Oncol Radiother 2016;21(2):108-112.

Keywords

Boron neutron capture therapy
High LET radiation
DSBs
γH2AX foci

Authors

Natsuko Kondo
Hiroyuki Michiue
Yoshinori Sakurai
Hiroki Tanaka
Yosuke Nakagawa
Tsubasa Watanabe
Masaru Narabayashi
Yuko Kinashi
Minoru Suzuki
Shin-ichiro Masunaga
Koji Ono

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