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Title: Wortmannin efficiently suppresses the recovery from radiation-induced damage in pimonidazole-unlabeled quiescent tumor cell population.
Authors: Masunaga, Shin-Ichiro  kyouindb  KAKEN_id
Sakurai, Yoshinori  kyouindb  KAKEN_id  orcid (unconfirmed)
Tanaka, Hiroki  kyouindb  KAKEN_id
Suzuki, Minoru  kyouindb  KAKEN_id  orcid (unconfirmed)
Kondo, Natsuko  kyouindb  KAKEN_id
Narabayashi, Masaru  KAKEN_id
Maruhashi, Akira
Ono, Koji
Author's alias: 増永, 慎一郎
Keywords: Quiescent cell
recovery from radiation-induced damage
Issue Date: Mar-2013
Publisher: Oxford University Press
Journal title: Journal of radiation research
Volume: 54
Issue: 2
Start page: 221
End page: 229
Abstract: Labeling of proliferating (P) cells in mice bearing EL4 tumors was achieved by continuous administration of 5-bromo-2'-deoxyuridine (BrdU). Tumors were irradiated with γ-rays at 1 h after pimonidazole administration followed by caffeine or wortmannin treatment. Twenty-four hours later, assessment of the responses of quiescent (Q) and total (= P + Q) cell populations were based on the frequencies of micronucleation and apoptosis using immunofluorescence staining for BrdU. The response of the pimonidazole-unlabeled tumor cell fractions was assessed by means of apoptosis frequency using immunofluorescence staining for pimonidazole. The pimonidazole-unlabeled cell fraction showed significantly enhanced radio-sensitivity compared with the whole cell fraction more remarkably in Q cells than total cells. However, a significantly greater decrease in radio-sensitivity in the pimonidazole-unlabeled than the whole cell fraction, evaluated using an assay performed 24 hours after irradiation, was more clearly observed in Q cells than total cells. In both the pimonidazole-unlabeled and the whole cell fractions, wortmannin efficiently suppressed the reduction in sensitivity due to delayed assay. Wortmannin combined with γ-ray irradiation is useful for suppressing the recovery from radiation-induced damage especially in the pimonidazole-unlabeled cell fraction within the total and Q tumor cell populations.
Rights: © The Author 2012. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited
DOI(Published Version): 10.1093/jrr/rrs094
PubMed ID: 23097299
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