ライフサイエンスコーパス: radiosensitivity

1 d Ku-DNA end-binding activity, and increases radiosensitivity).

2 l cell apoptosis boosts intestinal stem cell radiosensitivity.

3 and break repair, which both led to improved radiosensitivity.

4 in determining the cell-cycle phase-specific radiosensitivity.

5 fficiency as in other species, regardless of radiosensitivity.

6 ated a regulatory role for eIF4E in cellular radiosensitivity.

7 al therapeutic target to increase tumor cell radiosensitivity.

8 IF4E with ribavirin also enhanced tumor cell radiosensitivity.

9 g a previously unknown class of mediators of radiosensitivity.

10 deficiency syndrome associated with cellular radiosensitivity.

11 fect of miR-421 on cell cycle checkpoint and radiosensitivity.

12 usible factor leading to changes in cellular radiosensitivity.

13 comitantly with RT synergistically increases radiosensitivity.

14 ity, and colony survival assays for cellular radiosensitivity.

15 s in the regulation of tumor and normal cell radiosensitivity.

16 ating a ROS-dependent mechanism for curcumin radiosensitivity.

17 receptor CD47 could correspondingly increase radiosensitivity.

18 ential therapeutic target for adjusting cell radiosensitivity.

19 repair, thus resulting in increased cellular radiosensitivity.

20 iated with defective V(D)J recombination and radiosensitivity.

21 mechanisms underlying mutant EGFR-associated radiosensitivity.

22 d by exposure to ionizing radiation enhanced radiosensitivity.

23 obiota-associated enhancement of endothelial radiosensitivity.

24 ich reduced ErbB1 activity, had no effect on radiosensitivity.

25 volved in microbial regulation of intestinal radiosensitivity.

26 red for the ATM protein to regulate cellular radiosensitivity.

27 sulted in a significant enhancement in AsPC1 radiosensitivity.

28 e degradation of ErbB2, yet had no effect on radiosensitivity.

29 iation exposure, and promotes an increase in radiosensitivity.

30 and GADD45beta expression and increased cell radiosensitivity.

31 cogenic K-ras signaling to pancreatic cancer radiosensitivity.

32 ristic facial features, immunodeficiency and radiosensitivity.

33 ocked IGF signaling, and enhanced tumor cell radiosensitivity.

34 Gleevec resulted in an enhancement in their radiosensitivity.

35 been implicated as a determinant of cellular radiosensitivity.

36 AS could thus be targets for manipulation of radiosensitivity.

37 s the oxygen range where tumors have limited radiosensitivity.

38 chanism underlying flavopiridol-induced cell radiosensitivity.

39 evels of ATM expression, and restores normal radiosensitivity.

40 nd breaks, and telomere dysfunction provokes radiosensitivity.

41 d by other assays that can predict for their radiosensitivity.

42 sfunction, growth abnormalities, and extreme radiosensitivity.

43 tein potentiates p53-dependent apoptosis and radiosensitivity.

44 he IGF-IR pathway prevents correction of the radiosensitivity.

45 and HT1080, respectively) leads to increased radiosensitivity.

46 53BP1 pathway inactivation further increases radiosensitivity.

47 ce defects but not lymphocyte development or radiosensitivity.

48 eased polyploidy after IR, but did not alter radiosensitivity.

49 cells without BRCA1 showed decreased TCR and radiosensitivity.

50 a limited number of major genes determining radiosensitivity.

51 ific, indicating varying levels of intrinsic radiosensitivity.

52 tering to group patients based on esophageal radiosensitivity.

53 signaling activity, which is associated with radiosensitivity.

54 ate the mechanisms by which p16 may regulate radiosensitivity.

55 g its role as a key contributor to stem cell radiosensitivity.

56 on for future calculations of individualised radiosensitivity.

57 kout resulted in slower growth and increased radiosensitivity.

58 grow normally, and are fertile but show mild radiosensitivity.

59 -deficient tumors and consequently increased radiosensitivity.

60 effect of Atm loss on tumor endothelial cell radiosensitivity.

61 e autophagy-deficient mice display increased radiosensitivity.

62 gies to overcome radioresistance and improve radiosensitivity.

63 tion to normal tissues while enhancing tumor radiosensitivity.

64 croenvironment was sufficient to limit tumor radiosensitivity.

65 pairing checkpoint activation and increasing radiosensitivity.

66 gic approaches abolished intestinal T84 cell radiosensitivity.

67 n enhanced cetuximab efficacy and tumor cell radiosensitivity.

68 ect of parthenolide on tumor and normal cell radiosensitivity.

69 tumor control rate was 87% versus 54% using radiosensitivity (2-Gy surviving fraction S(2) < 0.70 vs

70 n in Atm(-/-) mice increased crypt stem cell radiosensitivity 3.7-fold without sensitizing the microv

71 This was greater than the radiosensitivity achieved using the phosphatidylinositol

72 The distribution of radiosensitivities among the family members showed a tri

73 Rif1 inhibition resulted in radiosensitivity and a defect in the intra-S-phase check

74 nvestigated gammaH2AX as a reporter of tumor radiosensitivity and a potential target to enhance the e

75 response in SCCs demonstrates enhancement in radiosensitivity and amplification of radiation-induced

76 e making them potential targets for altering radiosensitivity and apoptosis in tumors.

77 clusion, inhibition of XIAP rescues cellular radiosensitivity and both DIABLO and XIAP might be poten

78 he ATM gene that includes among its stigmata radiosensitivity and cancer susceptibility.

79 rad9-S4 and rad9-S5, reduced HU sensitivity, radiosensitivity and caused aberrant checkpoint function

80 g a checkpoint function and suggest that the radiosensitivity and chromosomal instability of Artemis-

81 hese include genetics, immune dysregulation, radiosensitivity and chronic infections such as Helicoba

82 risingly, both the Pin2/TRF1 mutants reduced radiosensitivity and complemented the G(2)/M checkpoint

83 vidualisation of radiotherapy dose to tumour radiosensitivity and could provide a framework to design

84 vidualisation of radiotherapy dose to tumour radiosensitivity and could provide a framework to design

85 in a NONO-deficient background led to severe radiosensitivity and delayed resolution of DSB repair fo

86 hortening, the G(2)/M checkpoint defect, and radiosensitivity and demonstrate a critical role for Pin

87 landscapes affect cellular heterogeneity in radiosensitivity and demonstrate the nonubiquitous natur

88 dicates that loss of PARP1 increases in vivo radiosensitivity and genomic instability in DNA-PKcs-def

89 by ionizing radiation, Dmp53 mutants exhibit radiosensitivity and genomic instability.

90 ts uncovered DNA variants that contribute to radiosensitivity and identified genes that can be target

91 sia-mutated (ATM) DSB response protein cause radiosensitivity and immunodeficiency in humans.

92 gulation of XLF in human cell lines leads to radiosensitivity and impaired NHEJ.

93 ATM activation and consequently resulted in radiosensitivity and impaired the G2/M checkpoint.

94 with C38 monoclonal antibody (Mab) enhanced radiosensitivity and increased the efficacy of radiation

95 Here we find that miR-205 promotes radiosensitivity and is downregulated in radioresistant

96 wild-type XLF into such cells corrects their radiosensitivity and NHEJ defects.

97 antiapoptotic function of Prx1 in modulating radiosensitivity and provides the impetus to monitor the

98 drome associated with cancer predisposition, radiosensitivity and radioresistant DNA synthesis-S phas

99 fore provide new insights into mechanisms of radiosensitivity and responses to radiotherapy as well a

100 m from normal control individuals: increased radiosensitivity and risk of cancer.

101 ese results indicate that MS-275 can enhance radiosensitivity and suggest that this effect may involv

102 Because of its radiosensitivity and tendency to concentrate (2)(1)(0)Po

103 rols showed evidence of enhanced chromosomal radiosensitivity and that this sensitivity was not age r

104 derstanding of the individual differences in radiosensitivity and the molecular basis of radiation re

105 rains that show large differences in in vivo radiosensitivity and tumor susceptibility.

106 nt arrest responses, increased apoptosis and radiosensitivity, and augmented genetic instability (i.e

107 e frequency, telomere signal level, cellular radiosensitivity, and DNA-PKcs protein expression level.

108 e phase arrest in PDAC cells, enhanced their radiosensitivity, and more potently abrogated PDAC growt

109 lts indicate that the effects of ATR on cell radiosensitivity are independent of NHEJ but are linked

110 vivo system developed to study IR-dependent radiosensitivity as a measure of clonogenic cell death.

111 These findings uncover radiosensitivity as a novel, therapeutically viable vuln

112 ng Atm expression also demonstrated enhanced radiosensitivity as determined via a clonogenic survival

113 relationship between DSB repair fidelity and radiosensitivity as well as the mechanisms associated wi

114 n of hsa-miR-125b in these cells resulted in radiosensitivity, as seen by reduced clonogenic survival

115 in a dose-dependent manner and enhanced cell radiosensitivity assessed by the clonogenic cell surviva

116 knockdown also reverses the cytotoxicity and radiosensitivity associated with PARP inhibition, sugges

117 in mammalian cells, and defects in it cause radiosensitivity at the cellular and whole-organism leve

118 ry of progenitor cells and, thus, red marrow radiosensitivity (because during the recovery period the

119 the size arrest via PTEN deletion conferred radiosensitivity both in vitro and in vivo.

120 ge response pathways are key determinants of radiosensitivity but the extent to which these overlappi

121 ombined immunodeficiency (SCID) and cellular radiosensitivity, but hypomorphic mutations can cause mi

122 arer gene with a similar, additive effect on radiosensitivity, but the data are clearly consistent wi

123 ol dose of 300 nM, given for 1 day, enhanced radiosensitivity by a factor of 2.1.

124 inhibits NPC tumor growth and increases NPC radiosensitivity by directly regulating Jab1/CSN5 and th

125 Rescue of SCID fibroblast radiosensitivity by human Artemis protein demonstrated t

126 Esophageal radiosensitivity can be quantified using esophageal expa

127 n disease displaying chromosome instability, radiosensitivity, cancer predisposition, immunodeficienc

128 ciency characterized among other symptoms by radiosensitivity, cancer, sterility, immunodeficiency an

129 To test for a role of CREB in cellular radiosensitivity, CHO cells were transfected with plasmi

130 cribed as RS-SCID, in which patients display radiosensitivity combined with severe combined immunodef

131 fibroblasts, HCT-116 cells display moderate radiosensitivity compared to the other MMR-deficient lin

132 maH2AX radiation-induced foci; and increased radiosensitivity compared with TGFbeta competent cells.

133 hree HNPCC lines investigated show levels of radiosensitivity consistent with that displayed by norma

134 ells derived from this patient show dramatic radiosensitivity, decreased double-strand break rejoinin

135 res of human tumor cells of varying in vitro radiosensitivity, derived from tumors of varying radiocu

136 rus vector, heat shocked 24 h later, and the radiosensitivity determined 12 h after heat shock.

137 Previous studies have demonstrated that radiosensitivity, determined as a reduction in colony fo

138 Cells lacking hTERT exhibit increased radiosensitivity, diminished capacity for DNA repair, an

139 , a recently discovered immunodeficiency and radiosensitivity disorder.

140 Mutations in Mre11 and nibrin result in the radiosensitivity disorders ataxia-telangiectasia-like di

141 nal stem cells and microvascular compartment radiosensitivity, EndoMT and rectal damage severity.

142 IP6K2 overexpression caused increased radiosensitivity, evidenced by decreased colony forming

143 d, in addition to cellular kinetics and cell radiosensitivities for the 2 studied lineages.

144 st postirradiation mitosis, and an increased radiosensitivity for cell killing.

145 have been associated with somewhat increased radiosensitivity for some end points, but none directly

146 The radiosensitivity for the prostate-specific antigen-posit

147 Loss of H2AX causes radiosensitivity, genome instability, and DNA double-str

148 neurodegenerative disorder characterized by radiosensitivity, genomic instability, and predispositio

149 The mechanism behind this increased radiosensitivity has been proposed to be secondary to de

150 Recently, strategies to enhance tumor radiosensitivity have begun to focus on targeting the mo

151 its biological function in pancreatic cancer radiosensitivity have not been previously described.

152 rmore, reduction of mdm2 in vivo resulted in radiosensitivity, highlighting the importance of mdm2 as

153 tified 16 mRNA gene expression signatures of radiosensitivity, HPV status, tumour hypoxia, and micros

154 adaptive responses as well as low-dose hyper-radiosensitivity (HRS) and increased radioresistance (IR

155 Among HPV-positive cases, signatures for radiosensitivity, hypoxia, and microsatellite instabilit

156 isease characterized by genetic instability, radiosensitivity, immunodeficiency and cancer predisposi

157 ibit clinical symptoms that include cellular radiosensitivity, immunodeficiency, and cancer predispos

158 drome, which we have termed RIDDLE syndrome (radiosensitivity, immunodeficiency, dysmorphic features

159 NG finger 168 (RNF168), mutated in the human radiosensitivity, immunodeficiency, dysmorphic features,

160 sophageal expansion, as a method to quantify radiosensitivity in 134 non-small-cell lung cancer patie

161 They also showed increased radiosensitivity in a clonogenic survival assay.

162 ll viability and induced apoptosis, enhanced radiosensitivity in BON1 and QGP1 cells, induced SSTR2 e

163 ssential for radiation-induced autophagy and radiosensitivity in caspase-3/7 double-knockout cells.

164 t this increases its potential for measuring radiosensitivity in cells and may therefore have value i

165 interpretations of energy dependent cellular radiosensitivity in culture vessels, and radiotherapeuti

166 IGF-1R inhibition enhanced radiosensitivity in DU145, PC3 and 22Rv1 prostate cancer

167 st to ATM, does not affect cell survival and radiosensitivity in hypoxia.

168 Some preclinical studies show reduced radiosensitivity in irradiated malignant mammary epithel

169 for the purpose of increasing IUdR-mediated radiosensitivity in MMR(-) cells.

170 eworthy that the drug did not decrease tumor radiosensitivity in mouse models.

171 h genetic and pharmacologic methods enhanced radiosensitivity in multiple basal-like cell lines.

172 review will discuss clinical implications of radiosensitivity in normal salivary glands, compare anim

173 LIF levels may predict local recurrence and radiosensitivity in NPC patients.

174 ct in NPC, and enhanced chemosensitivity and radiosensitivity in NPC.

175 ounds as novel therapeutic drugs to regulate radiosensitivity in NSCLC cells, NCI-H1299 and NCI-H460,

176 In a screen for compounds that restore radiosensitivity in p53 mutant zebrafish while tolerated

177 A strand break rejoining activity and normal radiosensitivity in response to ionizing radiation.

178 a potentially useful predictive biomarker of radiosensitivity in solid tumors and a generally applica

179 ell cycle phase distribution, apoptosis, and radiosensitivity in squamous cell carcinoma (SCC) cell l

180 sensitizing effects of 2DG, without altering radiosensitivity in the absence of 2DG.

181 In this study, we investigated radiosensitivity in the normal esophagus using an imagin

182 Increased radiosensitivity in the presence of rucaparib was associ

183 ing reduced clonogenic survival and enhanced radiosensitivity in these stem-like cells.

184 ed in our understanding of how P53 modulates radiosensitivity in tissues following IR as well as its

185 /7 inhibition induces autophagy and promotes radiosensitivity in vitro and in vivo.

186 Sa-II), and whether this results in enhanced radiosensitivity in vivo, as assessed by in vivo/in vitr

187 of As(2)O(3)-induced augmented oxygenation, radiosensitivity increased by 2.2-fold compared with con

188 not interphase cells, accompanied by mitotic radiosensitivity, increased micronuclei, and chromosomal

189 icity prediction modelling without utilizing radiosensitivity information.

190 models compared to model performance without radiosensitivity information.

191 cant defect in NHEJ that leads to pronounced radiosensitivity is compatible with normal human viabili

192 , indicating that the effect of Hus1 on cell radiosensitivity is independent of nonhomologous end-joi

193 Therefore, a means to characterize radiosensitivity is necessary.

194 ption as a contributor to the development of radiosensitivity-linked immunodeficiency in patients wit

195 cellular radiation response is complex, and radiosensitivity may be also regulated at different leve

196 ially important when attempting to translate radiosensitivity measurements at the experimental in vit

197 Discovery of this intestinal radiosensitivity mechanism allowed design of an antisens

198 umans are associated with increased cellular radiosensitivity, microcephaly, facial dysmorphisms, gro

199 t is characterized by cancer predisposition, radiosensitivity, neurodegeneration, sterility, and acqu

200 rdation, genomic instability, and organismal radiosensitivity observed in PARP1-deficient mice.

201 point abnormalities contribute little to the radiosensitivity observed.

202 17DMAG was previously shown to enhance the radiosensitivity of a number of human cell lines, which

203 o)-17-demethoxygeldanamycin (17DMAG), on the radiosensitivity of a panel of human tumor cell lines.

204 al results indicate that Ad/p16 enhanced the radiosensitivity of A549 but not H322 or H1299.

205 uced expression of IGF-IR contributes to the radiosensitivity of AT cells.

206 opriate target for selectively enhancing the radiosensitivity of brain tumor cells.

207 may serve as therapeutic targets to enhance radiosensitivity of breast cancers.

208 es a molecular explanation for the increased radiosensitivity of caffeine-treated cells.

209 treatment, but the relationship between the radiosensitivity of cancer cells and their genomic chara

210 trated to be a generic method to enhance the radiosensitivity of cancer cells with a supra-additive s

211 ream activation of MAPK which may affect the radiosensitivity of carcinoma cells.

212 poration of GNPs has a significant effect on radiosensitivity of cells and their dose-dependent clono

213 survival showed its capacity to stratify the radiosensitivity of cells based on aspects of their phen

214 pair DNA double-strand breaks, increases the radiosensitivity of cells, and enhances radiation-induce

215 o repair DNA double-strand breaks, increases radiosensitivity of cells, and enhances radiation-induce

216 stitutively expressing PCNA protein restored radiosensitivity of CHO cells back to wild-type levels.

217 iosensitivity of tumor cells but also on the radiosensitivity of endothelial cells lining the tumor v

218 CBD) can induce cell death and increases the radiosensitivity of GBM by enhancing apoptosis.

219 egulates DNA damage checkpoint responses and radiosensitivity of GSCs through nuclear translocation o

220 tal role of the BH3-only protein Puma in the radiosensitivity of hematopoietic stem cells (HSCs) and

221 Mechanistic investigations revealed that the radiosensitivity of heterozygous cells was independent o

222 ize the effects of iNOS gene transfer on the radiosensitivity of human colorectal cancer cells in vit

223 es can enhance both the in vitro and in vivo radiosensitivity of human tumor cell lines generated fro

224 are a plausible mechanism to understand the radiosensitivity of IDH1-mutated cancer cells.

225 These results demonstrate the increased radiosensitivity of intestinal stem cells within the cry

226 In vivo, parthenolide increases radiosensitivity of mouse xenograft tumors but protects

227 We examined the relative radiosensitivity of normal stem cell populations compare

228 The increased radiosensitivity of p50-/- mice was associated with an e

229 The radiosensitivity of PBSCs was determined by measuring su

230 tabolites may play a role in determining the radiosensitivity of prostate cancer cells, and that the

231 One variable that may affect the radiosensitivity of prostate tumor cells is their p53 st

232 Importantly, the radiosensitivity of Rad51C-deficient HeLa cells was evid

233 an established biological rationale for the radiosensitivity of renal-cell carcinoma to stereotactic

234 ss this notion was to determine the level of radiosensitivity of several MMR-deficient cell lines der

235 ypothesized that As(2)O(3) might enhance the radiosensitivity of solid tumors by increasing tumor oxy

236 The radiosensitivity of telomere dysfunctional cells correla

237 ma levels before RAIT may indicate increased radiosensitivity of the bone marrow, and use of this mea

238 Ku70 level, and significantly increases the radiosensitivity of the cells.

239 ese observations, Gleevec did not modify the radiosensitivity of the normal cell line.

240 justed according to the chemosensitivity and radiosensitivity of the tumor tissue in an individual pa

241 ow therapeutic interventions to increase the radiosensitivity of the tumors.

242 ing a mechanistic rationale for the clinical radiosensitivity of these cancers.

243 The radiosensitivity of transformed clones, as measured by a

244 iation classifier that predicts the inherent radiosensitivity of tumor cell lines as measured by surv

245 eIF4E silencing enhanced the radiosensitivity of tumor cell lines but not normal cell

246 of radiation therapy depends not only on the radiosensitivity of tumor cells but also on the radiosen

247 otein activity and potentially enhancing the radiosensitivity of tumor cells, we have investigated th

248 aluated the ability of dFdCyd to enhance the radiosensitivity of two human glioblastoma cell lines.

249 e effects of Gleevec on Rad51 levels and the radiosensitivity of two human glioma cell lines and a no

250 effects of the HDAC inhibitor MS-275 on the radiosensitivity of two human tumor cell lines (DU145 pr

251 and tumors, and also show that the intrinsic radiosensitivity of unsorted colony-forming tumor cells,

252 However, Ad-p53 will enhance the radiosensitivity of wild-type p53 glioma cells by increa

253 ontrast, IGF-1R inhibition did not influence radiosensitivity or gammaH2AX focus resolution in LNCaP-

254 opic expression of hTERT does not rescue the radiosensitivity or the telomere fusions in A-T fibrobla

255 Radiosensitivity parameters determined by clonogenic ass

256 cold effect and typical magnitude for tumor radiosensitivity parameters.

257 such as dose rate delivered, tumor size, and radiosensitivity play a major role in determining therap

258 ivariate linear regression model is used for radiosensitivity prediction.

259 ic tumors and were independent of tumor cell radiosensitivity, proliferation rate, rate of tumor shri

260 model was able to effectively stratify X-ray radiosensitivity (R (2) = 0.74) without the use of any c

261 ents with lymphoblastoid cell lines, we used radiosensitivity, radioresistant DNA synthesis, and irra

262 able to identify three patient subgroups of radiosensitivity: radiosensitive, radio-normal, and radi

263 esponse, a limiting factor in improving cell radiosensitivity, remains elusive.

264 Previous cellular radiosensitivity research using EBT may be underestimati

265 L)) to modify tumor cell or endothelial cell radiosensitivity, respectively.

266 in stem cells significantly decreased their radiosensitivity, restored DDR function, and increased s

267 ibution in tumor and (b) the increased tumor radiosensitivity resulting from the improved tumor oxyge

268 nomic regions of functional significance for radiosensitivity (RS) but have yet to be systematically

269 TK-dependent signaling nor an enhancement in radiosensitivity, suggesting the potential for a therape

270 However, the lack of severe radiosensitivity suggests that there must be alternative

271 n in late-generation Terc-/- mice imparted a radiosensitivity syndrome associated with accelerated mo

272 hese two approaches had no greater effect on radiosensitivity than either alone.

273 ed consecutively according to their inherent radiosensitivities that may be reordered therapeutically

274 th siRNA to ErbB3 or 17DMAG had no effect on radiosensitivity, the combination, which reduced both Er

275 ine decreased P-Akt expression and increased radiosensitivity to a similar extent as nelfinavir.

276 ceptor-mediated internalization and enhances radiosensitivity to both Er-filtered and standard 250 kV

277 t on DNA DSB rejoining and no effect on cell radiosensitivity to killing although it sensitized contr

278 Wortmannin did not affect the radiosensitivity to killing and produced only a modest i

279 recombination and support the view that the radiosensitivity to killing of cells deficient in BRCA1

280 in AT cells, it was unable to restore normal radiosensitivity to the cells.

281 to angiogenesis inhibition, endothelial cell radiosensitivity, tumor cell apoptosis, or a decrease in

282 ent a kinetic model incorporating effects of radiosensitivity, tumor repopulation, and dead-cell reso

283 s its ability to confer chemosensitivity and radiosensitivity upon tumor cells.

284 ons, and successfully fit to cellular proton radiosensitivity using a single dose-related parameter (

285 Although sorafenib does not affect intrinsic radiosensitivity using in vitro colony formation assays,

286 be determined by PET at a microscopic scale, radiosensitivity values extracted here by fitting models

287 lls were generated, and the effect of p16 on radiosensitivity was determined by clonogenic cell survi

288 is was strengthened by finding that cellular radiosensitivity was increased by genetic inhibition of

289 hypoxia, suggesting that the effect of DA on radiosensitivity was independent of these factors and a

290 Radiosensitivity was mediated, at least in part, through

291 Radiosensitivity was tested in combination with gamma-ir

292 Tumor cell radiosensitivity was the major determinant of tumor resp

293 ain insight into this important biomarker of radiosensitivity, we first examined genomic patterns ref

294 the rate of telomere attrition and apparent radiosensitivity weaken the intra-individual correlation

295 efects, genomic instability, infertility and radiosensitivity, were not rescued.

296 xpression by small interfering RNA increased radiosensitivity, whereas increased radioresistance was

297 ominant-negative TRAF2 mutant also conferred radiosensitivity, whereas overexpression of wild-type (W

298 entify species that exhibit widely different radiosensitivities, which in turn has hampered the ident

299 after irradiation resulted in an increase in radiosensitivity with dose enhancement factors of 1.9 an

300 fection resulted in little or no increase in radiosensitivity with respect to cell killing, a 1.5-fol