ライフサイエンスコーパス: radiosensitivity

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

2 ity, and colony survival assays for cellular radiosensitivity.

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

4 ating a ROS-dependent mechanism for curcumin radiosensitivity.

5 receptor CD47 could correspondingly increase radiosensitivity.

6 ential therapeutic target for adjusting cell radiosensitivity.

7 repair, thus resulting in increased cellular radiosensitivity.

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

9 mechanisms underlying mutant EGFR-associated radiosensitivity.

10 d by exposure to ionizing radiation enhanced radiosensitivity.

11 obiota-associated enhancement of endothelial radiosensitivity.

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

13 volved in microbial regulation of intestinal radiosensitivity.

14 red for the ATM protein to regulate cellular radiosensitivity.

15 sulted in a significant enhancement in AsPC1 radiosensitivity.

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

17 iation exposure, and promotes an increase in radiosensitivity.

18 and GADD45beta expression and increased cell radiosensitivity.

19 cogenic K-ras signaling to pancreatic cancer radiosensitivity.

20 ristic facial features, immunodeficiency and radiosensitivity.

21 ocked IGF signaling, and enhanced tumor cell radiosensitivity.

22 Gleevec resulted in an enhancement in their radiosensitivity.

23 been implicated as a determinant of cellular radiosensitivity.

24 AS could thus be targets for manipulation of radiosensitivity.

25 chanism underlying flavopiridol-induced cell radiosensitivity.

26 evels of ATM expression, and restores normal radiosensitivity.

27 nd breaks, and telomere dysfunction provokes radiosensitivity.

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

29 sfunction, growth abnormalities, and extreme radiosensitivity.

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

31 tein potentiates p53-dependent apoptosis and radiosensitivity.

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

33 and HT1080, respectively) leads to increased radiosensitivity.

34 on for future calculations of individualised radiosensitivity.

35 ce defects but not lymphocyte development or radiosensitivity.

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

37 cells without BRCA1 showed decreased TCR and radiosensitivity.

38 a limited number of major genes determining radiosensitivity.

39 re was no relationship between G1 arrest and radiosensitivity.

40 n most wt-p53+ lines and are associated with radiosensitivity.

41 owing gamma-irradiation, but failed to alter radiosensitivity.

42 mologue (Yku70p), does not lead to increased radiosensitivity.

43 kout resulted in slower growth and increased radiosensitivity.

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

45 -deficient tumors and consequently increased radiosensitivity.

46 tering to group patients based on esophageal radiosensitivity.

47 effect of Atm loss on tumor endothelial cell radiosensitivity.

48 e autophagy-deficient mice display increased radiosensitivity.

49 gies to overcome radioresistance and improve radiosensitivity.

50 tion to normal tissues while enhancing tumor radiosensitivity.

51 croenvironment was sufficient to limit tumor radiosensitivity.

52 pairing checkpoint activation and increasing radiosensitivity.

53 n enhanced cetuximab efficacy and tumor cell radiosensitivity.

54 signaling activity, which is associated with radiosensitivity.

55 ect of parthenolide on tumor and normal cell radiosensitivity.

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

57 fficiency as in other species, regardless of radiosensitivity.

58 ate the mechanisms by which p16 may regulate radiosensitivity.

59 ated a regulatory role for eIF4E in cellular radiosensitivity.

60 al therapeutic target to increase tumor cell radiosensitivity.

61 IF4E with ribavirin also enhanced tumor cell radiosensitivity.

62 deficiency syndrome associated with cellular radiosensitivity.

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

64 comitantly with RT synergistically increases radiosensitivity.

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

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

67 This was greater than the radiosensitivity achieved using the phosphatidylinositol

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

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

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

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

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

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

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

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

76 oint after ionizing irradiation and enhanced radiosensitivity and chromosomal breakage.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 - and XRCC4-deficient cells exhibit profound radiosensitivity and severe defects in V(D)J recombinati

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

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

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

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

102 ontains the PI-3 kinase domain, complemented radiosensitivity and the S-phase checkpoint and reduced

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

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

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

106 o study the relationships between G1 arrest, radiosensitivity, and genetic alterations.

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

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

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

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

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

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

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

114 orm of IkappaBalpha led to correction of the radiosensitivity associated with the AT phenotype.

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

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

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

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

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

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

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

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

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

124 Esophageal radiosensitivity can be quantified using esophageal expa

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

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

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

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

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

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

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

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

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

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

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

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

137 , a recently discovered immunodeficiency and radiosensitivity disorder.

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

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

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

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

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

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

144 e clues about how to modify a normal crypt's radiosensitivity for therapeutic benefit.

145 pathways controlling cell cycle checkpoints, radiosensitivity, genetic instability, and aging.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 othesis, we have studied the heritability of radiosensitivity in families of patients with breast can

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

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

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

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

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

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

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

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

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

171 uence cellular proliferation, apoptosis, and radiosensitivity in SCCs of the head and neck.

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

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

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

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

176 Increased radiosensitivity in the presence of rucaparib was associ

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

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

179 /7 inhibition induces autophagy and promotes radiosensitivity in vitro and in vivo.

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

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

182 icity prediction modelling without utilizing radiosensitivity information.

183 models compared to model performance without radiosensitivity information.

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

185 , the function of Atm in cellular growth and radiosensitivity is distinct.

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

187 Therefore, a means to characterize radiosensitivity is necessary.

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

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

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

191 Predisposition to cancer and radiosensitivity observed in AT has been linked to chrom

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

193 point abnormalities contribute little to the radiosensitivity observed.

194 rast to the results seen in tumor cells, the radiosensitivity of a normal human fibroblast cell line

195 17DMAG was previously shown to enhance the radiosensitivity of a number of human cell lines, which

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

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

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

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

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

201 e checkpoint responses and for the increased radiosensitivity of caffeine-treated cells [6] [7] [8].

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

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

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

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

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

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

208 osen for evaluation because of the increased radiosensitivity of cells derived from AT patients and o

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

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

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

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

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

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

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

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

217 nduction of apoptosis; and (b) increases the radiosensitivity of human prostate cancer cells by decre

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

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

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

221 s primarily a local treatment, the exquisite radiosensitivity of lymphomas to radiation has allowed r

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

223 The radiosensitivity of NIH 3T3 fibroblasts overexpressing e

224 ivity of tumor cells but does not affect the radiosensitivity of normal cells.

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

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

227 The radiosensitivity of PBSCs was determined by measuring su

228 alues for murine cellular turnover rates and radiosensitivity of progenitor cells were used in the mo

229 The radiosensitivity of proliferating crypt epithelial cells

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 enterocytes to the cell cycle increases the radiosensitivity of the crypt epithelium without changin

240 g activity correlates well with an increased radiosensitivity of the heat-shocked cells, and furtherm

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

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

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

244 ults indicate that p53 does not regulate the radiosensitivity of TK6 cells through the apoptotic path

245 The radiosensitivity of transformed clones, as measured by a

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

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

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

249 e that this anti-Ras adenovirus enhances the radiosensitivity of tumor cells but does not affect the

250 or neutralizing antibody to VEGF affects the radiosensitivity of tumor cells These findings support a

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

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

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

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

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

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

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

258 No effect on apoptosis, radiosensitivity or mutability was observed when the HPV

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

260 cold effect and typical magnitude for tumor radiosensitivity parameters.

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

262 ivariate linear regression model is used for radiosensitivity prediction.

263 uble strand break repair are associated with radiosensitivity, predisposition to cancer and immunodef

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 ld-type cells underwent G2 arrest, but their radiosensitivity was similar.

293 Tumor cell radiosensitivity was the major determinant of tumor resp

294 In an unique strategy to modify tumor radiosensitivity, we used an inhibitor of the protein ki

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

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

300 ers showed clear evidence of heritability of radiosensitivity, with a single major gene accounting fo