ライフサイエンスコーパス: bleomycin

1 dividual patients vary in their responses to bleomycin.

2 , and apoptosis in AECs of mice unexposed to bleomycin.

3 with cisplatin and etoposide with or without bleomycin.

4 three cycles of ifosfamide, vinblastine, and bleomycin.

5 t on the possible mechanism of action for Co-bleomycin.

6 tment with the DNA-cleaving antitumor agent, bleomycin.

7 te trafficking into the lungs in response to bleomycin.

8 age caused by diepoxybutane, mitomycin C and bleomycin.

9 ssion manifested as a phenotype resistant to bleomycin.

10 a single course of VEG-ECT with intravenous bleomycin (15,000 IU/m(2)) and concomitant electric puls

11 n patients receiving </= or > four cycles of bleomycin (5-year PFS difference, 1.7%; 95% CI, -4.2% to

12 transport of antimicrobial peptides such as bleomycin(7).

13 The hyper-sensitivity to bleomycin, a drug known to induce DSBs, further supports

14 Equipping this molecule with a bleomycin A5 cleaving module converts the simple binding

15 lore emerging RNA-target strategies, such as bleomycin A5 conjugates and ribonuclease targeting chime

16 binding to direct cleavage by conjugation to bleomycin A5 in a manner that imparts RNA-selective clea

17 Furthermore, skin fibrosis induced by bleomycin administration is also reduced by the thyroid

18 After 21 d of bleomycin administration, AT2CC(-/-) mice behaved in a m

19 some ultrastructural changes in response to bleomycin administration, including basement membrane th

20 This replicated the activity of bleomycin, an antibiotic that has been previously used i

21 lungs of Vim(-/-) mice challenged with LPS, bleomycin and asbestos.

22 ransport the unrelated hydrophilic compounds bleomycin and cobalamin.

23 d sensitivity to two chemotherapeutic drugs, bleomycin and etoposide (P < 0.001).

24 of pulmonary fibrosis in mice (intratracheal bleomycin and inducible TGF-beta1).

25 erin deficient (CLU-/-) mice persisted after bleomycin and it was associated with increased DNA damag

26 ression with shChk1 increased sensitivity to bleomycin and radiation.

27 as cisplatin, often used in combination with bleomycin and vinca alkaloids, can lead to vascular even

28 Bleomycin and vincristine discontinuation because of dru

29 The role of bleomycin and vincristine in the treatment of patients w

30 omputer system to receive either intravenous bleomycin and vincristine or oral etoposide (the investi

31 clitaxel plus ART (64%, 55 to 73; n=138) and bleomycin and vincristine plus ART (44%, 35 to 53; n=132

32 y was closed early due to inferiority of the bleomycin and vincristine plus ART arm, as per the recom

33 eriority to both oral etoposide plus ART and bleomycin and vincristine plus ART, supporting its use i

34 analyzed with respect to discontinuation of bleomycin and/or vincristine.

35 patients (4.7%) received </= four cycles of bleomycin, and 218 (6.6%) received </= three cycles of v

36 of exposure to bacterial lipopolysaccharide, bleomycin, and allergic airway inflammation induced by h

37 dCs) underwent fibrosis after treatment with bleomycin, and EdCs retrieved from the lung showed expre

38 b, doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone), with no significant impact o

39 C-Exo treatments could attenuate and resolve bleomycin- and silica-induced fibrosis by reestablishing

40 signed to continue ABVD (ABVD group) or omit bleomycin (AVD group) in cycles 3 through 6.

41 e, and cisplatin chemotherapy, given without bleomycin because of the anticipated need for postchemot

42 We reported that, following bleomycin (bleo), knockin mice harboring the human R213G

43 ut (il17a(-/-) ) mice were protected against bleomycin (BLEO)-induced fibrosis and collagen depositio

44 ransition (EndoMT) and fibrotic responses in bleomycin (BLM) induced lung fibrosis models.

45 In the bleomycin (BLM) model of lung fibrosis, CKO mice had red

46 ients with idiopathic pulmonary fibrosis and bleomycin (BLM)-induced fibrotic murine lungs.

47 thic pulmonary fibrosis and a mouse model of bleomycin (BLM)-induced PF.

48 d analysis was performed in a mouse model of bleomycin (BLM)-induced pulmonary fibrosis by micro-CT,

49 (n = 6) and patients with IPF (n = 6), aging bleomycin (BLM)-treated mice (n = 7), and BLM-treated AF

50 d 21 after single intratracheal injection of bleomycin (BLM).

51 ysM(Cre)) were exposed to the fibrotic agent bleomycin (BLM; 0.035 U/g body weight, i.p.).

52 , followed by a fixed dose of 15 000 IU/m(2) bleomycin by intravenous infusion on day 4.

53 vincristine, procarbazine, vinblastine, and bleomycin; CEC) in patients with advanced-stage Hodgkin

54 hi)Foxp3(+) cells undergo alterations during bleomycin challenge and the IL-2 complex had no effect o

55 Intranasal bleomycin challenge exacerbated lung inflammation in aut

56 Our data indicate that after bleomycin challenge, mice lacking IRAK-M have decreased

57 phangiogenesis peaked at 14 to 28 days after bleomycin challenge, was accompanied by doubling of chem

58 as necessary for CCR2 upregulation following bleomycin challenge.

59 p3(+) cells in the lung during intratracheal bleomycin challenge; however, this unexpectedly led to a

60 ation of the potent ATX inhibitor PAT-048 to bleomycin-challenged mice markedly decreased ATX activit

61 re system, macrophages isolated from in vivo bleomycin-challenged WT, but not IRAK-M(-/-), mice promo

62 who were clinically assessed as eligible for bleomycin chemotherapy from a single centre in the UK.

63 Bleomycin chemotherapy was not associated with pulmonary

64 the lungs of IPF patients, and in mice with bleomycin, cigarette smoke, silica, or sepsis-induced lu

65 Interestingly, the dimer-bleomycin conjugate cleaves the entire pri-miR-17-92 clu

66 Further, the bleomycin conjugate exerted selective effects on the miR

67 induced by an intratracheal instillation of bleomycin (control mice were instilled with a saline sol

68 Furthermore, bleomycin-dependent induction of T helper type 2-skewed

69 ould improve treatment outcomes by tailoring bleomycin dosages to each patient.

70 relation to age, cumulative cisplatin and/or bleomycin dose, time since chemotherapy, sociodemographi

71 Larger cumulative bleomycin doses (OR, 1.44 per 90,000 IU) were significan

72 n standardized uptake values correlated with bleomycin doses, histologic score of fibrosis, lung hydr

73 sions, DNA breaks induced by several agents (bleomycin, doxorubicin, topotecan, hydrogen peroxide, UV

74 demonstrate in mouse models of allergen- and bleomycin-driven airway inflammation that neutralization

75 is of patients with HL treated with BEACOPP (bleomycin, etoposide, adriamycin, cyclophosphamide, vinc

76 NS who experienced a relapse after adjuvant bleomycin, etoposide, and cisplatin (BEP) from 18 center

77 rs have been hypothesized for treatment with bleomycin, etoposide, and cisplatin (BEP).

78 nce only; retroperitoneal radiotherapy (RT); bleomycin, etoposide, and cisplatin (BEP); or more than

79 , and incurs less drug cost than 2 cycles of bleomycin, etoposide, and cisplatin.

80 cisplatin (EPX4) or three or four cycles of bleomycin, etoposide, cisplatin (BEPX3/BEPX4).

81 CTx was predominantly bleomycin, etoposide, doxorubicin cyclophosphamide, vinc

82 ieving CR on PET2 were switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

83 edian follow-up, 106 months), superiority of bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

84 -positive patients switched to two cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

85 lle score 4 to 5) were switched to escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

86 findings after two cycles received BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

87 calated plus two standard cycles of BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

88 atients treated with six to eight courses of bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

89 Treatment with bleomycin-etoposide-cisplatin (BEP; n = 1,819) was assoc

90 Pulmonary fibrosis after asbestos or bleomycin exposure was evaluated in 129SJ/wild-type and

91 l and prevents lung edema in mice induced by bleomycin exposure-a lung injury model in which TGF-beta

92 ttenuated lung injury and fibrosis following bleomycin exposure.

93 Bleomycin failed to induce miR-34a in p53- or plasminoge

94 ified noninferiority margin, the omission of bleomycin from the ABVD regimen after negative findings

95 The bleomycin group had rising hydroxyproline level on days

96 Therefore, using bleomycin has been questioned in older Hodgkin lymphoma

97 , we found a high risk of severe toxicity of bleomycin in older HL patients receiving more than 2 cyc

98 n mediating photochemical internalisation of bleomycin in patients with advanced and recurrent solid

99 Inclusion of bleomycin in this setting is not necessary.

100 r assessing the development of fibrosis in a bleomycin induced skin fibrosis mouse model.

101 bacterial pneumonia, ventilator-induced ALI, bleomycin-induced ALI) and indirect ALI (systemic LPS, c

102 demonstrate that TOLLIP protects cells from bleomycin-induced apoptosis using primary bronchial epit

103 roduction of Raf1-tr sensitized the cells to bleomycin-induced apoptosis.

104 ased Raf1-tr expression become sensitized to bleomycin-induced apoptosis.

105 IL-17A deficiency mitigates bleomycin-induced complement activation during lung fibr

106 as significantly reducing the development of bleomycin-induced dermal fibrosis in mice in vivo.

107 ion was significantly elevated in the murine bleomycin-induced dermal fibrosis model, which was assoc

108 sults indicate that glycyrrhizin ameliorates bleomycin-induced dermal fibrosis through the inhibition

109 nockout mice exhibited significantly reduced bleomycin-induced dermal fibrosis with greater preservat

110 and causes amplification of irradiation- and bleomycin-induced DNA damage.

111 Moreover, in vivo the bleomycin-induced down-regulation of peroxisomes was abr

112 ry fibrosis by heightening susceptibility to bleomycin-induced epithelial injury and diminishing epit

113 IRAK-M (IRAK-M(-/-)) were protected against bleomycin-induced fibrosis and displayed diminished coll

114 However, bleomycin-induced fibrosis in skin proceeded in a compar

115 gnaling in primary dermal fibroblasts and of bleomycin-induced fibrosis in vivo.

116 NJB2 also detected pulmonary fibrosis in a bleomycin-induced fibrosis model.

117 sis in vivo was assessed in a mouse model of bleomycin-induced fibrosis using PET imaging.

118 n these cells exacerbated the development of bleomycin-induced fibrosis, whereas mutation of REVERBal

119 ng inflammation, but does not play a role in bleomycin-induced fibrosis.

120 Redistribution of EC-SOD resolves bleomycin-induced inflammation via increased apoptosis o

121 1-alpha (HIF1A) inhibition in late stages of bleomycin-induced injury attenuates pulmonary fibrosis i

122 After bleomycin-induced injury, TH promoted mitochondrial biog

123 BX4 signaling attenuated lung fibrosis after bleomycin-induced injury.

124 nistration of artemisitene strongly inhibits bleomycin-induced lung damage.

125 We assessed FKBP10 expression in bleomycin-induced lung fibrosis (using quantitative reve

126 1 gene transfer in the mouse lung attenuated bleomycin-induced lung fibrosis and improved lung functi

127 ast differentiation of LR-MSC and attenuates bleomycin-induced lung fibrosis by targeting Smad7.

128 acterize the heterogeneity of macrophages in bleomycin-induced lung fibrosis in mice.

129 Bleomycin-induced lung fibrosis in wild-type and miR-155

130 In a bleomycin-induced lung fibrosis model we used wild-type

131 In the murine bleomycin-induced lung fibrosis model, GSK3008348 engage

132 itor displayed efficacy in a murine model of bleomycin-induced lung fibrosis similar to that of a kno

133 Asbestos- or bleomycin-induced lung fibrosis, AEC mtDNA damage, and a

134 In a mouse model of bleomycin-induced lung fibrosis, Lonidamine reduced the

135 d that Dio2-knockout mice exhibited enhanced bleomycin-induced lung fibrosis.

136 Sobetirome, a TH mimetic, also blunted bleomycin-induced lung fibrosis.

137 ynthase deficiency in AEC2 cells exacerbates bleomycin-induced lung fibrosis.

138 ponsiveness (AHR) and lung inflammation, and bleomycin-induced lung fibrosis; however, the cellular s

139 rthermore, HSM pretreatment markedly reduces bleomycin-induced lung injury and fibrosis in mice.

140 e Hodgkin lymphoma (HL) but carries risks of bleomycin-induced lung injury and radiation toxicity.

141 ression worsens fibroproliferation following bleomycin-induced lung injury in alcohol-fed mice.

142 nstrate that application of C1INH alleviates bleomycin-induced lung injury via direct interaction wit

143 ficiency markedly reduced recovery following bleomycin-induced lung injury.

144 g of CCN1 attenuates fibrogenic responses to bleomycin-induced lung injury.

145 nt antioxidant response and protects against bleomycin-induced lung injury.

146 es, which play a role in the pathogenesis of bleomycin-induced lung injury.

147 ased expression of Rpn6 were detected during bleomycin-induced lung remodeling and fibrosis.

148 oxicity in older patients, particularly from bleomycin-induced lung toxicity (BLT).

149 oducing Tc2 cells and play a major role in a bleomycin-induced model of fibrosis.

150 deposition of collagen in lung tissues in a bleomycin-induced model of pulmonary fibrosis.

151 roduction of interleukin-17B (IL-17B) during bleomycin-induced mouse lung fibrosis.

152 n of human IPF MPCs converted a self-limited bleomycin-induced mouse model of lung fibrosis to a mode

153 In a bleomycin-induced mouse pulmonary fibrosis model, 5d fro

154 hages to fibrotic disease progression in the bleomycin-induced murine model of pulmonary fibrosis.

155 EC-specific suppression of miR-34a inhibited bleomycin-induced p53, PAI-1, and apoptosis and prevente

156 In a bleomycin-induced PF model, mice deficient in p-rex1 had

157 Similar results were found in mice with bleomycin-induced PF.

158 ease or toxicity, including one patient from bleomycin-induced pneumonitis.

159 bit thrombin/PAR1 signaling and protect from bleomycin-induced pneumonitis.

160 signaling through PAR1 to ERK, and inhibits bleomycin-induced pneumonitis.

161 on (PGDHi) is protective in a mouse model of bleomycin-induced pulmonary fibrosis (PF).

162 d demonstrate an increased susceptibility to bleomycin-induced pulmonary fibrosis and collagen accumu

163 bone marrow-derived CD11c(+) cells promoted bleomycin-induced pulmonary fibrosis by activation of fi

164 Thus, vitamin D treatment could prevent bleomycin-induced pulmonary fibrosis by delaying or supp

165 we used a novel segmental challenge model of bleomycin-induced pulmonary fibrosis in sheep to evaluat

166 in vivo and was shown to be efficacious in a bleomycin-induced pulmonary fibrosis model in mice and i

167 ene-modified and inhibitor-treated mice in a bleomycin-induced pulmonary fibrosis model.

168 and inflammatory cell accumulationin in the bleomycin-induced pulmonary fibrosis mouse model on supp

169 ated from human IPF lungs and from mice with bleomycin-induced pulmonary fibrosis showed an increased

170 fibrosis and 16% of isolated fibroblasts in bleomycin-induced pulmonary fibrosis to be of endothelia

171 In the murine model of bleomycin-induced pulmonary fibrosis, the consequences o

172 in collagen-producing cells led to increased bleomycin-induced pulmonary fibrosis, which is mediated

173 n the lungs of IPF patients and of mice upon bleomycin-induced pulmonary fibrosis.

174 tissues from patients with IPF and mice with bleomycin-induced pulmonary fibrosis.

175 in vivo through lentiviral delivery blunted bleomycin-induced pulmonary fibrosis.

176 tion of the GLS1 inhibitor CB-839 attenuated bleomycin-induced pulmonary fibrosis.

177 antifibrotic efficacy in an animal model of bleomycin-induced pulmonary fibrosis.

178 P2 mutation (SHP2(D61G/+)) were resistant to bleomycin-induced pulmonary fibrosis.

179 AREG expression was significantly induced in bleomycin-induced pulmonary fibrosis.

180 on and activity were up-regulated in IPF and bleomycin-induced pulmonary fibrosis.

181 es/macrophages and protected from subsequent bleomycin-induced pulmonary fibrosis.

182 injections of sialidase inhibitors attenuate bleomycin-induced pulmonary fibrosis.

183 In conclusion, STC1 blunts bleomycin-induced rise in thrombin protein and activity,

184 Importantly, DMF prevented bleomycin-induced skin fibrosis in mice.

185 unological activation in mice with HOCl- and bleomycin-induced SSc.

186 CGEN25009 was effective at decreasing bleomycin-induced, acid-soluble collagen deposition in v

187 e demonstrate that in vehicle-treated sheep, bleomycin-infused lung segments had significantly higher

188 ession and endothelial cell proliferation in bleomycin-infused lung segments were significantly reduc

189 DSBs induced in pre-B cells by etoposide or bleomycin inhibit recombination of Igkappa loci and a ch

190 When introduced into dermis or bleomycin-injured lungs of mice, collectins MBL and SP-D

191 5, Smad2, and Smad3 levels were increased in bleomycin-injured lungs.

192 LPA and LPC species that increase in BAL of bleomycin-injured mice were discordant, inconsistent wit

193 e of C3aR and C5aR in lung fibrosis by using bleomycin-injured mice with fibrotic lungs, elevated loc

194 both in alveolar epithelial type I cells in bleomycin-injured mouse lungs and in lung sections from

195 tin 5 remodelling program after influenza or bleomycin injury in mice.

196 We found that bleomycin injury increases the bronchoalveolar lavage (B

197 remodeling in mice with lung fibrosis after bleomycin injury or telomere dysfunction.

198 After bleomycin injury, H2-K1 cells expand and differentiate i

199 acyl groups predominated in BAL fluid after bleomycin injury, with 22:5 and 22:6 species accounting

200 ated alpha6-expression protects mice against bleomycin injury-induced experimental lung fibrosis.

201 xin-like peptide, in lung fibroblasts and in bleomycin injury.

202 Leveraging the bleomycin-injury IPF model, we demonstrate that early-in

203 models of pulmonary fibrosis, intratracheal bleomycin instillation and thoracic irradiation, we find

204 Experiments performed using a bleomycin-instilled mouse model of pulmonary fibrosis sh

205 Bleomycin is a powerful chemotherapeutic drug used to tr

206 2a-mediated photochemical internalisation of bleomycin is safe and tolerable.

207 Using time-series single cell RNA-seq of the bleomycin lung injury model, we resolved transcriptional

208 ivo studies, the progression of TGF-beta and bleomycin mediated PF was significantly attenuated by 9-

209 masome activity and protects from subsequent bleomycin-mediated pulmonary fibrosis.

210 ivo therapeutic effects were assessed in the bleomycin model of lung fibrosis by SHP2-lentiviral admi

211 ch signaling is known to be activated in the bleomycin model of pulmonary fibrosis, control and Notch

212 ly attenuate pulmonary fibrosis in the mouse bleomycin model, and by breaking the feedback loop, caus

213 In the experimental bleomycin model, matriptase depletion, by the pharmacolo

214 ntly reduced fibrosis in a 14-day mouse lung bleomycin model.

215 in IPF precision cut lung slices and in the bleomycin model.

216 Using the bleomycin mouse model for fibrosis, we examined an array

217 ts of 15-PGDH inhibition were studied in the bleomycin mouse model of pulmonary fibrosis.

218 in in pleural thickening in the carbon-black bleomycin mouse model.

219 nary LPA production during fibrogenesis in a bleomycin mouse model.

220 ession significantly increases fibrosis in a bleomycin murine model, whereas FIEL1 knockdown attenuat

221 small-molecule DNA cleaving agents, such as bleomycin, neocarzinostatin chromophore, and lomaivitici

222 In conclusion, no effects of bleomycin on toxicity rates were detectable in older pat

223 red with patients receiving > four cycles of bleomycin or > three cycles of vincristine, respectively

224 Using intratracheal injection of bleomycin or hydrochloric acid in mice, we show that rep

225 rosis after a single round of treatment with bleomycin or hydrochloric acid, repeated injury leads to

226 n accumulation in response to either inhaled bleomycin or inducible lung targeted TGF-beta1 overexpre

227 In conclusion, brentuximab-AVD without bleomycin or radiation produced a high complete response

228 istinct murine models of fibrosis induced by bleomycin or targeted type II alveolar epithelial injury

229 Overexpression of Cav-1 suppressed bleomycin- or silica-induced activation of caspase-1 and

230 administration of cisplatin, etoposide, and bleomycin (PEb) is reduced from four to three cycles and

231 n club or myeloid cells had no effect on the bleomycin phenotype.

232 b, doxorubicin, cyclophosphamide, vindesine, bleomycin, prednisone (R-ACVBP) or rituximab, cyclophosp

233 6 strains, thereby leading to differences in bleomycin resistance.

234 matode-specific gene (scb-1) is required for bleomycin resistance.

235 elegans to identify genetic determinants of bleomycin-response differences by performing linkage map

236 enomic region on chromosome V that underlies bleomycin-response variation.

237 anism by which this gene causes variation in bleomycin responses is unknown, we suggest that a rare v

238 apies with lasers and other agents including bleomycin, salicylic acid, and light-emitting diode have

239 iflu) starting either 1 day or 10 days after bleomycin strongly attenuate pulmonary fibrosis in the m

240 induced by ionizing radiation, etoposide, or bleomycin suppress Rag1 and Rag2 mRNA levels in primary

241 Preoperative therapy (including use of bleomycin), surgical management, recurrence, and surviva

242 e the vitamin thiamine, the anti-cancer drug bleomycin, the antibacterial sulfathiazole and the antiv

243 rat pups, we intratracheally injected either bleomycin to induce ALI or saline as a sham control.

244 g hydroxyproline content after intratracheal bleomycin to levels comparable with that of wild-type co

245 ology after intra-tracheal administration of bleomycin to WT and STC1 Tg mice.

246 obstructive pulmonary disease, and mice with bleomycin-, transforming growth factor beta-, or passive

247 olin-1 scaffolding domain peptide suppressed bleomycin-, transforming growth factor beta-, or passive

248 se Tc2 cells in the lung requires IL-21, and bleomycin treated IL-21- and IL-21R-deficient mice devel

249 dialdehyde) and increase GSH content both in bleomycin treated mouse lungs and TGF-beta stimulated fi

250 ribution in other organs was similar between bleomycin-treated and sham mice.

251 r of bone marrow-derived CD11c(+) cells from bleomycin-treated donor mice exacerbated pulmonary fibro

252 of noggin, BAMBI, and FSTL1 in the lungs of bleomycin-treated mice and in the lungs of idiopathic pu

253 o as well as to reduce pulmonary fibrosis in bleomycin-treated mice in vivo.

254 ion, vasculopathy, and tissue fibrosis, with bleomycin-treated mice mimicking the fibrotic and inflam

255 day 7), but not the fibrotic phase (day 23), bleomycin-treated mice presented with an enhanced leukoc

256 2- to 8-fold-greater uptake in the lungs of bleomycin-treated mice than sham-treated mice, whereas t

257 In bleomycin-treated mice, a higher metabolic activity was

258 igher and early recruitment of leukocytes in bleomycin-treated mice, compared with control mice.

259 significantly ameliorated dermal fibrosis in bleomycin-treated mice, which was partly attributable to

260 in fibrotic lungs from patients with IPF and bleomycin-treated mice.

261 modeling, and improved pulmonary function in bleomycin-treated mice.

262 Lungs of bleomycin-treated WT mice display: severe pneumonitis; i

263 d DNA double-strand break (DSB) levels after bleomycin treatment and a reduced ability to repair thes

264 espread lymphangiogenesis was observed after bleomycin treatment and in fibrotic lungs of prospero ho

265 evealed that lymphangiogenesis 14 days after bleomycin treatment was dependent on vascular endothelia

266 enhanced survival of ionizing radiation and bleomycin treatment, agents that induce double-strand br

267 However, upon bleomycin treatment, they exhibited enhanced lung injury

268 and fibrosis and accelerated recovery after bleomycin treatment.

269 ce that are subjected to a fibrosis-inducing bleomycin treatment.

270 KO mice were analyzed for their responses to bleomycin treatment.

271 Mice uniformly died after challenge with bleomycin, underscoring an essential role for telomere f

272 ival analyses received standard doxorubicin, bleomycin, vinblastine and dacarbazone (ABVD) therapy si

273 Doxorubicin, bleomycin, vinblastine sulfate, and dacarbazine (ABVD) i

274 d by the combination regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine (19%), or other

275 med after two initial cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) and was l

276 ed with six to eight courses of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) despite m

277 PET (ePET) after two cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) in previo

278 th Hodgkin's Lymphoma) compared doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) with mech

279 Doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) with or w

280 Patients received 2 cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD).

281 ith the chemotherapy regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine (or equivalent).

282 ted States by widespread use of doxorubicin, bleomycin, vinblastine, and dacarbazine and diminishing

283 core, 3 to 5) received a fourth doxorubicin, bleomycin, vinblastine, and dacarbazine cycle and involv

284 fully treated with a regimen of doxorubicin, bleomycin, vinblastine, and dacarbazine for Hodgkin dise

285 y treatment (CMT) with 2x ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) and small-field

286 n, received two cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) chemotherapy, a

287 suitable for standard ABVD (ie, doxorubicin, bleomycin, vinblastine, and dacarbazine) therapy.

288 al compared six cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine), four escalated

289 ssessment after three cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine; 143 PET-positiv

290 noninferiority of two cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) plus 20 Gy in

291 se monitoring after 2 cycles of doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) to guide trea

292 patients received doxorubicin (Adriamycin), bleomycin, vinblastine, dacarbazine chemotherapy along w

293 h mechlorethamine, doxorubicin, vincristine, bleomycin, vinblastine, etoposide, and prednisone (Stanf

294 l scanned at baseline and after 2 adriamycin-bleomycin-vinblastine-dacarbazine (ABVD) courses with (1

295 Bleomycin was adjusted on the basis of PFT results and w

296 Moreover skin fibrosis induced by bleomycin was dependent on endogenous LIGHT activity.

297 According to local protocol, bleomycin was discontinued if hemoglobin-corrected DLCO

298 With 3,309 patients with HL analyzed, bleomycin was discontinued in 17.6% and vincristine in 3

299 Induction bleomycin was not associated with pulmonary complication

300 e propenal) as formed by the natural product bleomycin, with product assignments by mass spectrometry

301 After bleomycin, WT macrophages displayed an alternatively act