ライフサイエンスコーパス: bleomycin

1 three cycles of ifosfamide, vinblastine, and bleomycin.

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

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

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

5 age caused by diepoxybutane, mitomycin C and bleomycin.

6 ngs of patients with IPF and mice exposed to bleomycin.

7 uch as cyclosporine, and cytostatics such as bleomycin.

8 however, better tolerated compared to PCI of bleomycin.

9 of patients with IPF and in mice exposed to bleomycin.

10 cted on the basis of their strong binding to bleomycin.

11 A damage caused by the chemotherapeutic drug bleomycin.

12 nin deficiency showed delayed recovery after bleomycin.

13 or both (CD39/CD73DKO) were challenged with bleomycin.

14 econstitutes their lung fibrotic response to bleomycin.

15 with cisplatin and etoposide with or without bleomycin.

16 Mice were given intratracheal bleomycin (0.04 units) and assessed for AEC death, infla

17 to 3, etoposide 167 mg/m(2) on days 1 to 3, bleomycin 15 U/m(2) on day 1).

18 mesna (500 mg/m(2) at 0, 3, 7 and 11 h), and bleomycin (25 units per day, by continuous infusion for

19 or 5 days], and intramuscular or intravenous bleomycin [30 mg per day on days 1, 8, and 15]), patient

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

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

22 Clinically used bleomycin A5 has been employed in a study of double-stra

23 Bleomycins A5 and B2 were used to study the structural f

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

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

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

27 addition, when c03958 larvae were exposed to bleomycin, an agent that produces oxidative DNA damage,

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

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

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

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

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

33 nd increased tolerability compared to PCI of bleomycin and may represent an interesting clinical futu

34 ression with shChk1 increased sensitivity to bleomycin and radiation.

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

36 Bleomycin and vincristine discontinuation because of dru

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

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

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

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

41 In both bleomycin- and radiation-induced pulmonary fibrosis muri

42 med in two preclinical murine models of IPF, bleomycin- and radiation-induced pulmonary fibrosis.

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

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

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

46 targeting properties of the antitumor agent bleomycin (BLM) were studied in cell culture using micro

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

48 We used a mouse model of bleomycin (BLM)-induced lung injury to understand the in

49 art of human MC chymase, in a mouse model of bleomycin (BLM)-induced lung injury.

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

51 e for the tumor cell targeting properties of bleomycin (BLM).

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

53 brogates their lung inflammatory response to bleomycin, but reconstitutes their lung fibrotic respons

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

55 ic subunits (DNA-PKcs) in response to IR and bleomycin can be quantified by Number and Brightness ana

56 ion increased susceptibility for phleomycin, bleomycin, capreomycin, amikacin, kanamycin, cetylpyridi

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

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

59 Intranasal bleomycin challenge exacerbated lung inflammation in aut

60 e, lung fibrosis induced after intratracheal bleomycin challenge in mice could be prevented by pretre

61 apoptosis of alveolar epithelial cells under bleomycin challenge.

62 tion of lung fibrosis in mice in response to bleomycin challenge.

63 ickening and tensile strength increase after bleomycin challenge.

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

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

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

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

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

69 tegrin binding was increased in the lungs of bleomycin-, compared with saline-, exposed mice and was

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

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

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

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

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

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

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

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

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

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

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

81 uction of BEACOPP(escalated) (escalated-dose bleomycin, etoposide, doxorubicin, cyclophosphamide, vin

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

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

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

85 xia-inducible factor 1alpha and treatment of bleomycin-exposed mice with a DCK inhibitor attenuated p

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

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

88 ttenuated lung injury and fibrosis following bleomycin exposure.

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

90 n AECs had greater AEC death at 1 week after bleomycin, followed by increased numbers of fibroblasts

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

92 rker, in the vitamin D group compared to the bleomycin group (P < 0.001).

93 The bleomycin group had rising hydroxyproline level on days

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

95 ntial of GRN510 to limit fibrosis induced by bleomycin in mTERT heterozygous mice.

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

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

98 aling in vitro, and skin fibrosis induced by bleomycin in vivo was attenuated in mice harboring a mut

99 iation (IR) or radiomimetic drugs, including bleomycin, in living cells.

100 ittermate genotype control mice injured with bleomycin indicating that fibrocytes are not a necessary

101 FTY720 fails to protect against bleomycin-induced acute lung injury in mice, while FTY72

102 After naphthalene, ozone or bleomycin-induced airway epithelial injury, surviving ep

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

104 ro studies demonstrated that LYCAT modulated bleomycin-induced cardiolipin remodeling, mitochondrial

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

106 beta-catenin-deficient AECs showed increased bleomycin-induced cytotoxicity as well as reduced prolif

107 uation for wound closure, proliferation, and bleomycin-induced cytotoxicity.

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

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

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

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

112 In vitro, bleomycin-induced expression of SphK1 in lung fibroblast

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

117 In this model of bleomycin-induced fibrosis, treatment with GRN510 suppre

118 ockout mice are significantly protected from bleomycin-induced fibrosis.

119 fibrotic human lung tissue and in mice with bleomycin-induced fibrosis.

120 in the alveolar epithelium protects against bleomycin-induced fibrosis.

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

122 1-alpha (HIF1A) inhibition in late stages of bleomycin-induced injury attenuates pulmonary fibrosis i

123 After bleomycin-induced injury, TH promoted mitochondrial biog

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

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

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

127 1 gene transfer in the mouse lung attenuated bleomycin-induced lung fibrosis and improved lung functi

128 FKBP10 expression was up-regulated in bleomycin-induced lung fibrosis and IPF.

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

130 rofibrotic effects of IPF LFs and attenuates bleomycin-induced lung fibrosis in mice.

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

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

133 Using an in vivo bleomycin-induced lung fibrosis model, we reveal a clock

134 d S1P generation and TGF-beta secretion in a bleomycin-induced lung fibrosis mouse model that was acc

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

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

137 miR-145 deficiency is protective against bleomycin-induced lung fibrosis, suggesting that miR-145

138 In mice, injections of Slit2 inhibit bleomycin-induced lung fibrosis.

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

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

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

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

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

144 ed reduced pulmonary fibrosis in response to bleomycin-induced lung injury, relative to wild-type con

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 inflammation and fibroblast proliferation in bleomycin-induced lung injury.

148 uman syndecan-2 during the fibrotic phase of bleomycin-induced lung injury.

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

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

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

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

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

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

155 Administration of SphK inhibitor reduced bleomycin-induced mortality and pulmonary fibrosis in mi

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

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

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

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

160 550 prevented the onset of both hypoxia- and bleomycin-induced PH and produced a significantly greate

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

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

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

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

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

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

167 tissues and is required for pathogenesis of bleomycin-induced pulmonary fibrosis in mice.

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

169 ent with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pulmonary fibrosis model reduced fibro

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

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

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

173 Moreover, using a murine treatment model of bleomycin-induced pulmonary fibrosis we found that inhib

174 Lrp5 null mice were protected against bleomycin-induced pulmonary fibrosis, an effect that was

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

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

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

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

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

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

181 nd that miR-145(-/-) mice are protected from bleomycin-induced pulmonary fibrosis.

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

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

184 Skin wound healing and bleomycin-induced skin fibrosis are thought to reflect c

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

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

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

188 ute respiratory distress syndrome, aspirated bleomycin induces a significant increase in the number o

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

190 CCL2 expression increased in bleomycin-injured bronchoalveolar lavage (BAL), but sign

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

192 nate every other day for 1 week in normal or bleomycin-injured mice maintains significantly higher lu

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

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

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

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

197 development or progression of fibrosis in a bleomycin injury model during both acute and chronic rem

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

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

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

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

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

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

204 2a-mediated photochemical internalisation of bleomycin is safe and tolerable.

205 tes DNA cleavage in much the same fashion as bleomycin, it exhibits diminished cytotoxicity in compar

206 d1 progenitor-derived pericytes expand after bleomycin lung injury, and activate expression of collag

207 pe and Adam9(-/-) mice in bacterial LPS- and bleomycin-mediated acute lung injury (ALI).

208 gradation of lung elastin during LPS- and/or bleomycin-mediated ALI.

209 ells are sources of profibrotic MMP-8 during bleomycin-mediated lung fibrosis.

210 Thus, during bleomycin-mediated lung injury, MMP-8 dampens the lung a

211 ceptor 1 levels and improves outcomes in the bleomycin model of acute lung injury.

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

213 nts with rapidly progressing IPF and a mouse bleomycin model of lung fibrosis.

214 growth factor stimulation and in the murine bleomycin model of lung fibrosis.

215 ed against perturbed lung fluid balance in a bleomycin model of lung injury, highlighting a role for

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

217 ant attenuation of pulmonary fibrosis in the bleomycin model of the disease.

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

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

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

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

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

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

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

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

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

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

228 r Lrp5 in models of lung fibrosis induced by bleomycin or an adenovirus encoding an active form of tr

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

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

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

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

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

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

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

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

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

238 lung injury was induced in C57BL/6 mice with bleomycin to assess effects of sphingosine 1-phosphate r

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

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

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

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

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

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

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

246 n inflammatory or immune cell influx between bleomycin-treated CKO and control mouse lungs.

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

248 es not regulate collagen accumulation in the bleomycin-treated lung.

249 rted by immunostaining of lung sections from bleomycin-treated mice and from ILD patients.

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

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

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

253 2- to 8-fold-greater uptake in the lungs of bleomycin-treated mice than sham-treated mice, whereas t

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

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

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

257 e sections from ILD patients and in lungs of bleomycin-treated mice.

258 17~92 expression was reduced in the lungs of bleomycin-treated mice.

259 in skin from CD39KO, CD73KO, or CD39/CD73DKO bleomycin-treated mice.

260 sfer of BM-derived CD11c(+) cells from donor bleomycin-treated mice.

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

262 Studies of bleomycin-treated Mmp-8 bone marrow chimeric mice show t

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

264 x vivo was increased in wild-type mice after bleomycin treatment but remained low in skin from CD39KO

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

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

267 The number of LHPCs increased rapidly after bleomycin treatment.

268 population was significantly increased after bleomycin treatment.

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

270 PKcs quickly mobilized in response to IR and bleomycin treatments consistent with prior reports using

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

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

273 2496 Intergroup trial comparing doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) and Stanf

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

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

276 ree cycles of chemotherapy with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) require r

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

278 The majority received doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD)-like chem

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

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

281 scan after two cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) as compared wit

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

283 Although ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) has been establ

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

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

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

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

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

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

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

291 ury, with a more severe fibrotic effect when bleomycin was applied at a circadian nadir in NRF2 level

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

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

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

295 th compressed PEB (cisplatin, etoposide, and bleomycin) was initiated every 3 weeks for three cycles

296 compared the PCI of VEGF121/rGel to that of bleomycin which is currently under clinical evaluation.

297 ere found for PCI of VEGF121/rGel and PCI of bleomycin with cure rates of 40% and 33% respectively.

298 pulmonary fibrosis induced by intratracheal bleomycin, with minimal alterations in the early inflamm

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

300 After bleomycin, WT macrophages displayed an alternatively act