ライフサイエンスコーパス: cyclophosphamide

1 colorectal cancer cells to UV radiation and cyclophosphamide.

2 ow transplantation with post-transplantation cyclophosphamide.

3 ltimore group using high-dose posttransplant cyclophosphamide.

4 transplantation received posttransplantation cyclophosphamide.

5 cells from 4 to 24 hours was observed after cyclophosphamide.

6 ophenolate mofetil, and post-transplantation cyclophosphamide, 0.98 (0.76-1.27; p=0.92) for tacrolimu

7 ine 30 mg/m(2) on days -6 to -2, intravenous cyclophosphamide 14.5 mg/kg on days -6 and -5, and total

8 s were randomized to receive HSCT along with cyclophosphamide (200 mg/kg) and antithymocyte globulin

9 mg/m(2) on days 1, 8, and 15, and daily oral cyclophosphamide 25 mg/m(2), on days 1-28).

10 avenous fludarabine (25 mg/m(2) per day) and cyclophosphamide (250 mg/m(2) per day) for the first 3 d

11 ously of fludarabine (25 mg/m(2), days 1-3), cyclophosphamide (250 mg/m(2), days 1-3), and rituximab

12 ion, or with (2) irradiation (3 x 8 Gy), (3) cyclophosphamide, (4) cisplatin or (5) doxorubicin, all

13 , and post-transplantation cyclophosphamide (cyclophosphamide 50 mg/kg on days 3 and 4, followed by t

14 GVHD prophylaxis comprised intravenous cyclophosphamide 50 mg/kg per day on days 3 and 4 after

15 nt, patients were randomly assigned (1:1) to cyclophosphamide (500 mg daily orally on days 1, 8, and

16 udarabine (30 mg/m(2) body-surface area) and cyclophosphamide (500 mg/m(2) body-surface area) on days

17 [500 mg/m(2)], epirubicin [75 mg/m(2)], and cyclophosphamide [500 mg/m(2)]; day 1 of cycles 5-8) the

18 ; D7), busulfan (8 mg/kg D6 through D4), and cyclophosphamide (60 mg/kg/d D3; D2).

19 eting conditioning chemotherapy (intravenous cyclophosphamide [60 mg/kg] daily for 2 days followed by

20 ks x 4 doses) or AC (doxorubicin 60 mg/m(2); cyclophosphamide 600 mg/m(2) every 2-3 weeks x 4 doses)

21 rms by four times epirubicin 90 mg/m(2) plus cyclophosphamide 600 mg/m(2) every 3 weeks.

22 ive six cycles of docetaxel (75 mg/m(2)) and cyclophosphamide (600 mg/m(2)) every 3 weeks (DC) or thr

23 three cycles of epirubicin (90 mg/m(2)) and cyclophosphamide (600 mg/m(2)) followed by three cycles

24 ophenolate mofetil, and post-transplantation cyclophosphamide; 73 [82%] for tacrolimus, methotrexate,

25 All patients received cyclophosphamide 750 mg/m(2) and doxorubicin 50 mg/m(2)

26 Patients received cyclophosphamide 750 mg/m(2) on day 1 intravenously, dox

27 prednisolone (R-CHOP; rituximab 375 mg/m(2), cyclophosphamide 750 mg/m(2), doxorubicin 50 mg/m(2), an

28 x cycles of R-CHOP (rituximab [375 mg/m(2)], cyclophosphamide [750 mg/m(2)], doxorubicin [50 mg/m(2)]

29 phamide (TC) was superior to doxorubicin and cyclophosphamide (AC) in a trial in early breast cancer.

30 le-agent cisplatin (CDDP) versus doxorubicin-cyclophosphamide (AC) in BRCA carriers with stage I-III

31 tem cell transplantation with posttransplant cyclophosphamide, achieving results comparable to those

32 dministered KGF to mice 24 hours before i.p. cyclophosphamide administration, followed by histologic

33 pproaches that increase the response rate to cyclophosphamide, adriamycin, vincristine, and prednison

34 by 3 cycles of fluorouracil, epirubicin, and cyclophosphamide after surgery.

35 ioning can be safely combined with high-dose cyclophosphamide after transplantation, and the risk of

36 y, TH-MYCN transgenic mice were administered cyclophosphamide alone or in combination with an anti-GD

37 pression of MYC and BCL2 in combination with cyclophosphamide also significantly slowed tumor growth

38 As proof of principle, cyclophosphamide and diethylstilbestrol (DES), for which

39 We tested this hypothesis by administering cyclophosphamide and doxorubicin (Cyclo/Dox), a common t

40 osphamide, methotrexate, and fluorouracil or cyclophosphamide and doxorubicin) or capecitabine.

41 cutaneous enfuvirtide during post-transplant cyclophosphamide and during oral medication intolerance.

42 ctinomycin, and doxorubicin alternating with cyclophosphamide and etoposide) and radiation therapy.

43 Twenty of 24 patients received cyclophosphamide and fludarabine lymphodepletion and CD1

44 in patients with aggressive NHL treated with cyclophosphamide and fludarabine lymphodepletion followe

45 ) treated on a phase 1/2 clinical trial with cyclophosphamide and fludarabine lymphodepletion followe

46 ter lymphodepletion, and higher intensity of cyclophosphamide and fludarabine lymphodepletion was ass

47 h marrow tumor burden, lymphodepletion using cyclophosphamide and fludarabine, higher CAR T-cell dose

48 receiving a conditioning regimen of low-dose cyclophosphamide and fludarabine.

49 tine alone, bendamustine and fludarabine, or cyclophosphamide and fludarabine.

50 The remission was achieved with cyclophosphamide and methylprednisolone systemic therapy

51 s generated by MVA-5T4 vaccination; however, cyclophosphamide and MVA-5T4 each independently induced

52 etoposide, vincristine, and doxorubicin with cyclophosphamide and prednisone (EPOCH), were identified

53 e breast cancer (TNBC) include anthracycline-cyclophosphamide and taxane-based chemotherapy.

54 mice were given carboplatin, doxorubicin, or cyclophosphamide and were cotreated with AAV9-MIS, recom

55 apy, typically with mycophenolate mofetil or cyclophosphamide and with glucocorticoids, although thes

56 mmendations, alkylating drugs (bendamustine, cyclophosphamide) and proteasome inhibitors (bortezomib,

57 D prophylaxis of tacrolimus, post-transplant cyclophosphamide, and CD28 blockade induces multi-lineag

58 EPOCH (etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin) is a preferred regime

59 r Study 5 (NWTS-5; vincristine, doxorubicin, cyclophosphamide, and etoposide plus radiotherapy) would

60 Doses of doxorubicin, cyclophosphamide, and etoposide were reduced midstudy be

61 ing regimen (2 Gy of total-body irradiation, cyclophosphamide, and fludarabine) and graft-versus-host

62 el of chemotherapy-induced gonadotoxicity by cyclophosphamide, and inhibition of mTOR complex 1 (mTOR

63 gemcitabine group; n=1576) or to epirubicin, cyclophosphamide, and paclitaxel (control group; n=1576)

64 o one of two treatment regimens: epirubicin, cyclophosphamide, and paclitaxel (four cycles of 90 mg/m

65 received neoadjuvant dose-dense doxorubicin, cyclophosphamide, and paclitaxel chemotherapy, followed

66 usion on day 1 every 3 weeks) or epirubicin, cyclophosphamide, and paclitaxel plus gemcitabine (the s

67 Fludarabine, cyclophosphamide, and rituximab (FCR) can improve diseas

68 Fludarabine, cyclophosphamide, and rituximab (FCR) has become a gold-

69 (U-MRD) status after first-line fludarabine, cyclophosphamide, and rituximab (FCR) have prolonged pro

70 tandard chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab, in patients with previo

71 cles of chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab.

72 5 of whom were conditioned with fludarabine, cyclophosphamide, and total-body irradiation, underwent

73 ophenolate mofetil, and post-transplantation cyclophosphamide; and six were excluded.

74 cal transplantation with the post-transplant cyclophosphamide approach but with differing patterns of

75 ve non-Hodgkin lymphoma, and doxorubicin and cyclophosphamide are both associated with left ventricul

76 We used post-transplant cyclophosphamide as graft-versus-host disease (GVHD) pro

77 By using post-transplant cyclophosphamide as GVHD prophylaxis, we successfully ex

78 nab-paclitaxel followed by doxorubicin plus cyclophosphamide as neoadjuvant treatment for early-stag

79 (sb) paclitaxel followed by epirubicin plus cyclophosphamide as neoadjuvant treatment in patients wi

80 g on day -3 (except the post-transplantation cyclophosphamide, as indicated), with a target level of

81 ks followed by doxorubicin at 60 mg/m(2) and cyclophosphamide at 600 mg/m(2) every 2 weeks for 8 week

82 sity conditioning regimen and posttransplant cyclophosphamide-based graft-versus-host disease (GVHD)

83 Conclusion Post-transplantation cyclophosphamide-based HAPLO transplantation results in

84 n lymphoma who received post-transplantation cyclophosphamide-based haploidentical (HAPLO) allogeneic

85 edge, this is the first systematic report on cyclophosphamide-based treatment of acute AMR based on m

86 les, chemotherapy was reinforced with either cyclophosphamide (BD group) or thalidomide (C-BD group).

87 ponse-adapted intensification treatment with cyclophosphamide, bortezomib, and dexamethasone (CVD) ve

88 e approved for light chain (AL) amyloidosis, cyclophosphamide, bortezomib, and dexamethasone (CyBorD)

89 splantation platform: 247 receiving busulfan/cyclophosphamide (BuCy) conditioning (data collected ret

90 The clinical success of cyclophosphamide (C)-based haploidentical stem-cell tran

91 rtezomib plus dexamethasone (BD), or BD plus cyclophosphamide (C-BD).

92 nly for adults who receive anthracycline and cyclophosphamide chemotherapy; and the addition of a neu

93 We investigated whether cyclophosphamide combined with plasmapheresis and intrav

94 report that lymphodepleting chemotherapy by cyclophosphamide (CTX) does not lead to increased availa

95 s significantly increased when the alkylator cyclophosphamide (CTX) is added to TLI/ATS conditioning.

96 orts: 1) 1-5 x 108 CART-BCMA cells alone; 2) Cyclophosphamide (Cy) 1.5 g/m2 + 1-5 x 107 CART-BCMA cel

97 cells transferred after lymphodepletion with cyclophosphamide (Cy) transiently control tumor growth b

98 tcomes in response to rituximab (RTX) versus cyclophosphamide (CYC) and plasma exchange (PLEX).

99 ophenolate mofetil, and post-transplantation cyclophosphamide (cyclophosphamide 50 mg/kg on days 3 an

100 Cyclophosphamide (CyP) immunosuppressed or RAG2 knockout

101 regimens involving the anti-CD3 (alphaCD3), cyclophosphamide (CyP), and IAC (IL-2/JES6-1) antibody c

102 ding omalizumab, as well as corticosteroids, cyclophosphamide, dapsone, mycophenolate mofetil, plasma

103 Cyclophosphamide depleted regulatory T cells in 24 of 27

104 Prior depletion of regulatory T cells by cyclophosphamide did not increase immune responses gener

105 ministration with docetaxel, epirubicin, and cyclophosphamide did not prolong RFS or survival compare

106 Adding cyclophosphamide did not sufficiently improve the effica

107 ssigned to an intergroup metronomic trial of cyclophosphamide, doxorubicin, and paclitaxel were queri

108 efficacy and safety of brentuximab vedotin, cyclophosphamide, doxorubicin, and prednisone (A+CHP) ve

109 brentuximab vedotin (BV) in combination with cyclophosphamide, doxorubicin, and prednisone (BV-CHP) v

110 mbination with rituximab or obinutuzumab and cyclophosphamide, doxorubicin, and prednisone (CHP) in p

111 adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R

112 the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednison

113 uximab (DA-EPOCH-R) with standard rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

114 s had inferior outcomes after rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

115 o were uniformly treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

116 cristine, prednisone; n = 45, rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

117 ived one 21-day cycle of standard rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

118 tatistic, 0.75; P = .011; and rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

119 ide, doxorubicin, and prednisone (BV-CHP) vs cyclophosphamide, doxorubicin, vincristine, and predniso

120 , doxorubicin, and prednisone (A+CHP) versus cyclophosphamide, doxorubicin, vincristine, and predniso

121 omised trial of front-line chemotherapy with cyclophosphamide, doxorubicin, vincristine, and predniso

122 ing long-term progression-free survival over cyclophosphamide, doxorubicin, vincristine, and predniso

123 of the addition of bortezomib to rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

124 dipasvir and chemotherapy (14 rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

125 xorubicin, vincristine, and prednisone and 6 cyclophosphamide, doxorubicin, vincristine, and predniso

126 DLBCL cases treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

127 tients uniformly treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

128 cles of rituximab followed by four cycles of cyclophosphamide, doxorubicin, vincristine, and predniso

129 Anthracycline-containing regimens, namely cyclophosphamide, doxorubicin, vincristine, and predniso

130 Cyclophosphamide, doxorubicin, vincristine, and predniso

131 unconfirmed after first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

132 luate the benefit of RT after rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

133 cohort comprising 395 patients treated with cyclophosphamide, doxorubicin, vincristine, and predniso

134 oma (DLBCL) is rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and predniso

135 b, plus chemotherapy (six-to-eight cycles of cyclophosphamide, doxorubicin, vincristine, and predniso

136 We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

137 and prednisone) with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

138 m 1998 to 2009 with frontline rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

139 ront-line therapy with either rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

140 ival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

141 hem treated with R-CHOP biweekly (rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

142 A regimen of cyclophosphamide, doxorubicin, vincristine, and predniso

143 ammes used for other diseases, such as CHOP (cyclophosphamide, doxorubicin, vincristine, and predniso

144 The integration of rituximab (R) into cyclophosphamide, doxorubicin, vincristine, and predniso

145 Immunochemotherapy with rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

146 esponding patients to R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and predniso

147 referred treatment is abbreviated rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

148 e of PMBCL primarily treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

149 in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

150 The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and predniso

151 mbination with rituximab or obinutuzumab and cyclophosphamide, doxorubicin, vincristine, and predniso

152 leomycin, prednisone (R-ACVBP) or rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (

153 classifier was not prognostic for rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone o

154 of plasma samples collected under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-C

155 el plus capecitabine followed by 3 cycles of cyclophosphamide, epirubicin, and capecitabine (TX+CEX).

156 cycles of docetaxel followed by 3 cycles of cyclophosphamide, epirubicin, and fluorouracil (T+CEF),

157 Jude Lifetime Cohort treated with cyclophosphamide equivalent dose (CED) >=4,000 mg/m(2).

158 herapy at any dose, and alkylating agents at cyclophosphamide equivalent doses of 4,000 mg/m(2) or gr

159 higher doses of testicular radiotherapy, and cyclophosphamide equivalent doses.

160 ow transplantation with post-transplantation cyclophosphamide expanded the donor pool while limiting

161 ly leads to abnormal urothelial repair after cyclophosphamide exposure from pathologic basal cell end

162 ent solid cancers and breast cancer, whereas cyclophosphamide exposure increases the risk of subseque

163 and basal cell endoreplication 3 days after cyclophosphamide exposure versus controls.

164 Three days after cyclophosphamide exposure, Fgfr2KO urothelium had defect

165 nitors or other urothelial cells 1 day after cyclophosphamide exposure.

166 factor receptor (FGFR) 2 in urothelium after cyclophosphamide exposure.

167 cells reproduced Fgfr2KO abnormalities after cyclophosphamide exposure.

168 The preparative regimen included busulfan, cyclophosphamide, fludarabine, and rabbit anti-thymocyte

169 area after lymphodepleting conditioning with cyclophosphamide/fludarabine (Cy/Flu).

170 e treated by sequential NAC (epirubicin plus cyclophosphamide followed by docetaxel with or without c

171 d to receive tandem transplant with thiotepa/cyclophosphamide followed by dose-reduced carboplatin/et

172 acil, epirubicin [100 mg/m(2) per dose], and cyclophosphamide), followed by 3 cycles of concurrent do

173 oadjuvant chemotherapy with doxorubicin plus cyclophosphamide, followed by paclitaxel, and had a comp

174 monotherapy; GFR=30-59 ml/min per 1.73 m(2): cyclophosphamide for 3 months followed by azathioprine p

175 raviroc, bortezomib, or post-transplantation cyclophosphamide for GvHD prophylaxis compared with cont

176 completed 4 cycles of dose-dense doxorubicin-cyclophosphamide for stage I-III breast cancer received

177 concentrations of the chemotherapeutic drugs cyclophosphamide, gemcitabine (GEM) and oxaliplatin (OXP

178 We hypothesized that high-dose cyclophosphamide given after G-CSF-mobilized blood cell

179 Patients randomized to a cyclophosphamide group received 50 mg twice daily on tre

180 ing chemotherapy included high-dose (3 g/m2) cyclophosphamide (HD-Cy) for 17 patients and low-dose (<

181 , cyclosporine, plasmapheresis, thalidomide, cyclophosphamide, hemoperfusion, tumor necrosis factor i

182 Taken together, these results indicate that cyclophosphamide improves Fli1 deficiency-dependent vasc

183 men that contains docetaxel, epirubicin, and cyclophosphamide improves survival outcomes of patients

184 10(-8) M for paclitaxel and 5 x 10(-9) M for cyclophosphamide in blood serum.

185 ates were utilized for TDM of paclitaxel and cyclophosphamide in blood serum.

186 ate cytotoxicity of platinum-based drugs and cyclophosphamide in cancer cells.

187 cal transplantation with posttransplantation cyclophosphamide in combination with CTLA4Ig-based T-cos

188 sensitivity to a standard chemotherapy drug, cyclophosphamide, in DLBCL cell lines.

189 oxic injury, thereby preventing both IR- and cyclophosphamide-induced alopecia.

190 Keratinocyte growth factor (KGF) improves cyclophosphamide-induced bladder injury.

191 Cyclophosphamide-induced immunosuppression led to recrud

192 KGF pretreatment blocks cyclophosphamide-induced intermediate and basal cell apo

193 Consistent with these findings, during cyclophosphamide-induced myeloablation or specific monoc

194 During myeloid replenishment after cyclophosphamide-induced myeloablation, BCAP(-/-) mice h

195 Biweekly cyclophosphamide injection improved vascular permeabilit

196 otrexate, and fluorouracil (CMF; 600 mg/m(2) cyclophosphamide intravenously on days 1 and 8 or 100 mg

197 Dexamethasone-rituximab-cyclophosphamide is an alternative, particularly for non

198 em cell transplantation using posttransplant cyclophosphamide is associated with low rates of severe

199 At 6 and 24 hours after cyclophosphamide, KGF-pretreated mice also had apparent

200 y) for 17 patients and low-dose (<=1.5 g/m2) cyclophosphamide (LD-Cy) for 8 patients.

201 -eligible pathways for patients treated with cyclophosphamide, lenalidomide, and dexamethasone (CRD)

202 osphamide, thalidomide, and dexamethasone or cyclophosphamide, lenalidomide, and dexamethasone) and a

203 set of patients who received fludarabine and cyclophosphamide lymphodepletion.

204 Cyclophosphamide may cause hemorrhagic cystitis and even

205 owed by four 4-week cycles of either classic cyclophosphamide, methotrexate, and fluorouracil (CMF; 6

206 t chemotherapy (physician's choice of either cyclophosphamide, methotrexate, and fluorouracil or cycl

207 Immunosuppressive therapies (ie, intravenous cyclophosphamide, methotrexate, and infliximab) in these

208 investigate the molecular mechanism by which cyclophosphamide mitigates SSc vasculopathy, we employed

209 al protocol) or with busulfan, thiotepa, and cyclophosphamide (modified protocol).

210 y (n = 19), and a combination of MVA-5T4 and cyclophosphamide (n = 18).

211 transplanted recipients (TBI of 850 cGy plus cyclophosphamide of 60 mg/kg per day for 2 days).

212 fludarabine of 100 mg/kg per day for 5 days, cyclophosphamide of 60 mg/kg per day for 2 days, and tot

213 n and 600 mg/m(2) intravenously administered cyclophosphamide on day 1 every 3 weeks, followed by fou

214 gether with vinorelbine on days 1 and 8, and cyclophosphamide on day 1 for a maximum of 12 cycles.

215 may help to explain the beneficial effect of cyclophosphamide on SSc vasculopathy.

216 lymphocyte response upon immunotherapy with cyclophosphamide or anti-PD-1 antibodies.

217 When use of cyclophosphamide or rituximab was compared with all othe

218 All patients received cyclophosphamide or rituximab.

219 g cytotoxic agents was found for exposure to cyclophosphamide (OR, 3.58; 95% CI, 0.91-14.11) followed

220 increased using MVA-5T4, metronomic low-dose cyclophosphamide, or a combination of both treatments.

221 Conditioning was performed with busulfan and cyclophosphamide (original protocol) or with busulfan, t

222 nd the United States (P = .017), with either cyclophosphamide (P = .01) or rituximab therapy (P = .00

223 0.001) and the US (P=0.017), as well as with cyclophosphamide (P=0.01) and rituximab therapy (P=0.001

224 nrolled and randomly assigned to epirubicin, cyclophosphamide, paclitaxel, and gemcitabine (gemcitabi

225 y adopted in the United States: doxorubicin, cyclophosphamide, paclitaxel, and trastuzumab (ACTH) and

226 itaxel portion of the dose-dense doxorubicin-cyclophosphamide-paclitaxel regimen.

227 Cyclophosphamide plus fludarabine conditioning chemother

228 ow-dose chemotherapy conditioning regimen of cyclophosphamide plus fludarabine.

229 h melphalan-prednisone-lenalidomide (MPR) or cyclophosphamide-prednisone-lenalidomide (CPR) or lenali

230 Future studies will show, whether cyclophosphamide proves to be a valuable alternative for

231 The use of posttransplant cyclophosphamide (PT-Cy) as graft-versus-host disease (G

232 Posttransplantation cyclophosphamide (PTCy) can function as single-agent GVH

233 The safety and feasibility of posttransplant cyclophosphamide (PTCY) in this setting have been report

234 Post-transplantation cyclophosphamide (PTCy) recently has had a marked impact

235 transplantation (h-HSCT) with posttransplant cyclophosphamide (PTCY) using peripheral blood stem cell

236 ies, including high-dose posttransplantation cyclophosphamide (PTCy), have been developed to allow fo

237 em cell transplantation using posttransplant cyclophosphamide (PTCy).

238 Intravenous cyclophosphamide pulse, a standard treatment for systemi

239 re significantly increased after intravenous cyclophosphamide pulse.

240 ith biopsy-proven acute AMR with intravenous cyclophosphamide pulses (15 mg/kg adapted to age and ren

241 Treatment was completed after 6 cyclophosphamide pulses or in case of return to baseline

242 patients received second-line immunotherapy (cyclophosphamide, rituximab, or both).

243 vival (PFS) after treatment with fludarabine-cyclophosphamide-rituximab (FCR) chemoimmunotherapy.

244 ergoing 2 types of chemotherapy: oxaliplatin/cyclophosphamide, shown to induce immunogenic cell death

245 Guidelines recommend steroid plus cyclical cyclophosphamide (St-Cp) therapy for patients with idiop

246 Immunosuppression with cyclophosphamide stabilised luciferase expression, sugge

247 Cyclophosphamide, systemic cytarabine, and central nervo

248 ompared TC6 with docetaxel, doxorubicin, and cyclophosphamide (TAC6).

249 disease (GVHD) prophylaxis included post-HCT cyclophosphamide, tacrolimus, and mycophenolate mofetil.

250 Purpose Docetaxel and cyclophosphamide (TC) was superior to doxorubicin and cy

251 herapy standard (six cycles of docetaxel and cyclophosphamide [TC]) in the routine treatment of human

252 ophenolate mofetil, and post-transplantation cyclophosphamide; ten (11%) had grade 3 and 68 (76%) had

253 k of VTE compared with patients treated with cyclophosphamide, thalidomide, and dexamethasone (CTD) (

254 assigned induction therapy as per protocol (cyclophosphamide, thalidomide, and dexamethasone or cycl

255 zero) occurred more often in patients given cyclophosphamide than mycophenolate mofetil.

256 Most patients (80/103, 77.7%) received cyclophosphamide therapy.

257 or immunotherapy, using prior treatment with cyclophosphamide to create a therapeutic window of minim

258 rapy, we delivered multicycle treatment with cyclophosphamide to Th-MYCN mice, individualizing therap

259 l neutralizing monoclonal antibody using the cyclophosphamide transient suppression model.

260 Throughout decades, cyclophosphamide treatment has been proven to be effecti

261 age injected dose per gram), but oxaliplatin/cyclophosphamide treatment led to close to a 2.4-fold hi

262 er and randomized to watch and wait (n = 9), cyclophosphamide treatment only (n = 9), MVA-5T4 only (n

263 nction with transcriptome analyses following cyclophosphamide treatment to reveal that Atm deficiency

264 At 10 and 28 days after cyclophosphamide treatment, KGF-pretreated mice had litt

265 At 1 to 28 days after cyclophosphamide treatment, mostly KRT14(+) basal progen

266 may be preferentially eradicated by low-dose cyclophosphamide treatment.

267 g induction regimen (cisplatin, carboplatin, cyclophosphamide, vincristine, and etoposide with or wit

268 ith rituximab, when used in combination with cyclophosphamide, vincristine, and prednisone (CVP) in p

269 inetics, and pharmacodynamics of GP2013 plus cyclophosphamide, vincristine, and prednisone (GP2013-CV

270 ne, and prednisone [CHOP] or eight cycles of cyclophosphamide, vincristine, and prednisone [CVP]), ev

271 FOLL05 trial compared R-CVP (rituximab plus cyclophosphamide, vincristine, and prednisone) with R-CH

272 142 patients with FL treated with rituximab, cyclophosphamide, vincristine, and prednisone, and a cli

273 a historical cohort treated with rituximab, cyclophosphamide, vincristine, and prednisone, event-fre

274 of the hyper-CVAD regimen (hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexameth

275 plant-eligible patients randomly assigned to cyclophosphamide, vincristine, doxorubicin, and dexameth

276 uding twice-daily plasma exchange; pulses of cyclophosphamide, vincristine, or cyclosporine A; or sal

277 d that dose-adjusted etoposide, doxorubicin, cyclophosphamide, vincristine, prednisone, and rituximab

278 d in the independent cohorts (rituximab plus cyclophosphamide, vincristine, prednisone: OR, 2.95; c-s

279 systemic treatment (n = 138, rituximab plus cyclophosphamide, vincristine, prednisone; n = 45, ritux

280 ourses of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

281 escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

282 iority of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

283 cycles of bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

284 escalated bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

285 BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednis

286 dominantly bleomycin, etoposide, doxorubicin cyclophosphamide, vincristine, procarbazine, and prednis

287 r half with R-ACVBP (rituximab, doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone),

288 e efficacy of either rituximab, doxorubicin, cyclophosphamide, vindesine, bleomycin, prednisone (R-AC

289 ificant increase in signal after oxaliplatin/cyclophosphamide was also observed in the A9F1 model (0.

290 The use of cyclophosphamide was associated with a greater chance of

291 In addition, cyclophosphamide was found to increase sarcoma risk in a

292 oietic transplantation using post-transplant cyclophosphamide was originally described using bone mar

293 pecific Fli1 knockout mice, a single dose of cyclophosphamide was sufficient to normalize the decreas

294 ophenolate mofetil, and post-transplantation cyclophosphamide was the most promising intervention, yi

295 responses following induction of cystitis by cyclophosphamide were also observed in both NaV 1.7(Nav1

296 de with alternating periods of etoposide and cyclophosphamide, whereas the other arm received placebo

297 ne and 50% for vincristine, doxorubicin, and cyclophosphamide, which shortened the treatment duration

298 derwent lymphodepletion with fludarabine and cyclophosphamide with or without alemtuzumab, then child

299 patients with recurrences were treated with cyclophosphamide with or without plasmapheresis, and 2 o

300 whether use of oral capecitabine instead of cyclophosphamide would be non-inferior in terms of patie