ライフサイエンスコーパス: chemotherapy

1 herapy boost based on margins with continued chemotherapy).

2 reduced therapeutic efficacy of conventional chemotherapy.

3 pplements, other than a multivitamin, during chemotherapy.

4 platinum to anthracycline- and taxane-based chemotherapy.

5 n patients who received rituximab-containing chemotherapy.

6 use of DC compared with anthracycline-based chemotherapy.

7 r that should be given prior to conventional chemotherapy.

8 capacity for self-renewal and resistance to chemotherapy.

9 ors associated with the use of postoperative chemotherapy.

10 logram of body weight) after lymphodepleting chemotherapy.

11 ut less than 60 mL/min, or those who refused chemotherapy.

12 d antitumor efficacy when administered after chemotherapy.

13 cal cancer who received rituximab-containing chemotherapy.

14 reatment opportunity for patients undergoing chemotherapy.

15 es that are currently treated with high-dose chemotherapy.

16 sed apoptosis following serum deprivation or chemotherapy.

17 vomiting (CINV) is a significant toxicity of chemotherapy.

18 r shorter-term mortality after intensive AML chemotherapy.

19 iprocal interaction of circadian rhythms and chemotherapy.

20 shed disease after abrogation of the initial chemotherapy.

21 se rates despite best-available conventional chemotherapy.

22 nd increased overall survival, compared with chemotherapy.

23 ing chemotherapy and enhance the efficacy of chemotherapy.

24 asis of MammaPrint may safely avoid adjuvant chemotherapy.

25 oprotective therapeutic agents during cancer chemotherapy.

26 of cancer progression, and poor responses to chemotherapy.

27 nd evaluates the immunomodulatory effects of chemotherapy.

28 nts and evaluating disease persistence after chemotherapy.

29 ncy factor gene transcription in response to chemotherapy.

30 me integrity, tumorigenesis, and response to chemotherapy.

31 cell death; an effect further potentiated by chemotherapy.

32 nduced neuropathic pain models during cancer chemotherapy.

33 ly poor, as they are resistant to first line chemotherapy.

34 event and the time to first use of cytotoxic chemotherapy.

35 umor grade, poor survival, and resistance to chemotherapy.

36 e consistent with effects of the preparative chemotherapy.

37 within 12 months of neoadjuvant or adjuvant chemotherapy.

38 target for HDT in TB in adjunct to canonical chemotherapy.

39 ed inhibitor rather than a broadly cytotoxic chemotherapy.

40 tructure, and engineer NPs of this polymeric chemotherapy.

41 oor prognosis when treated with conventional chemotherapy.

42 rior anthracycline- and/or taxane-containing chemotherapy.

43 when treated with atezolizumab but not with chemotherapy.

44 ts tend to tolerate these agents better than chemotherapy.

45 duction of apoptosis and re-sensitization to chemotherapy.

46 w reduction in the intensity and duration of chemotherapy.

47 genome evolution in response to hormonal and chemotherapy.

48 ) were developed as a carrier of DOX for GBM chemotherapy.

49 need for cardiac monitoring during and after chemotherapy.

50 resection and adjuvant radiotherapy (RT) and chemotherapy.

51 84 (75.4%) patients who received neoadjuvant chemotherapy, 105 (89%) simultaneous venous resections,

52 xygen species (ROS), ionizing radiation, and chemotherapies, activate acid sphingomyelinase (ASMase)

53 Cytotoxic chemotherapy administration was not significantly associ

54 eases sensitivity to the DNA damage-inducing chemotherapy agent doxorubicin.

55 Cisplatin is a commonly used chemotherapy agent with significant dose-limiting neurot

56 outcomes due to development of resistance to chemotherapy agents and the EGFR inhibitors, which resul

57 n CSS was significantly superior compared to chemotherapy alone (56 vs 30 months, P < 0.001).

58 on provides a better survival advantage over chemotherapy alone after upfront resection of PDAC.

59 ight have been treatment-related (one in the chemotherapy alone group and four in the chemotherapy pl

60 doubling the duration of mouse survival over chemotherapy alone, whilst protecting endogenous HSC.

61 deficit unpredicted by our previous study of chemotherapy alone.

62 alins B (LMB) chemotherapy with standard LMB chemotherapy alone.

63 132 patients were assigned chemotherapy and 129 surveillance.

64 therapy), and neoadjuvant chemoradiotherapy (chemotherapy and 45 Gy radiotherapy, then surgery and ra

65 , radiotherapy (55.8 Gy), chemoradiotherapy (chemotherapy and 55.8 Gy radiotherapy), and neoadjuvant

66 eatectomy, 155 (63%) initiated postoperative chemotherapy and 90 (37%) did not.

67 reduction and discontinuation of life-saving chemotherapy and a permanently impaired quality of life

68 tients who underwent surgery and gemcitabine chemotherapy and analyzed them by immunohistochemistry.

69 re intrinsically resistant to platinum-based chemotherapy and are enriched with intracellular antioxi

70 uropathy on the systemic interaction between chemotherapy and cancer.

71 cells survive unfavorable conditions such as chemotherapy and cause relapse.

72 h (y)pT and (y)pN, and predicted response to chemotherapy and chemoradiation irrespective of anatomic

73 h-dose (HD; 74 Gy) radiation with concurrent chemotherapy and determined the efficacy of cetuximab fo

74 lter the biological response to DNA-damaging chemotherapy and enhance the efficacy of chemotherapy.

75 x microenvironment, and is resistant to both chemotherapy and immune checkpoint blockade.

76 e activity in the standard mouse model of TB chemotherapy and in a mouse model of human-like necrotic

77 ta highlight a role for A3B in resistance to chemotherapy and indicate that stimulation of A3B expres

78 sive TNBC biology by promoting resistance to chemotherapy and inducing a prometastatic transcriptiona

79 Progression during initial or reinduction chemotherapy and initial high-risk disease are risk fact

80 ct [APD] cohort) treated with combined BVZ + chemotherapy and investigated previously reported predic

81 Chemotherapy and irradiation cause DNA damage to hematop

82 o accelerate immune reconstitution following chemotherapy and is being pursued for biosimilar develop

83 ncer response after one cycle of neoadjuvant chemotherapy and may improve response prediction when us

84 ion of adjunctive upfront treatments such as chemotherapy and novel anti-androgen agents has further

85 n our quest to circumvent the limitations of chemotherapy and photodynamic therapy, we have engineere

86 A predicts inferior response to preoperative chemotherapy and poor survival in patients with CLM.

87 Inhibition of PIM sensitized NSCLC cells to chemotherapy and produced a synergistic antitumor respon

88 sk feature, and an indicator for neoadjuvant chemotherapy and prognosis.

89 s are frequently resistant to platinum-based chemotherapy and provide TP53 mutations as potential tar

90 nvestigated the benefit of combined adjuvant chemotherapy and radiotherapy (CTRT) versus radiotherapy

91 isted of surgical resection during induction chemotherapy and radiotherapy after last SCT.

92 RAD51AP1 KD improved chemotherapy and radiotherapy response by inhibiting BCS

93 therapy), were not candidates for high-dose chemotherapy and subsequent autologous stem-cell transpl

94 tent with the known sensitivity of LELC-B to chemotherapy and suggests that immune checkpoint therapy

95 jority of patients received a combination of chemotherapy and surgery.

96 ients received no therapy, 113 received just chemotherapy, and 20 received just radiation.

97 ensity score based on age, staging, surgery, chemotherapy, and center size.

98 lity of TNBC cells, sensitized TNBC cells to chemotherapy, and restricted the TNBC stem cell populati

99 clinical complete response after neoadjuvant chemotherapy, and who were subsequently managed by a wat

100 y but did not receive it; those who received chemotherapy; and those for whom chemotherapy was not re

101 r dietary supplements both before and during chemotherapy are consistent with recommendations for cau

102 differential responses of APC-mutant CRCs to chemotherapy are not well understood.

103 inoma after progression on gemcitabine-based chemotherapy are urgently needed.

104 o cooperate with DNA-damaging or antimitotic chemotherapies as the former prevent cell-cycle entry, t

105 We applied the PDXGEM to several cytotoxic chemotherapies as well as targeted therapy agents that a

106 Addition of atezolizumab to platinum-based chemotherapy as first-line treatment prolonged progressi

107 tions in polyamine metabolism in response to chemotherapy, as well as DFMO-induced preferential sensi

108 he remaining recommendations for second-line chemotherapy, as well as other recommendations related t

109 s that aneuploidy brings about resistance to chemotherapies because of a general feature of the aneup

110 years but considered unsuitable for standard chemotherapy because of a cardiac ejection fraction of l

111 A patient-specific estimator of absolute chemotherapy benefit was computed using individualized r

112 nto three groups: those who were recommended chemotherapy but did not receive it; those who received

113 ntly worse prognosis and do not benefit from chemotherapy, but the mechanisms underlying the differen

114 ceive appropriate surgery, radiotherapy, and chemotherapy by 2023, which would increase to 90% by 203

115 Potentiating radiotherapy and chemotherapy by inhibiting DNA damage repair is proposed

116 sent a therapeutic strategy termed "targeted chemotherapy" by depleting protein phosphatase 2A (PP2A)

117 Chemotherapy causes off-target toxicity and is often ine

118 Chemotherapy consisted of oxaliplatin 85 mg/m(2) adminis

119 fety run-in with VEN 600 mg, patients in the chemotherapy-containing cohort were randomized to either

120 totic-tumor bodies, such as those induced by chemotherapies, contributes to the formation of an immun

121 , and the relationship between the number of chemotherapy cycles and time between two consecutive che

122 rapy cycles and time between two consecutive chemotherapy cycles.

123 We noted that SNI-1 enhances chemotherapy-dependent growth inhibition of a variety of

124 The addition of capivasertib to chemotherapy did not extend cPFS in mCRPC irrespective o

125 Perioperative FOLFOX chemotherapy did not improve major pathological response

126 t regeneration, and strongly synergizes with chemotherapy, doubling the duration of mouse survival ov

127 tment decisions have largely centered around chemotherapy drug intensity.

128 he DHCR7 inhibitors including AY9944 and the chemotherapy drug tamoxifen promoted clearance of Zika v

129 potentially be developed for vaccination and chemotherapy drug transportation.

130 id tumors are dominated by a set of standard chemotherapy drugs, and alternative therapies are used o

131 DNA damage induced by chemotherapy drugs, such as topoisomerase I inhibitors,

132 in, and A3B knockout enhances sensitivity to chemotherapy drugs.

133 t was computed using individualized relative chemotherapy effect from the randomized TAILORx and B-20

134 onal program; inhibition of TRIM37 increases chemotherapy efficacy and reduces metastasis risk in pat

135 fered significantly in preoperative systemic chemotherapy exposure, node-positive primary status, and

136 ion of ABCB1 by diverse stressors, including chemotherapy, facilitated escape of leukemia cells from

137 Patients received neoadjuvant SOC chemotherapy (FOLFIRINOX or gemcitabine/nab-paclitaxel)

138 effectively treated or cured with high-dose chemotherapy followed by autologous haematopoietic stem

139 Platinum-based neoadjuvant chemotherapy followed by delayed primary surgery (DPS) i

140 atients receiving platinum-based neoadjuvant chemotherapy followed by DPS in the ICON8 trial.

141 odal or margin involvement or LVI), adjuvant chemotherapy followed by radiation provides a better sur

142 Patients receiving second-line chemotherapy followed by resection had significantly wor

143 S and PFS than patients receiving first-line chemotherapy followed by resection.

144 despite the combined treatment of radio- and chemotherapy following surgical removal.

145 Second-line (2 L) chemotherapies for advanced or metastatic gastric cancer

146 half of patients received monotherapy as 2 L chemotherapy for advanced/metastatic gastric cancer and

147 for human therapeutics and an alternative to chemotherapy for cancer.

148 zation (5%, 9%, 9%, P = 0.001), preoperative chemotherapy for colorectal liver metastases (70%, 82%,

149 CIST and GCIG CA125 responses to neoadjuvant chemotherapy for epithelial ovarian cancer should not be

150 ave received more than two previous lines of chemotherapy for metastatic breast cancer.

151 and had received up to two previous lines of chemotherapy for metastatic disease.

152 rity of 3 months versus 6 months of adjuvant chemotherapy for patients with stage III colon cancer wa

153 Docetaxel (DTX) has been used as a standard chemotherapy for the mCRPC.

154 lymphoma warrants further investigation as a chemotherapy-free option in this setting.

155 formed in an independent cohort with primary chemotherapy from Heidelberg, Germany.

156 group versus 12.1 months (10.9-14.0) in the chemotherapy group (0.85, 95% CI 0.72-1.02; p=0.075).

157 d pneumonitis), and one (<1%) patient in the chemotherapy group (acute kidney injury).

158 n=209) versus 12.1 months (10.4-15.0) in the chemotherapy group (n=207; hazard ratio 0.89, 95% CI 0.7

159 nths (IQR 8.7-24.9) in the atezolizumab plus chemotherapy group and 19.8 months (8.1-24.5) in the pla

160 d 19.8 months (8.1-24.5) in the placebo plus chemotherapy group.

161 to receive atezolizumab plus platinum-based chemotherapy (group A), atezolizumab monotherapy (group

162 py (group B), or placebo plus platinum-based chemotherapy (group C).

163 Women who did not receive chemotherapy had a more than 97% rate of 8-year freedom

164 55 (44%) of 126 participants who started chemotherapy had acute grade 3 or worse treatment-emerge

165 These multiple activities driven by chemotherapy have tradeoffs that depend on the specific

166 unresolvable UPR and possibly other forms of chemotherapy helping in a better stratification GBM pati

167 vasion (HR = 1.50 [1.01-2.23]), and adjuvant chemotherapy (HR = 0.69 [0.48-0.97]) were independent pr

168 t eye, 3 years after the last intra-arterial chemotherapy (IAC) injection.

169 ntil neutrophil recovery following induction chemotherapy (IC) in 97 AML patients.

170 ch CD82 promotes AML survival in response to chemotherapy identified a crucial role for enhanced prot

171 ed chemoradiation and postoperative adjuvant chemotherapy impairs tolerability and feasibility and do

172 Addition of trastuzumab to first-line chemotherapy improves overall survival in patients with

173 Perioperative or adjuvant chemotherapy improves survival in patients with stage 1B

174 of venetoclax in combination with intensive chemotherapy in AML is unknown.

175 placebo in combination with trastuzumab and chemotherapy in first-line HER2-positive metastatic oeso

176 tegies for overcoming resistance to platinum chemotherapy in lung adenocarcinoma has previously been

177 ignancies who are hospitalized for cytotoxic chemotherapy in noncritical care units.

178 The safety and activity of venetoclax plus chemotherapy in paediatric patients with heavily relapse

179 mab would enhance the antitumour activity of chemotherapy in patients with metastatic triple-negative

180 and PD-1 blockade may expand the benefit of chemotherapy in PDAC and warrants confirmation in subseq

181 alue in patients receiving atezolizumab plus chemotherapy in the first-line setting.

182 nd previous treatment with the same class of chemotherapy in the neoadjuvant or adjuvant setting (yes

183 oresistant MYCN-overexpressing PDX models to chemotherapy in vivo.

184 Chemotherapy included six cycles of ifosfamide 3 g/m(2)

185 tment of leishmaniasis relies exclusively on chemotherapy including amphotericin B (AmB), miltefosine

186 Platinum-based chemotherapies, including oxaliplatin, are a mainstay in

187 Here, we show that cytotoxic chemotherapies induce dynamic changes in the tumor immun

188 macological inhibition of KDM6A also impairs chemotherapy-induced BCSC enrichment.

189 trient-starved tumors and protects them from chemotherapy-induced death.

190 MIR1249 modulated the chemotherapy-induced enrichment of CD133+ cells by contr

191 Chemotherapy-induced hair loss (alopecia) (CIA) remains

192 se results pinpoint the mechanistic basis of chemotherapy-induced hyperprogression and illustrate a t

193 Cannabinoids can alleviate chemotherapy-induced nausea and emesis and chronic pain.

194 Chemotherapy-induced nausea and vomiting (CINV) is a sig

195 Chemotherapy-induced peripheral neuropathy is among the

196 nstellation of neurologic disorders known as chemotherapy-induced peripheral neuropathy, mechanistic

197 A patient-reported outcome measure for chemotherapy-induced peripheral neurotoxicity in childre

198 metric properties of assessment measures for chemotherapy-induced peripheral neurotoxicity.

199 -derived TNBC cells in vitro, and attenuates chemotherapy-induced secretion of the pro-inflammatory c

200 These findings show that chemotherapy-induced small extracellular vesicles accele

201 em and progenitor cells, LSCs expanded under chemotherapy-induced stress.

202 Targeted chemotherapy induces the DNA damage response without cau

203 FL received obinutuzumab- or rituximab-based chemotherapy induction.

204 Gemcitabine-platinum combination chemotherapy initiated within 90 days after nephroureter

205 lerance, compliance to oral supplementation, chemotherapy interruptions and delays, quality of life,

206 sponds to microstructural changes induced by chemotherapy, is feasible within clinical scan times and

207 ase-related (acute leukemia, curative intent chemotherapy), laboratory-related (platelet count < 50 x

208 etastatic breast cancer who had received <=2 chemotherapy lines in the metastatic setting.

209 o ameliorate the acute toxicities induced by chemotherapy, long-term comorbidities including bone los

210 Rituximab added to standard LMB chemotherapy markedly prolonged event-free survival and

211 ether, this research uncovers a mechanism of chemotherapy-mediated metastasis by which drug-induced u

212 It also resulted in increased chemotherapy (melphalan) activity, as measured by format

213 ons possibly associated with radiotherapy or chemotherapy (n = 13) caused the death in the majority o

214 ith multi-drug resistance to the neoadjuvant chemotherapy (NAC).

215 or without fulvestrant with standard-of-care chemotherapy of physician's choice plus trastuzumab in w

216 The effect of treatment with platinum-based chemotherapy on CTGCT risk was assessed using multivaria

217 city of the method allows its application to chemotherapy optimization in different cancers.

218 s are quiescent, and thus, do not respond to chemotherapies or radiation therapies, and they are not

219 cultures of 24 pediatric patients undergoing chemotherapy or hematopoietic stem cell transplantation

220 e less responsive than cutaneous melanoma to chemotherapy or immune checkpoint inhibitors, encouragin

221 there is evidence that genotoxic stress from chemotherapy or radiation therapy, ribosome biogenesis s

222 ide effects associated with the treatment of chemotherapy or radiotherapy.

223 ogic disease prognosis, and future plans for chemotherapy or transplantation.

224 cizumab, platinum-based two-drug combination chemotherapy, or non-platinum-based two-drug therapy.

225 53) when cardiac function was evaluated post-chemotherapy (p=0.017).

226 mellitus type II [OR, 2.9, P=0.041], certain chemotherapies [platinum derivatives; OR, 3.0, P=0.034],

227 the chemotherapy alone group and four in the chemotherapy plus cetuximab group).

228 ession-free survival versus standard-of-care chemotherapy plus trastuzumab while showing a tolerable

229 Nineteen dogs at the end of the 19-week chemotherapy protocol (8 Complete Response and 11 Progre

230 pite the introduction of anthracycline-based chemotherapy protocols, with or without autologous haema

231 ational platform developed allows optimizing chemotherapy protocols, within admissible limits of toxi

232 itors with immune checkpoint blockade (ICB), chemotherapy, radiation, and/or diet now offer new appro

233 undergoing multimodal therapy (surgery with chemotherapy, radiation, or chemoradiation).

234 th pillar of cancer care, alongside surgery, chemotherapy, radiotherapy, and targeted therapy.

235 egy could be further explored to combine the chemotherapy/radiotherapy treatment to enhance the thera

236 astic tumors (GTT) resistant to single-agent chemotherapy receive alternative chemotherapy regimens,

237 under anti-PD-L1 monotherapy as compared to chemotherapy, reflecting the Th17 polarization of these

238 rded with frequently reported events for the chemotherapy regimen.

239 nase inhibitor, despite the use of high-risk chemotherapy regimens and frequent HSCT upon first remis

240 ideline on the selection of optimal adjuvant chemotherapy regimens for early breast cancer and adjuva

241 n of SMPD1 was associated with resistance to chemotherapy regimens that include 5-FU.

242 are important components of prostate cancer chemotherapy regimens, but their oral administration is

243 ingle-agent chemotherapy receive alternative chemotherapy regimens, which, although effective, cause

244 Most conventional chemotherapies remain limited by ineffective blood-brain

245 preferential sensitization of TNBC cells to chemotherapy, reported here suggest that ODC may be a ta

246 Since chemotherapy represents the established backbone of PDAC

247 Patients with primary chemotherapy resected at the Massachusetts General Hospi

248 critical need to identify key regulators of chemotherapy resistance in AML.

249 tion in vitro and promoted tumor aggression, chemotherapy resistance, and MEK inhibitor resistance in

250 verexpressed in various cancers and mediates chemotherapy resistance.

251 eutrophils result in enhanced metastasis and chemotherapy resistance.

252 t a biocompatible drug delivery platform for chemotherapy resistant tumor treatment.

253 and can act as anti-cancer agents to inhibit chemotherapy-resistant tumor growth by consuming intrace

254 l features (K/N-RAS status), and response to chemotherapy (Response Evaluation Criteria in Solid Tumo

255 er xenografts (PDX), similar in genetics and chemotherapy responsiveness to human tumors, was exposed

256 BAY 1895344 with certain DNA damage inducing chemotherapy resulted in synergistic antitumor activity.

257 hemoresistance, i.e., tumor insensitivity to chemotherapy, shortens life expectancy of cancer patient

258 Adjuvant platinum-based chemotherapy should be considered a new standard of care

259 A 60-Gy radiation dose with concurrent chemotherapy should remain the standard of care, with th

260 with nab-paclitaxel and anthracycline-based chemotherapy significantly improved pathological complet

261 risks could not be explained by exposure to chemotherapy, stem-cell transplantation, or rituximab, e

262 rent strategies, including combinations with chemotherapy, targeted therapy, radiation therapy, intra

263 omisation was stratified by type of on-study chemotherapy (taxane or gemcitabine-carboplatin), PD-L1

264 cordingly, they show that the combination of chemotherapy, TGFbeta signaling inhibition, and immune c

265 may lead to lasting breakthroughs in malaria chemotherapy that can prevent recrudescences and protect

266 cells to arginine deprivation treatment and chemotherapy through targeting ASS1- and GLUT1-mediated

267 Adding pemetrexed and carboplatin chemotherapy to gefitinib significantly prolonged PFS an

268 Data to support administering postoperative chemotherapy to patients who received preoperative thera

269 improvement in survival with the addition of chemotherapy to surgery.

270 nd evaluated enhanced delivery of irinotecan chemotherapy to the brain and a rat glioma model.

271 tablets (300 mg twice daily) or single-agent chemotherapy TPC (21-day cycles of either capecitabine,

272 inded independent central review, versus the chemotherapy TPC arm (5.7 vs 4.2 months; HR = 0.53 [95%

273 ed in high-grade PC tumors (P < 0.05) and in chemotherapy-treated patients compared to chemo-naive pa

274 n in combination may identify which adjuvant chemotherapy-treated TNBC patients have a higher risk of

275 vels are associated with shorter survival in chemotherapy-treated TNBC patients.

276 er (PLL) for simultaneous synergistic thermo-chemotherapy treatment and MRI imaging.

277 tablet monotherapy (300 mg twice daily) over chemotherapy treatment of physician's choice (TPC) in pa

278 rapeutic strategy to improve the efficacy of chemotherapy treatment.

279 s a selective benefit to cancer cells during chemotherapy treatment.

280 either surveillance or four 21-day cycles of chemotherapy, using a minimisation algorithm with a rand

281 , we developed novel nanocarrier delivery of chemotherapy via TFR1-mediated endocytosis, assessing th

282 Bleomycin chemotherapy was not associated with pulmonary complicat

283 ho received chemotherapy; and those for whom chemotherapy was not recommended and not given.

284 a between in vitro and human sputum prior to chemotherapy was quantified using different model-based

285 Chemotherapy was quickly started.

286 ants, vitamin B12 use both before and during chemotherapy was significantly associated with poorer di

287 Use of iron during chemotherapy was significantly associated with recurrenc

288 Doublet chemotherapy was used in 36.4% of 2 L patients, most com

289 ment modalities for patients who progress on chemotherapy, we explored the effects of long-term gemci

290 age, N-stage, resection margin, and adjuvant chemotherapy were correlated with OS and DFS.

291 cordant response assessments after induction chemotherapy were evaluated with the Wilcoxon test.

292 PMBCL treated with curative intent rituximab-chemotherapy were identified.

293 angiocarcinoma (CCA) is its poor response to chemotherapy, which is partly due to reduction of intrac

294 vasive fungal diseases (IFDs) during initial chemotherapy, which need to be considered when assessing

295 or-bearing mice against the toxic effects of chemotherapy while enhancing therapeutic efficacy.

296 treated with gemcitabine and S-1 (GS)-based chemotherapies with/without radiation.

297 djuvant therapy and 90 who received adjuvant chemotherapy with or without radiation (22%).

298 tuximab to standard lymphomes malins B (LMB) chemotherapy with standard LMB chemotherapy alone.

299 ents received BL-8040 and pembrolizumab with chemotherapy, with an ORR, DCR and median duration of re

300 o suppressed response to cisplatin-etoposide chemotherapy, with similar findings made upon MYCL overe

301 One participant allocated chemotherapy withdrew consent for data use after randomi