ライフサイエンスコーパス: tumor regression

1 control, yet low-avidity T cells can promote tumor regression.

2 aring mice with an IKK inhibitor resulted in tumor regression.

3 survival and achieve a high rate of complete tumor regression.

4 g these 5 genes with PI3K inhibition induced tumor regression.

5 coadministration with 5-NIdR caused complete tumor regression.

6 and expansion of polyfunctional CD8 CTLs and tumor regression.

7 d ROS as hallmarks of the cells that survive tumor regression.

8 lowed for the imaging of viral infection and tumor regression.

9 models inhibited PI3K signaling and promoted tumor regression.

10 lection of disease stabilization rather than tumor regression.

11 I3K and MAPK signaling and triggers dramatic tumor regression.

12 , their recruitment into the tumor site, and tumor regression.

13 ING agonist 3'3'-cGAMP induced apoptosis and tumor regression.

14 innate immune cell subsets were required for tumor regression.

15 e, and in multiple instances led to complete tumor regression.

16 fer into a patient with melanoma resulted in tumor regression.

17 ration and increased apoptosis, resulting in tumor regression.

18 ous tumor antigens are powerful mediators of tumor regression.

19 hin the tumor microenvironment and eliciting tumor regression.

20 rapeutic manipulation of immunity can induce tumor regression.

21 t cancer, BHPI induced rapid and substantial tumor regression.

22 sufficient to suppress temozolomide-induced tumor regression.

23 -FOXO1-mediated gene expression and elicited tumor regression.

24 lone, the addition of AZD8055 induced potent tumor regression.

25 optosis in tumor tissue, leading to complete tumor regression.

26 n of MEK together with JAK and FGFR enhanced tumor regression.

27 ensitivity of breast tumors to tamoxifen and tumor regression.

28 nd 4-1BB is essential for CAR-T cell-induced tumor regression.

29 on of MYC and beta-catenin induces sustained tumor regression.

30 PTK787 treatment also facilitated long-term tumor regression.

31 n-reactive T(H)1 cells and again experienced tumor regression.

32 eting significantly enhanced the NK-mediated tumor regression.

33 t decrease, as would have been expected with tumor regression.

34 , and SERD/MEK inhibitor combinations induce tumor regression.

35 every alternate day resulted in significant tumor regression.

36 in patients with prostate cancer results in tumor regression.

37 on analysis, gene knockdown assay and animal tumor regression.

38 DK4 inhibition), resulting in cell death and tumor regression.

39 ealed that direct killing was sufficient for tumor regression.

40 te of CTLs in vivo was insufficient to cause tumor regression.

41 hat induces anti-tumor immunity and promotes tumor regression.

42 sorafenib cooperatively and safely triggered tumor regressions.

43 forms and androgen receptor results in major tumor regressions.

44 h GLV-1h153 resulted in a 6-fold increase in tumor regression (24 compared to 146 mm(3) for the virus

45 metronomic chemotherapy induced the greatest tumor regression (6.2-fold reduction in size compared to

46 At last visit, eyes with follow-up showed tumor regression (66%), stability (12%), growth (14%), r

47 d an ordinary differential equation model of tumor regression after adoptive transfer of a population

48 Tumor regression after radiation therapy for melanomas w

49 Furthermore, 17d demonstrated potent in vivo tumor regression against the BT474 xenograft model.

50 The most efficacious ADC showed complete tumor regression and 10/10 tumor free survivors at a sin

51 elicits superb anticancer efficacy with >98% tumor regression and 60% cure rate.

52 ith these targeted inhibitors could increase tumor regression and decrease the likelihood of eventual

53 ered locally or systematically, resulting in tumor regression and enhanced survival when combined wit

54 wn (using uncontrolled sonication) to induce tumor regression and improve survival in rat glioma.

55 d tumor xenograft (PDX) models, resulting in tumor regression and improved disease control.

56 intrinsic cobalt toxicity, leads to complete tumor regression and improved overall survival in an in

57 iltrating T cells, which was associated with tumor regression and increased mice survival.

58 fficacy on xenografted mice with significant tumor regression and increased survival.

59 ficacy in xenografted mice, with significant tumor regression and increased survival.

60 T cells in the tumor, which induce complete tumor regression and long-lasting immunologic memory in

61 ade, chemotherapy, or low-dose TNF, complete tumor regression and long-lasting tumor immunity were ob

62 e, ionized radiation, STAT3i SPNPs result in tumor regression and long-term survival in 87.5% of GBM-

63 n excellent therapeutic effect with profound tumor regression and low systemic toxicity.

64 A combined classification of primary tumor regression and lymph node status in 3 grades repre

65 early showed the best accuracy in predicting tumor regression and may be particularly useful in guidi

66 n of EGFR* induction that led to significant tumor regression and prolonged animal survival.

67 a week for 1.5 weeks resulted in significant tumor regression and prolonged mouse median survival wit

68 - and cholesterol-dependent fashion, causing tumor regression and prolonged survival in mouse models.

69 tic tumors to anti-PD1 therapy, resulting in tumor regression and prolonged survival.

70 e peptides, 11, was shown to induce complete tumor regression and protective immunity following intra

71 d in combination with irinotecan, leading to tumor regression and replacement of Ewing sarcoma cells

72 nd doxorubicin (EAD) resulted in significant tumor regression and restoration of epigenetically silen

73 K expression in vivo, we were able to induce tumor regression and significantly increase survival; ho

74 Silencing of HBEGF in vivo resulted in tumor regression and significantly increased survival, s

75 ab for the prediction of complete pathologic tumor regression and survival in patients with MRI-defin

76 esulted in infiltration of T cells, complete tumor regression, and 100% survival of immunocompetent h

77 PI3K and BET inhibition induced cell death, tumor regression, and clamped inhibition of PI3K signali

78 s approach delayed tumor growth, facilitated tumor regression, and cured tumors in both A20 and CT26

79 3 target genes triggering massive apoptosis, tumor regression, and long-term cure of the majority of

80 on boosts low-avidity T cell responsiveness, tumor regression, and prevents T cell exhaustion.

81 e expression of a UBC-targeting shRNA led to tumor regression, and substantial long-term survival ben

82 llow patient monitoring of immune responses, tumor regression, and tumor dissemination during and aft

83 tivation of DCs and effector T cells, marked tumor regression, and tumor-specific antitumor immune me

84 drug-resistant cell expansion versus overall tumor regression as a function of induction length, but

85 n of an ABD resulted in HN3-ABD-T20-mediated tumor regression at 1 mg/kg.

86 daily dosing of compound 28 resulted in 33% tumor regression at 100 mg/kg.

87 licited superb anticancer efficacy with >98% tumor regression at a low X-ray dose of 5 x 1 Gy.

88 reasing aromatase expression, induces Leydig tumor regression both in vitro and in vivo, suggesting t

89 ng cancer with erlotinib results in dramatic tumor regression but it is invariably followed by drug r

90 ls (TSCM) can trigger profound and sustained tumor regression but their rareness poses a major hurdle

91 eus) induces systemic antitumor immunity and tumor regression, but not in TME with scarce TILeus, suc

92 uces Bim expression and apoptosis and causes tumor regression, but these effects are profoundly atten

93 an nanobody (HN3) immunotoxins causes potent tumor regression by blocking protein synthesis and down-

94 e induction of Ag-specific CTL responses and tumor regression by dipalmitoylated peptides was TAP ind

95 as a key molecule limiting this IFN-induced tumor regression by DMXAA.

96 or effects, as confirmed by re-initiation of tumor regression by fresh injections of SIRPalpha-inhibi

97 Tumor regression by LATS1/2 deletion requires adaptive i

98 sts that immune checkpoint inhibitors induce tumor regressions by reactivating a population of endoge

99 CAR T cell treatment resulted in significant tumor regression compared to untransduced T cells.

100 ificantly repressed tumor growth and induced tumor regressions compared with either drug alone.

101 Tumor regression correlated with reduced accumulation of

102 Ionizing radiation-mediated tumor regression depends on type I interferon (IFN) and

103 have been noted long after initial objective tumor regression despite continuous therapy.

104 In comparison, tumor regressions did not occur when ABT-737 was combine

105 Eliminating PEPD causes cell death and tumor regression due to p53 activation.

106 oncogenes often fails to result in sustained tumor regression due to the emergence of therapy-resista

107 erns of tumor expansion before treatment and tumor regression during treatment are tied to the dynami

108 which may be generated by or participate in tumor regressions during chemotherapy.

109 ransferred T cells disappeared shortly after tumor regression, endogenous T cells secured long-term m

110 oparticles led to effective and long-lasting tumor regression/eradication in subcutaneous and intrape

111 (PD-L1) resulted in synergistic and durable tumor regression even where either agent alone was only

112 with the BRAF inhibitor PLX4720 resulted in tumor regression followed by relapse.

113 ed blockade of EGFR and ERBB3 promotes rapid tumor regression, followed by the eventual outgrowth of

114 s directed toward cancer neoantigens mediate tumor regression following checkpoint blockade or adopti

115 oth cDC1 and CD8(+) T cells are required for tumor regression following combination therapy.

116 lpha-inhibited macrophages in tumors favored tumor regression for 1-2 weeks, but donor macrophages qu

117 e proportion of false-negative patients with tumor regression grade (TRG) 3-4 (>10% vital residual tu

118 Response to nCRT was assessed based on tumor regression grade (TRG) in the resection specimen.

119 Tumor Regression Grade (TRG1) of Ryan et al was the prim

120 ological complete or near-complete response (tumor regression grade 1-2) were classified as good resp

121 pTR was defined as Mandard tumor regression grade 1-3; imaging parameters included

122 idues in R0-specimens of partial responders (tumor regression grade 2-3: N = 90) were found in- and o

123 nearly no response (tumor regression grade: tumor regression grade 4-5).

124 complete versus incomplete response (Mandard tumor regression grade system 1 vs. 2-5).

125 After surgery the pathological tumor regression grade was assessed according to the cla

126 Histopathologic tumor regression grade was the reference standard.

127 d a pCR (ypT0N0) and 14% nearly no response (tumor regression grade: tumor regression grade 4-5).

128 eatment of esophageal cancer such as Mandard tumor regression grading focus on the effect on the prim

129 o independent pathologists using the Mandard tumor regression grading system (TRG).

130 and prognostic performance of commonly used tumor regression grading systems, namely College of Amer

131 the importance of CD4+ T cells in mediating tumor regression has become apparent.

132 Tumor regression has been observed following transfer of

133 r responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targetin

134 diate tumor surveillance and therapy-induced tumor regression; however, tumor-associated macrophages

135 bove transgenic mice resulted in significant tumor regression, implying an essential role of androgen

136 otypes, blocked tumor metastasis, and caused tumor regression in 60% of MMTV-Neu mice.

137 with a CD19-specific CAR achieved sustained tumor regression in a B cell lymphoma model.

138 icacy and robust abscopal effects with >97 % tumor regression in a bilateral breast cancer model.

139 The optimized compound led to tumor regression in a CARD11 mutant ABC-DLBCL lymphoma x

140 both AR signaling and AR levels and leads to tumor regression in a CRPC mouse xenograft model.

141 e now produced a compound that shows durable tumor regression in a lymphoma xenograft model.

142 utologous lymphocytes, can mediate objective tumor regression in a majority of patients with metastat

143 and MEK inhibition has been shown to induce tumor regression in a minority of patients; however, no

144 This response translated to significant tumor regression in a mouse model of high-risk neuroblas

145 mmunoglobulin G4 antibody nivolumab mediates tumor regression in a portion of patients with advanced

146 ppressive properties in vivo and facilitated tumor regression in a suppression of tumorigenicity 2 re

147 tion with H3B-6527 could effectively trigger tumor regression in a xenograft model of HCC.

148 o dual HER2 and p110alpha inhibition induced tumor regression in a xenograft model of HER2+/PTEN-defi

149 kg as PEG-b-PLA micelles, o(LA)8-PTX induced tumor regression in A549 tumor-bearing mice, whereas PTX

150 Two pathologists individually evaluated tumor regression in accordance with the CAP, Evans', JPS

151 bination of compound 28 and ibrutinib led to tumor regression in an ABC-DLBCL mouse model.

152 trations and is capable of achieving partial tumor regression in an MV4;11 xenograft tumor model in m

153 ctivated T cells in vitro and mediated rapid tumor regression in an orthotopic xenograft model of mul

154 s showed superior efficacy with complete NDL tumor regression in both treated and abscopal sites achi

155 bined BRAF and autophagy inhibition promoted tumor regression in BRAFi-resistant xenografts.

156 umbers of tumor-infiltrating CD8 T cells and tumor regression in caveolin-2 deficient mice, suggestin

157 h a CD137 agonist resulted in complete FBL-3 tumor regression in CD8(+) T cell-deficient mice.

158 Indeed, eIF4E inhibition induces tumor regression in cell line and patient-derived tumorg

159 ich was expressed in CD4+ T cells and caused tumor regression in combination with NY-ESO-1-redirected

160 to melanoma-bearing mice resulted in lasting tumor regression in contrast to temporary responses achi

161 hared oncogenic mutations can induce durable tumor regression in epithelial cancer patients.

162 The DDM were able to significantly induce tumor regression in ES2 ovarian xenograft mouse models b

163 ctive compounds identified by HT-DBP induced tumor regression in genetically engineered and patient-d

164 JNJ-64407564 can recruit T cells and induce tumor regression in GPRC5D+ MM murine models, which coin

165 d SVC112 combined with radiation resulted in tumor regression in HPV-positive and HPV-negative HNSCC

166 d dose-dependent manner in vitro and induced tumor regression in human NSCLC xenografts in vivo.

167 sts as well as their molecular mechanisms of tumor regression in LTED BC through triggering a rapid U

168 ved both efficient in vitro cell killing and tumor regression in Mcl-1 dependent cancer models.

169 Recently, imiquimod has demonstrated tumor regression in melanoma and breast cancer skin meta

170 n CD8(+) cytotoxic T lymphocytes can mediate tumor regression in melanoma through the specific recogn

171 (PDCD1; also known as PD-1) elicits durable tumor regression in metastatic cancer, but these dramati

172 poptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly revers

173 capacity in vitro and leads to neuroblastoma tumor regression in mice, while high levels of lncNB1 an

174 esulted in impaired cellular persistence and tumor regression in mouse models following ACT.

175 lele of MYC, termed OmoMYC, can induce rapid tumor regression in mouse models with little toxicity fo

176 pable of producing complete and long-lasting tumor regression in mouse xenograft models.

177 iogenesis, and blockade of RLIP76 results in tumor regression in multiple models.

178 hermore, single treatment of hYP7-PC induced tumor regression in multiple mouse models.

179 SD-36 achieves complete and long-lasting tumor regression in multiple xenograft mouse models at w

180 ation and promoted cancer cell apoptosis and tumor regression in murine models.

181 eases in CD8 T cell infiltration followed by tumor regression in murine models.

182 improved therapeutic efficacy with complete tumor regression in NIR irradiated ICG conjugated micell

183 HL001 with cisplatin synergistically enhance tumor regression in orthotopic NSCLC mouse model.

184 overcome immunosuppression and thus promote tumor regression in ovarian cancer (and other tumor type

185 RORgamma antagonists cause tumor regression in patient-derived xenografts and immun

186 n and cyclophosphamide can result in durable tumor regression in patients with advanced mesothelioma

187 antigen receptor (CAR.CD19) induces complete tumor regression in patients with lymphoid malignancies.

188 thus it may be most practical for assessing tumor regression in post-neoadjuvant resections for PDAC

189 he STING pathway can lead to T cell-mediated tumor regression in preclinical tumor models, and novel

190 ic melanoma who had had an initial objective tumor regression in response to anti-PD-1 therapy (pembr

191 PD-1/PD-L1 blockade is associated with tumor regression in several malignancies, but single-age

192 ght explain why cancer immunotherapy induces tumor regression in some individuals, while others do no

193 ent with IL-21 results in complete FC-muMCL1 tumor regression in syngeneic mice via NK- and T-cell-de

194 xhibited potent target engagement and strong tumor regression in the BRAF(V600E) xenograft model.

195 SD-36 achieves complete and long-lasting tumor regression in the Molm-16 xenograft tumor model at

196 The (131)I-ELP depots achieved >95% tumor regression in the prostate tumors (n=8); with a me

197 s excellent chemical stability, and achieves tumor regression in the SJSA-1 xenograft tumor model in

198 ecan/temozolomide combination induced strong tumor regression in the TCLT and in a model derived from

199 I) conjugates (2P-EPI) demonstrated complete tumor regression in the treatment of mice bearing ovaria

200 riven differentiation to achieve significant tumor regression in TNBC.

201 Dual HER2 and CDK7 inhibition induced tumor regression in two HER2iR BC xenograft models in vi

202 tion of RS4;11 cell growth and induces rapid tumor regression in vivo against RS4;11 xenograft tumors

203 MD-224 achieves complete and durable tumor regression in vivo in the RS4;11 xenograft tumor m

204 poptosis and growth inhibition in vitro, and tumor regression in vivo.

205 tumor cell proliferation in vitro and caused tumor regression in vivo.

206 mall cell population resulted in significant tumor regression in vivo.

207 led to sustained MAPK pathway inhibition and tumor regression in vivo.

208 ting cancer promotes rapid and comprehensive tumor regression in vivo.

209 mor spheroid formation in vitro and complete tumor regression in vivo.

210 ed a more robust and significantly prolonged tumor regression in xenograft models.

211 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regression in xenograft models.

212 he above-described EGFR variants and induces tumor regressions in a cross-resistant EGFR(del19 T790M

213 ve than paired combinations, provoking rapid tumor regressions in a PDX model.

214 onistic antibodies (aCD40) produced complete tumor regressions in a therapy-resistant pancreas cancer

215 tolerable and induced pCRs and radiographic tumor regressions in approximately one half of treated p

216 lin-expressing cancer cells lines and causes tumor regressions in mice.

217 nduced marked apoptosis in vitro, as well as tumor regressions in multiple SCLC xenograft models.

218 targeting mesothelin produced durable major tumor regressions in patients with extensive treatment-r

219 n clinical trials and has produced objective tumor regressions in patients.

220 intrinsic and adaptive resistance leading to tumor regressions in PIK3CA mutant xenografts.

221 g in enhanced tumor-specific immune-mediated tumor regressions in primary tumors and colorectal liver

222 xpressing xenograft tumors, which has led to tumor regressions in several SSTR2-expressing xenograft

223 ed additive antitumor activity with complete tumor regressions in some mice; tumors intrinsically sen

224 Cancer immunotherapy can result in durable tumor regressions in some patients.

225 ibition of PI3K and mTOR resulted in durable tumor regressions in three of five PDXs, and therapeutic

226 T790M in vitro, which translated into strong tumor regressions in vivo in several patient-derived xen

227 antly, our combinatorial therapy resulted in tumor regression, including regression in PDX samples fr

228 ib, which target c-Kit, resulted in complete tumor regression, indicating that c-Kit activity is cruc

229 In vivo, the extent of tumor regression induced by combination treatment with C

230 +) tumor-associated macrophages, and enables tumor regression induced by STING activation.

231 s produce high response rates, the degree of tumor regression is heterogeneous.

232 ponses are not durable, and the magnitude of tumor regression is variable, suggesting the existence o

233 but PEG-[SN22](4) treatment caused complete tumor regression lasting over 6 months (tumor free at ne

234 the intent to achieve complete and permanent tumor regression (local control).

235 n BRAF(V600E)mitf melanoma leads to dramatic tumor regression marked by melanophage infiltration and

236 taneous tumors by CD8(+) T cells and induced tumor regression, mediated by CD8(+) T cells.

237 We extended the classical tumor regression models such as Skipper's laws and the N

238 -catenin inhibition alone results in initial tumor regression, most tumors ultimately recurred, mimic

239 Pretreatment with 3TSR induced tumor regression, normalized tumor vasculature, and impr

240 Complete and durable tumor regression occurred with ORY-1001-induced NOTCH ac

241 ional treatment capable of inducing complete tumor regression of B-cell malignancies when there is su

242 owth of all four tumor types and resulted in tumor regression of breast and bladder xenografts.

243 to a significant tumor growth inhibition or tumor regression of cell line-based or patient-derived x

244 3-MDM2 interaction, DS-5272, causes dramatic tumor regressions of MLL-AF9-driven AML in vivo with a t

245 NCN-null phenotypes was confirmed by uniform tumor regression on single-dose cross-linker therapy in

246 tment of tumors with STING agonists leads to tumor regression, optimal STING-mediated immunity and re

247 atinum therapy rarely results in substantial tumor regression or a dramatic extension in patient surv

248 y help to provide more reliable estimates of tumor regression or regrowth following globe-preserving

249 ed cancer therapies fail to achieve complete tumor regressions or attain durable remissions.

250 ty for treating localized tumors, can induce tumor regression outside the radiation field through an

251 d Mut H-ras-specific effectors induced rapid tumor regression, overcoming established tumor suppressi

252 ted in the tumor (4.6% on day 7) and induced tumor regression (P < .05 on day 7).

253 tumor-infiltrating T cells, stimulates rapid tumor regression, prevents metastasis and leads to long-

254 , FAK inhibitors may trigger immune-mediated tumor regression, providing previously unrecognized ther

255 Tumor regression rate is negatively correlated with Ve a

256 was highly efficacious, leading to complete tumor regressions, reduced metastasis, and greatly exten

257 find that clonal diversity decreases during tumor regression, residual disease, and recurrence.

258 It is unknown if a greater tumor regression response after iodine 125 (I(125)) brac

259 The tumor regression score as an indicator of histopathologi

260 ethods correlate better with histopathologic tumor regression score in NSCLC patients under neoadjuva

261 responders (CR = 14) to CRT, as defined by a tumor regression score, were examined.

262 respectively; P = .027) and improved Mandard tumor regression scores (P = .001).

263 profile, in vitro cytotoxicity, and in vivo tumor regression studies by this lead compound.

264 nts that elicit cell arrest, the preclinical tumor regression studies, and the inorganic medicinal ch

265 en-specific CD8+ T cell responses paralleled tumor regression, suggesting that anti-PD-1 therapy enha

266 can be dramatic, sometimes causing complete tumor regression, the majority of melanomas eventually b

267 /or cMet, JNJ-61186372 treatment resulted in tumor regression through inhibition of signaling/recepto

268 thio-2'-deoxyguanosine (6-thio-dG), leads to tumor regression through innate and adaptive immune-depe

269 ncer model and their molecular mechanisms of tumor regression through the unfolded protein response a

270 Inducing tumor regression to permit BCT is often cited to support

271 anges were compared with pathologic complete tumor regression (TRG1) versus incomplete tumor regressi

272 te tumor regression (TRG1) versus incomplete tumor regression (TRG2-TRG5), progression-free survival,

273 rved, resulting in enhanced overall survival tumor regression up to 50% in the treatment of lung squa

274 We further confirmed that tumor regression upon infection was associated with an i

275 r this derives from clinical observations of tumor regressions upon antiviral treatments.

276 mor-bearing mice with PT2385 caused dramatic tumor regressions, validating HIF2alpha as a pivotal onc

277 nths (median, 6 months; range, 1-68 months), tumor regression was achieved in all cases, without recu

278 Tumor regression was assessed radiographically and micro

279 Furthermore, tumor regression was correlated with massive immune infi

280 were calculated, and their relationship with tumor regression was evaluated.

281 with MHIRE were tumor-free, whereas complete tumor regression was not observed in the control and IRE

282 treated with pembrolizumab, nearly complete tumor regression was observed after 4 cycles of therapy.

283 Complete tumor regression was observed in all PDX models, includi

284 Concomitant with IR-mediated tumor regression, we observed that IR and anti-PD-L1 syn

285 he chemokine gene CCL5 Such infiltration and tumor regression were abrogated by silencing CCL5 in BEC

286 Tumor regressions were also seen in a long-term estrogen

287 Complete and intermediate tumor regressions were associated with improved long-ter

288 Durable tumor regressions were observed in seven (70%) of 10 pat

289 mmediate reversal of all stromal changes and tumor regression, which are independent of CD4(+)CD8(+)

290 riggers acute metabolic stress, which causes tumor regression while inducing epigenetic reprogramming

291 ession, and the inhibition of C1QBP enhances tumor regression with chemotherapy.

292 the activity of T-DM1, resulting in complete tumor regression with combination treatment.

293 interferon-beta secretion in tumors, induced tumor regression with durable antitumor immunity, and sy

294 sion led to proliferation arrest and partial tumor regression with loss of anaplasia.

295 he subsequent 8 months resulted in extensive tumor regression with no detectable metastases.

296 reactive stromal fibroblasts and to trigger tumor regression, with implications for stromal-based st

297 lia/macrophage barrier, thereby facilitating tumor regression without causing a spread of the virus t

298 n selectively within the tumor, resulting in tumor regression without toxicity when tumor cells were

299 ectron transport chain proteins, and induced tumor regression without toxicity.

300 PD-1/PD-L1 blockade can promote robust tumor regression yet secondary resistance often occurs a