ライフサイエンスコーパス: tumor regression

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

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

3 ration and increased apoptosis, resulting in tumor regression.

4 ous tumor antigens are powerful mediators of tumor regression.

5 hin the tumor microenvironment and eliciting tumor regression.

6 rapeutic manipulation of immunity can induce tumor regression.

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

8 sufficient to suppress temozolomide-induced tumor regression.

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

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

11 coadministration with 5-NIdR caused complete tumor regression.

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

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

14 ensitivity of breast tumors to tamoxifen and tumor regression.

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

16 and expansion of polyfunctional CD8 CTLs and tumor regression.

17 PTK787 treatment also facilitated long-term tumor regression.

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

19 eting significantly enhanced the NK-mediated tumor regression.

20 tory roles in Leishmania major infection and tumor regression.

21 ectedly as effective as BEZ235 in triggering tumor regression.

22 cence, and apoptosis and abrogates sustained tumor regression.

23 ers cancer stem cell eradication and durable tumor regression.

24 rved with either small RNA alone, leading to tumor regression.

25 n contrast, 5FU promoted immune recovery and tumor regression.

26 25(-)CD127(-) CD4(+) T cells correlated with tumor regression.

27 e increased PD-1 on T cells with concomitant tumor regression.

28 tablish the immune cell subsets required for tumor regression.

29 elanoma, whereas Tc1 cells induced long-term tumor regression.

30 ICs from the perivascular niche, followed by tumor regression.

31 effector T cell activity capable of inducing tumor regression.

32 responses, effectively leading to sustained tumor regression.

33 -1, a receptor for one such ligand, impaired tumor regression.

34 t, boosting antitumor immunity and promoting tumor regression.

35 ells are superior to Tc17 cells in mediating tumor regression.

36 SCC induced rapid and dramatic apoptosis and tumor regression.

37 n-specific CTL responses and, in some cases, tumor regression.

38 this combination and the capacity to mediate tumor regression.

39 ered with high-affinity TCR can offer better tumor regression.

40 -1:10 000) Abs that correlated with clinical tumor regression.

41 es, and dendritic cells that leads to marked tumor regression.

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

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

44 models inhibited PI3K signaling and promoted tumor regression.

45 lection of disease stabilization rather than tumor regression.

46 I3K and MAPK signaling and triggers dramatic tumor regression.

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

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

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

50 innate immune cell subsets were required for tumor regression.

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

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

53 sorafenib cooperatively and safely triggered tumor regressions.

54 forms and androgen receptor results in major tumor regressions.

55 ted patients with melanoma can cause durable tumor regressions.

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

57 Among 33 patients with objective tumor regressions (31%), the Kaplan-Meier estimated medi

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

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

60 mab/LJM716/BYL719 exhibited similar rates of tumor regression after 3 weeks of treatment.

61 Tumor regression after radiation therapy for melanomas w

62 on, serial MR studies can be used to monitor tumor regression after surgery or chemotherapy.

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

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

65 uring ovariectomy-induced weight gain caused tumor regression and downregulation of PR expression in

66 Factors predicting tumor regression and eye salvage were bilateral retinobl

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

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

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

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

71 he molecular and phenotypic parallel between tumor regression and mammary gland involution suggests t

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

73 yc-dependent transcription, correlating with tumor regression and prolonged survival in a mouse model

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

75 ermore, in vivo brentuximab vedotin promoted tumor regression and prolonged survival of mice bearing

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

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

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

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

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

81 PFS and OS were comparable for patients with tumor regression and stable disease.

82 oth MYC and beta-catenin promoted more rapid tumor regression and successfully prevented tumor recurr

83 bits post-proline cleaving enzymes, mediates tumor regression and tested whether this agent could ser

84 ompleting preoperative chemotherapy, all had tumor regression and TME without preoperative chemoradio

85 al subset that experienced complete, lasting tumor regression - and may be cured.

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

87 tial for acute graft versus tumor responses, tumor regression, and prolonged survival.

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

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

90 CI, 1.20-2.27; P = 0.002) when analyzed with tumor regression as an additional independent factor (HR

91 toma in this mouse model, but does not drive tumor regression, as it does in Pten-wild-type medullobl

92 -specific T cell responses without sustained tumor regression because immunosuppressive elements with

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

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

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

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

97 -cell receptors (TCRs) can mediate effective tumor regression, but they often also are accompanied by

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

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

100 Tumor regression by LATS1/2 deletion requires adaptive i

101 nhanced inhibition of tumor growth (complete tumor regression) by paclitaxel and gemcitabine conjugat

102 3 is a viable strategy to initiate sustained tumor regression; combining p53 reactivation while inhib

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

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

105 T cells at the tumor site and also enhanced tumor regressions, compared with treatments with either

106 ons of RECIST, including its overemphasis on tumor regression, concerns about the accuracy of tumor m

107 Tumor regression correlated with increased CTL activity

108 Tumor regression correlated with reduced accumulation of

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

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

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

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

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

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

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

116 a receptor II induces complete and sustained tumor regression, enhances survival, and leads to restor

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

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

119 agents with CSF1R blockade potently elicited tumor regressions, even in larger established tumors.

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

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

122 melanoma that were associated with objective tumor regressions following adoptive transfer.

123 ge within tumor cells and causes substantial tumor regressions following two weekly doses of 3.0 mg/k

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

125 -docetaxel at 10mg/kg resulted in maintained tumor regression for a period of 30 days.

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

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

128 Tumor regression grade (TRG) was meticulously scored for

129 -related liver injuries (CALI), pathological tumor regression grade (TRG), and micrometastases on lon

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

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

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

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

134 Histopathologic tumor regression grade was the reference standard.

135 ied, all with prospectively recorded Mandard tumor regression grades (TRG).

136 reviously described the prognostic impact of tumor regression grading (TRG) on the outcome of patient

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

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

139 Tumor regression has been observed following transfer of

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

141 Mechanisms of spontaneous tumor regression have been difficult to characterize in

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

143 can sometimes result in rapid and sustained tumor regression, illustrating that cancers can be 'onco

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

145 anned by predictive dosimetry achieved index tumor regression in 8 of 8 patients, with a median size

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

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

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

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

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

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

152 ed death 1 [PD-1] receptor) produced durable tumor regression in a phase 1 trial.

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

154 PD-1 blockade can mediate tumor regression in a substantial proportion of patients

155 hed data on monotherapy, with rapid and deep tumor regression in a substantial proportion of patients

156 he recruited pDCs were CD8alpha+ and induced tumor regression in a TLR7/MyD88- and IFNAR1-dependent m

157 tion was efficacious in vivo, causing marked tumor regression in a UM xenograft model.

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

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

160 t with p8032 and 7DW8-5 resulted in complete tumor regression in A20 lymphoma-bearing mice, where pro

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

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

163 44 nM and achieves complete and long-lasting tumor regression in an animal model of human cancer.

164 Compound 49 achieved substantial tumor regression in an NPM-ALK driven murine tumor xenog

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

166 ombination of phenformin and PLX4720 induced tumor regression in both nude mice bearing melanoma xeno

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

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

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

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

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

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

173 molecule Shh pathway inhibitors have induced tumor regression in mice and patients with medulloblasto

174 nsfer of specific CD4(+) T cells can promote tumor regression in mice and patients.

175 or-bearing mice treated with IL PV-10 led to tumor regression in mice bearing B16 melanoma.

176 salinomycin, and demonstrated orally potent tumor regression in mouse MCF-7 xenografts.

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

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

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

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

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

182 0 inhibitors result in growth inhibition and tumor regression in NSCLC cell lines and tumor xenograft

183 ty and pharmacokinetics and induced complete tumor regression in nude mice explanted with lung cancer

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

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

186 and oral BRAF inhibitors induce substantial tumor regression in patients with BRAF(V600E) metastatic

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

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

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

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

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

192 er-specific receptors can mediate impressive tumor regression in terminally ill patients.

193 tment of Mito-CP and 2-DG led to significant tumor regression in the absence of significant morpholog

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

195 und 30 achieves rapid, complete, and durable tumor regression in the H146 small-cell lung cancer xeno

196 nt and effective antitumor agent that caused tumor regression in the MDA-MB-231 breast cancer xenogra

197 effective in induction of rapid and durable tumor regression in the MDA-MB-231 xenograft model.

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

199 SAR405838 is sufficient to achieve complete tumor regression in the SJSA-1 model.

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

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

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

203 riven differentiation to achieve significant tumor regression in TNBC.

204 le of achieving rapid, complete, and durable tumor regression in two types of xenograft models of hum

205 or-infiltrating lymphocytes (TIL) can induce tumor regression in up to 50% or more of patients with u

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

207 le of achieving rapid, complete, and durable tumor regression in vivo at a well-tolerated dose schedu

208 levels in hypoxic cells in vitro and induced tumor regression in vivo by facilitating NK-mediated tum

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

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

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

212 leading to tumor cell apoptosis in vitro and tumor regression in vivo.

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

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

215 This combination caused marked in vivo tumor regressions in KRAS mutant xenografts and in a gen

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

217 inhibitors (MEKi/PI3Ki) can induce dramatic tumor regressions in mouse models of KRAS-mutant non-sma

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

219 or vemurafenib (PLX4032) frequently produced tumor regressions in patients with BRAF V600-mutant meta

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

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

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

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

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 BEZ235 treatment induced apoptotic tumor regressions in vivo that correlated with suppressi

228 y synergistic in vitro, and provided durable tumor regressions in vivo without notable hematologic su

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

230 decrease in FDG uptake, preceding effects on tumor regression, irrespective of the baseline level of

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

232 Minor responses (tumor regression less than 30%) were seen in eleven of 2

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

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

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

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

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

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

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

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

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

242 schedules, SAR405838 achieves either durable tumor regression or complete tumor growth inhibition in

243 Tc1-dependent immunity capable of mediating tumor regression or extending overall survival.

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

245 LX4720 improved survival but did not lead to tumor regression or suppress signaling through the MAPK

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

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

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

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

250 Tumor regression rate is negatively correlated with Ve a

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

252 Val-boroPro -mediated tumor regression requires dendritic cells and is associa

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

254 e immune cell recruitment and the associated tumor regression response.

255 The tumor regression score as an indicator of histopathologi

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

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

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

259 In addition, not only was greater tumor regression seen in a second distant ear tumor impl

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

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

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

263 reveal an innate immunity-based mechanism of tumor regression that can be activated by a traditional

264 or incidence, slower growth, and spontaneous tumor regression that occurred in allografts generated f

265 ents with advanced melanoma has demonstrated tumor regressions that are associated with a suppression

266 l of MLL-rearranged leukemia caused complete tumor regressions that were sustained well beyond the co

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

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

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

270 ion [20], but also appear to be essential to tumor regression upon oncogene inactivation [21,22(**),2

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

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

273 Tumor regression was accompanied by mild toxicity, manif

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

275 Furthermore, tumor regression was correlated with massive immune infi

276 mor CD8(+) T cells are induced, and systemic tumor regression was documented.

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

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

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

280 Although activity that induced tumor regression was observed and termed tumor necrosis

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

282 P-activated protein kinase signaling, and no tumor regression was observed.

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

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

285 ategory, ypN-category, and histopathological tumor regression were assigned a value from 1 to 3 as fo

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 of ErbB2-positive breast cancer cells showed tumor regression when treated with small-molecule inhibi

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

291 managing the adverse effects and kinetics of tumor regression with ipilimumab and provide guidelines

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

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

294 E) inhibitors have been suggested to promote tumor regression with the help of host immunity, but thi

295 f patients treated with selumetinib achieved tumor regression, with 14% achieving an objective radiog

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

297 lizumab resulted in a high rate of sustained tumor regression, with mainly grade 1 or 2 toxic effects

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

299 i.v. or intratumoral routes achieves partial tumor regression without clinical or histopathologic tox

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