ライフサイエンスコーパス: tumor growth

1 D8(+) T cells that express PD-1 and suppress tumor growth.

2 ive and sustain malignant transformation and tumor growth.

3 reduced AR and AR-V7 levels to mitigate CRPC tumor growth.

4 at GATA3 relies on SEMA3B for suppression of tumor growth.

5 mbinatorial activity with taxanes to inhibit tumor growth.

6 ereby inhibiting BRAF(V600E)-driven melanoma tumor growth.

7 ts by selectively antagonizing YAP-dependent tumor growth.

8 limination from plasma, and subject-specific tumor growth.

9 7)Lu-IMP288 showed significant inhibition of tumor growth.

10 hese effects resulted in a profound delay in tumor growth.

11 kines they release on cancer development and tumor growth.

12 to escape immune surveillance for successful tumor growth.

13 monary metastasis, with no effect on primary tumor growth.

14 P450 pathway are angiogenic, inducing cancer tumor growth.

15 overexpress murine MCAD markedly suppresses tumor growth.

16 ctions, cell invasion and proliferation, and tumor growth.

17 refore an attractive strategy for inhibiting tumor growth.

18 at expressed full levels of Zeb1 accelerated tumor growth.

19 d gemcitabine failed to significantly reduce tumor growth.

20 m intestinal epithelial cells did not affect tumor growth.

21 WASp decreases colony formation and in vivo tumor growth.

22 cancers, in particular in the prevention of tumor growth.

23 ly, this antibody inhibited PDGFRA-dependent tumor growth.

24 hangioleiomyomatosis patients contributes to tumor growth.

25 -repressive effect on cell proliferation and tumor growth.

26 p24a1-null)) exhibited a 4-fold reduction in tumor growth.

27 ole in development, tissue regeneration, and tumor growth.

28 cer cells resistant to therapy and inhibited tumor growth.

29 RAS (mt) caused increased cell viability and tumor growth.

30 and disease recurrence, and is a read-out of tumor growth.

31 ed to facilitate increased MDSC presence and tumor growth.

32 aimed at restoring PP2A function to inhibit tumor growth.

33 n, and inhibits sphere-formation ability and tumor growth.

34 dels, epithelial HIF-2alpha was essential in tumor growth.

35 the activity of specific proteins that drive tumor growth.

36 dampens oncogenic transcription and inhibits tumor growth.

37 R in vivo was sufficient to strongly inhibit tumor growth.

38 us cancers leading to aberrant signaling and tumor growth.

39 ic glycolysis, cell proliferation, and brain tumor growth.

40 (EDHB) on liver regeneration and metastatic tumor growth.

41 maturation and antitumor immunity and reduce tumor growth.

42 nt roles in breast cancer cell migration and tumor growth.

43 critical role in cancer cell metabolism and tumor growth.

44 reased EET concentration and mildly promoted tumor growth.

45 yclin proteins, without enhancing metastatic tumor growth.

46 HSD2 silencing inhibited OCDO production and tumor growth.

47 Increased AFP levels correlated with tumor growth.

48 lly, depletion of CHIP leads to promotion of tumor growth.

49 rmation, as elevated CPT1A expression limits tumor growth.

50 y and globally modify ER action to attenuate tumor growth.

51 cancer xenografts, significantly inhibiting tumor growth.

52 aken the hypoxia-driven pathways and inhibit tumor growth.

53 ges and reduces CD8+ T cells to promote lung tumor growth.

54 alpha)-activated MSCs significantly promoted tumor growth.

55 n promoted tumor growth, and oxamate delayed tumor growth.

56 n and diminished both lung MDSC presence and tumor growth.

57 eas LOXL2 overexpression promoted metastatic tumor growth.

58 irin and a PI3K inhibitor further attenuated tumor growth.

59 vivo promoted lung metastasis independent of tumor growth.

60 tor 1 (PD-1) were ineffective in controlling tumor growth.

61 rolongs survival, without directly affecting tumor growth.

62 from other DLBCL subtypes and contributes to tumor growth.

63 state to drive malignant transformation and tumor growth.

64 ells at the hypoxic core of connexin-coupled tumor growths.

65 CTX014 decreased tumor growth, affected the accumulation and tolerogenic

66 Effects on tumor growth after fractionated alpha-radioimmunotherapy

67 Recurrence was defined as presence of tumor growth after treatment.

68 Despite its critical importance for tumor growth, alloimmune responses, and inflammation, th

69 r role in driving the stimulation of distant tumor growth and (b) use adjuvant drug therapies to bloc

70 ncer development and evolution by regulating tumor growth and altering metastatic properties.

71 ect the host from age-related progression of tumor growth and amyloid-beta accumulation.

72 library can be used to build simulations of tumor growth and angiogenesis with realistic vessel netw

73 cidic extracellular pH (pHe), which promotes tumor growth and builds resistance to therapy.

74 genes, and knockdown of circCCDC66 inhibited tumor growth and cancer invasion in xenograft and orthot

75 B20-4.1.1 inhibited subcutaneous tumor growth and decreased vascular density in both fs12

76 man TNBC, administration of C1572 suppressed tumor growth and depleted CSCs in a manner correlated wi

77 n leads to a profound repression of prostate tumor growth and distal metastasis and substantially pro

78 forward loop between IL-6 and STAT3 driving tumor growth and endocrine therapy resistance.

79 Stabilizing IFNAR1 inhibits tumor growth and improves immunotherapy efficacy.

80 During normal tumor growth and in response to some therapies, tumor ce

81 (mTORC2) nucleation and activity leading to tumor growth and increased invasive characteristics in g

82 not free alendronate, abrogated PLN-induced tumor growth and increased progression-free survival.

83 es LINC00152 plays an important role in lung tumor growth and is potentially a diagnostic/prognostic

84 hat AACOCF3 treatment effectively attenuated tumor growth and LD biogenesis.

85 arcomas, observing marked inhibition of both tumor growth and lung metastases.

86 latelets have been associated with increased tumor growth and metastasis but the mechanistic details

87 ting host defense to infection and promoting tumor growth and metastasis by converting resting B and

88 cell migration in vitro as well as xenograft tumor growth and metastasis in an orthotopic mouse model

89 analysis demonstrated that the inhibition of tumor growth and metastasis was associated with activati

90 ere combined immunodeficient mice; xenograft tumor growth and metastasis were assessed.

91 As a suppressor of tumor growth and metastasis, Capicua may be an important

92 xia is recognized to be an adverse factor in tumor growth and metastasis, the role of G9a in regulati

93 KA inhibitor impaired ES cell proliferation, tumor growth and metastasis, which was rescued by the co

94 on, proliferation, and migration and in vivo tumor growth and metastasis.

95 microenvironment plays an important role in tumor growth and metastasis.

96 gically tractable pathway necessary for PDAC tumor growth and metastasis.

97 oring cells and distant organs, thus fueling tumor growth and metastasis.

98 t with potential functional consequences for tumor growth and metastasis.

99 sed matrix stiffness has profound effects on tumor growth and metastasis.

100 e used to evaluate the role of ALCAM in lung tumor growth and metastasis.

101 vironment including platelets is crucial for tumor growth and metastasis.

102 greatly inhibits mutant p53 GOF in promoting tumor growth and metastasis.

103 ern recognition receptors, thereby promoting tumor growth and metastasis.

104 PUMA, which induces anoikis to suppress PDAC tumor growth and metastasis.

105 reported to play a more active role in solid tumor growth and metastatic dissemination than simply pr

106 expression of IL-6 and IL-8 and rescued the tumor growth and migratory phenotypes of ovarian cancer

107 f tumor-bearing mice results in cessation of tumor growth and partial rescue of cytokine production b

108 ration of leukocytes into the tumor, slowing tumor growth and preventing metastasis in poorly immunog

109 potential therapeutic targets for inhibiting tumor growth and progression in patients with GBM.

110 ltered signaling pathways and contributes to tumor growth and progression.

111 uocarmycin-based ADC, significantly impaired tumor growth and prolonged median survival from 13 d (ph

112 atment resulted in significant inhibition of tumor growth and prolonged mouse median survival.

113 te that OPA treatment reduces progression of tumor growth and prolongs survival in mice.

114 th intracranial GBM xenograft markedly slows tumor growth and provides a significant survival benefit

115 ignature in patient samples and its roles in tumor growth and radioresistance.

116 cells may provide a selective advantage for tumor growth and resistance to apoptosis.

117 of immunosuppressive adenosine in promoting tumor growth and spread in a number of cancer types, res

118 2, or 17 MBq) and (177)Lu-IMP288 (60 MBq) on tumor growth and survival was assessed.

119 Effects on tumor growth and survival was largely driven by CD8(+) T

120 origenic properties, causing them to support tumor growth and to convert and suppress adaptive immune

121 release of the active MMAE toxin to inhibit tumor growth and to extend animal survival to >90 days i

122 n and lung cancer cells results in increased tumor growth and upregulation of genes overexpressed in

123 IV treatment with HPssCD-HET0016 decreased tumor growth, and altered vascular kinetics in early and

124 tion, COX-2 overexpression, cancer stemness, tumor growth, and drug resistance.

125 of SFN on HCC tumor angiogenesis as well as tumor growth, and indicate that SFN has potential for th

126 ts with agents, such as cisplatin, to impair tumor growth, and observational studies suggest that sta

127 In vivo, LDHA overexpression promoted tumor growth, and oxamate delayed tumor growth.

128 a-AMOT-YAP1 signaling axis that promotes OSC tumor growth, and provide a rationale for therapeutic ta

129 cells decreased B16-F10 metastasis and s.c. tumor growth, and this was IFN-gamma dependent.

130 serves as a key nodal point in coordinating tumor growth, angiogenesis, and metastatic spread in ccR

131 ert their detrimental functions by promoting tumor growth, angiogenesis, and subsequent metastasis de

132 s a combination of pathological evidence and tumor growth at follow-up CT/MR at 12 months.

133 fluorescence imaging from the first week of tumor growth, before they became visible to the naked ey

134 mice with Lp/OVA/StII significantly reduced tumor growth being more noticeable in the preventive ass

135 icantly increased mouse survival and reduced tumor growth both directly on tumor cells and indirectly

136 e B-cell lymphoma (DLBCL) xenografts blocked tumor growth, both when delivered in viral vectors or as

137 ha in breast cancer models initially impairs tumor growth but later leads to the convergent evolution

138 Mutations in EGFR drive tumor growth but render tumor cells sensitive to treatme

139 y of CD39(high)CD8(+) T cells increased with tumor growth but was absent in lymphoid organs.

140 cer reprogram amino acid metabolism to drive tumor growth, but the molecular mechanisms are not well

141 In a cHL xenograft model, SEL24-B489 delayed tumor growth by 95.8% (P = .0002).

142 Although ARF can suppress tumor growth by activating p53 function, the mechanisms

143 Vgll4 inhibits cell proliferation and tumor growth by competing with YAP for binding to TEA-do

144 ast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity.

145 This interaction promotes tumor growth by facilitating recruitment of these cells

146 lects metastasizing tumor cells and supports tumor growth by immunological and metabolic mechanisms.

147 TOR inhibitors were effective in suppressing tumor growth by inhibiting both AR-induced transcription

148 B1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression.

149 mor stroma contributes to the suppression of tumor growth by releasing soluble factors that promote n

150 While blocking tumor growth by targeting autophagy is well established,

151 therapeutic strategies tailored to different tumor growth characteristics.

152 mory potential and capability of controlling tumor growth compared to transiently inhibiting Akt.

153 Results Pazopanib inhibited ovarian tumor growth compared with control (0.054 g +/- 0.041 vs

154 geted silencing of HuR significantly reduced tumor growth compared with PARPi therapy alone.

155 , whereas overexpression, suppressed mammary tumor growth, consistent with a significant association

156 t provides an improved theoretical basis for tumor growth control and may also find utility in therap

157 All individual tumor growth curves were decoded via separate measuremen

158 s determined by clonogenic cell survival and tumor growth delay assays.

159 CXCR4 blockade enhanced anti-VEGFR2-induced tumor growth delay but specific depletion of Ly6G(+) neu

160 HIP results in significant inhibition of the tumor growth examined by in vitro and in vivo experiment

161 tor interacting protein kinase 1 (RIPK1) and tumor growth factor-beta activated kinase 1 (TAK1)-media

162 lymphoma xenograft and efficiently inhibited tumor growth following treatment with the therapeutic an

163 man Burkitt's lymphoma xenograft and inhibit tumor growth, generating complete responses in the major

164 the metabolic requirements of ovarian cancer tumor growth has not been performed.

165 wever, factors that drive HGS ovarian cancer tumor growth have not been fully elucidated.

166 gulation, cell proliferation, and HBV-driven tumor growth.IMPORTANCE Hepatitis B virus (HBV) HBx prot

167 ermittent schedule, this treatment inhibited tumor growth in 11/11 PDXs of lung cancer or melanoma wi

168 Genetic deletion of Fos and Dusp1 suppressed tumor growth in a BCR-ABL fusion protein kinase-induced

169 ellent platform to study tissue behavior and tumor growth in a controlled, three-dimensional (3D) env

170 use model, JNK-IN-8 significantly suppressed tumor growth in a dose-dependent manner by inhibiting ac

171 of BKM120 and Olaparib cooperated to inhibit tumor growth in a genetic mouse model of Pten-deficient

172 Stroma slowed down tumor growth in a lymphocyte-deprived environment but pr

173 In addition, SFN significantly reduced HepG2 tumor growth in a modified chick embryo chorioallantoic

174 pared to normal ones and effectively reduced tumor growth in a mouse xenograft model.

175 asal-like TNBC cells in vitro and attenuates tumor growth in a mouse xenograft model.

176 g cell lines, and suppress H1299 lung cancer tumor growth in a mouse xenograft NOD-SCIDgamma model.

177 kinra abrogates IL-22 production and reduces tumor growth in a murine breast cancer model.

178 hout an HDAC inhibitor significantly delayed tumor growth in a radiation-treated xenograft model.

179 ng in a less transformed phenotype, it slows tumor growth in a xenograft model and correlates with pr

180 that LZK silencing was sufficient to reduce tumor growth in a xenograft model of HNSCC.

181 n of TCF7L1 and its paralogue TCF7L2 reduces tumor growth in a xenograft model of human skin SCC.

182 both in vitro and in vivo, which suppressed tumor growth in a xenograft model that specifically corr

183 tion of (131)I-CLR1404 significantly delayed tumor growth in all rodent pediatric xenograft models an

184 6 E6/E7 peptides significantly inhibited the tumor growth in both early and late therapeutic groups.

185 alances EMT, cancer stem cell potential, and tumor growth in colorectal cancer.

186 ally engineered mouse models of TNBC reduced tumor growth in culture and in vivo.

187 h cyclophosphamide also significantly slowed tumor growth in DLBCL xenograft mice.

188 GTPs and BSp significantly inhibited breast tumor growth in ERalpha-negative mouse xenografts, espec

189 st colon cancer cell lines and b) in vivo on tumor growth in mice following oral administration.

190 ine constructs effectively inhibited EG7-OVA tumor growth in mice, however only treatment with the th

191 KRAS-mutant lung cancer cells and inhibited tumor growth in murine models.

192 on in primary human cancers, facilitation of tumor growth in murine xenograft models, and centrosomal

193 is required for oncogenic transcription and tumor growth in non-small-cell lung cancer (NSCLC).

194 K inhibitor Bay 117085 significantly reduces tumor growth in nude mice compared with control untreate

195 xel and rubone inhibited orthotopic prostate tumor growth in nude mice, compared with monotherapy, by

196 restrained cell proliferation, migration and tumor growth in nude mice.

197 d EGFR phosphorylation, Ki-67 expression and tumor growth in nude mice.

198 of anti-PD-1 antibody therapy on inhibiting tumor growth in the BRAF V600E/PTEN-null melanoma mouse

199 -3 and RT112 xenografts selectively arrested tumor growth in UM-UC-3 xenografts, which had reduced tu

200 ses YAP1 nuclear localization and blocks OSC tumor growth in vitro and in vivo.

201 defects associated with OGT suppression, and tumor growth in vitro and in vivo.

202 d in reduced microvessel density and reduced tumor growth in vivo compared with CCL2-expressing cells

203 The dual drug HA conjugate can inhibit 4T1 tumor growth in vivo during treatment through both intra

204 bit breast cancer cell viability, as well as tumor growth in vivo EPI and NE activate the tumor suppr

205 his regulates SCC cell-cycle progression and tumor growth in vivo Furthermore, we identified a novel

206 E2-dependent cell proliferation in vitro and tumor growth in vivo in a reversible manner, suggesting

207 ly inhibited cell proliferation in vitro and tumor growth in vivo of lung cancer cells.

208 Accordingly, CNTD2 enhanced tumor growth in vivo on A549 xenograft models.

209 liferation in vitro and to abolish xenograft tumor growth in vivo Taken together, our findings establ

210 eam genes and promote cell proliferation and tumor growth in vivo Taken together, our findings reveal

211 hat lipin-1 knockdown significantly inhibits tumor growth in vivo using an orthotopic xenograft breas

212 lockade of miR-24 in tumor cells accelerated tumor growth in vivo, and prevented tumor growth inhibit

213 was synergistic with sunitinib in impairing tumor growth in vivo, indicating that these responses ar

214 YBL1 led to a reduced population of CCSC and tumor growth in vivo, similar to the effects of OGT sile

215 r, and genetic inhibition of JMJD2B impaired tumor growth in vivo.

216 ion in vitro and accompanied by promotion of tumor growth in vivo.

217 nt cell proliferation in vitro and xenograft tumor growth in vivo.

218 lar proliferation and migration in vitro and tumor growth in vivo.

219 ptosis in 2 in vivo syngeneic models of bone tumor growth in which apoptosis-inducible prostate cance

220 respect, our results show that MtRS induces tumor growth independent of the HIF-1alpha pathway.

221 ction, the mechanisms by which it suppresses tumor growth independently of p53 are not well understoo

222 ared with vehicle, FPS-ZM1 inhibited primary tumor growth, inhibited tumor angiogenesis and inflammat

223 with high specific activity induced superior tumor growth inhibition (P = 0.021, n = 5/group) without

224 elerated tumor growth in vivo, and prevented tumor growth inhibition by PMPs.

225 dent PK studies and demonstrated significant tumor growth inhibition efficacy in mouse flank xenograf

226 ly during the early stages of melanoma, poor tumor growth inhibition has been observed in more advanc

227 ced apoptosis, which resulted in significant tumor growth inhibition in CRC mouse models that express

228 tosis in different models, and also leads to tumor growth inhibition in vivo.

229 cancer prodrug molecules and shows effective tumor growth inhibition in vivo.

230 cancer cell lines and was able to induce 60% tumor growth inhibition of the CW22Rv1 in vivo xenograft

231 erapy using both sorafenib and MEAN enhanced tumor growth inhibition over monotherapy with either age

232 ing the affinity of cell binding and ensuing tumor growth inhibition reveal the linker length to be a

233 mplex-specific antibodies led to significant tumor growth inhibition.

234 to model-dependent tumor cell apoptosis and tumor growth inhibition.

235 n BITC, p53/LKB1 and p73/LKB1 axes in breast tumor growth-inhibition.

236 , cyr61 and survivin and upregulation of the tumor growth inhibitor molecule p38 MAPK.

237 ar signals into transcriptional programs for tumor growth, invasion and maintenance of the tumor-init

238 In line, WNT2 also promotes tumor growth, invasion and metastasis in vivo.

239 ote an environment that is less conducive to tumor growth, invasion, and metastasis.

240 Moreover, tumor growth is accelerated, not only in tristetraprolin

241 een increased HIF2alpha levels and inhibited tumor growth is reflected in large neuroblastoma patient

242 r, the impact of efferocytosis in metastatic tumor growth is unknown.

243 oblastoma, whereas temozolomide only delayed tumor growth, its coadministration with 5-NIdR caused co

244 ta1 in vivo showed a significant increase in tumor growth kinetics in both cell types, suggesting a p

245 ted daily with aspirin resulted in decreased tumor growth kinetics, whereas combination therapy of as

246 ution of EETs to angiogenesis and subsequent tumor growth may be attributed to downstream metabolites

247 egulated in Glioblastoma and is required for tumor growth mechanistically, such upregulation is due t

248 ufficient to delay tumor onset and to impair tumor growth, metastasis, and cancer stem-like cell form

249 ed RN7SL1 activates the PRR RIG-I to enhance tumor growth, metastasis, and therapy resistance.

250 eta signaling pathways facilitates efficient tumor growth, migration, and metastatic colonization.

251 s expression of JMJD2B enhanced subcutaneous tumor growth of colon cancer cells in a p53-dependent ma

252 ll migration and invasion, and inhibited the tumor growth of MDA-MB-231 TNBC cell xenografts in the m

253 expressing xenografts, effectively inhibited tumor growth of PSMA-expressing tumors, and significantl

254 ancer cells, the mechanism for dependency of tumor growth on mutant p53 is unknown.

255 o subtypes with targeted therapies inhibited tumor growth only in the subtype of tumor where the ther

256 shed into the blood and its relationship to tumor growth or progression must be validated.

257 a mathematical model was developed to model tumor growth over extended periods of time, and can be u

258 ver, the requirement for endogenous Muc4 for tumor growth progression has not been previously explore

259 ppressed postablation stimulation of distant tumor growth, proliferation, and microvascular density (

260 macologic stabilization of IFNAR1 suppressed tumor growth providing the rationale for upregulating IF

261 The Gompertz model was used to describe tumor growth, radiation effect was simulated by the line

262 Tumor growth rate and uptake varied among the different

263 gnificantly decreases disease penetrance and tumor growth rate in a MYCN-driven transgenic zebrafish

264 parate set of mice in which subject-specific tumor growth rates were accurately predicted.

265 Average tumor growth ratios were 103.0% +/- 75.8 with control tr

266 sets of cancer stem cells (CSC) that sustain tumor growth, recurrence, and therapy resistance.

267 se breast cancer cells, decreased orthotopic tumor growth, reduced tumor angiogenesis and recruitment

268 iferation of tumor cells in vitro and led to tumor growth regression in xenograft models with a KRAS,

269 Tumor growth relies on efficient DNA repair to mitigate

270 cell proliferation and suppressed metastatic tumor growth, respectively.

271 s, we observed that although some markers of tumor growth such as vascularity and cyclin D1 expressio

272 at activates both mTORC1 and MAPK to promote tumor growth, suggesting a combination of mTORC1 and MAP

273 bryonic development, wound healing, and even tumor growth, suggesting more complex physiological role

274 th sEH and COX led to a dramatic decrease in tumor growth, suggesting that the contribution of EETs t

275 angiogenesis and is an important protein for tumor growth, survival, and cancer cell metastasis.

276 We show that, in addition to inhibiting tumor growth, targeting BECN1 increased the infiltration

277 Kp46-iCre mice were also more susceptible to tumor growth than were their littermate controls when ch

278 dings suggest new strategies for controlling tumor growth that avoid the resistance to existing mTOR

279 markedly decreased glycolysis and restrained tumor growth, these signaling and metabolic restrictions

280 ese two led to improved survival and delayed tumor growth; this was accompanied by augmented antitumo

281 at HPssCD-HET0016 is effective in inhibiting tumor growth through decreasing proliferation, and neova

282 l line and xenograft models markedly reduces tumor growth through inhibition of mTOR pathway.

283 identified a novel mechanism of PLN-induced tumor growth through macrophage polarization and immunos

284 nal experiments revealed that MEAN inhibited tumor growth through mechanisms distinct from those of e

285 o the regulatory effect exerted by JMJD2B on tumor growth through the modulation of p53 target genes.

286 oral T reg and effector T cells in promoting tumor growth through the production of factors normally

287 astatic sites, but not primary growth sites, tumor growth was associated with increased megakaryopoie

288 tumor microenvironment and that PLN-induced tumor growth was dependent on macrophages.

289 ice, which develop chronic liver damage, and tumor growth was monitored.

290 c subunit PI3K(p110alpha), which can promote tumor growth, was remarkably downregulated, while the tu

291 nes, melanoma cell proliferation and in vivo tumor growth were significantly increased in the presenc

292 ts of PDZK1 on SHP-1 phosphorylation and the tumor growth were verified in vivo by xenograft tumor st

293 Activated form of Notch1 promotes xenograft tumor growth when expressed ectopically.

294 cluding consistency in predictions of single tumor growth when no secondary tumor was present.

295 -tissue resident Rorc(fm+) ILCs can suppress tumor growth, whereas intestinal Rorc(fm-) ILC1s or NK c

296 microparticles (MPs), supported accelerated tumor growth which was halted by PMP transfusion.

297 lar and molecular determinants that maintain tumor growth, will undoubtedly yield more effective ther

298 iltration into tumors enhanced inhibition of tumor growth with anti-VEGFR2 therapy.

299 ents of the V-SVZ that may permit or promote tumor growth within the region.

300 PD-1 blockade delays tumor growth without changing TIL metabolism or function

301 er inhibiting cytokinesis in the liver slows tumor growth without compromising the health of normal h