ライフサイエンスコーパス: tumor growth

1 iate into defined progenies and initiate the tumor growth.

2 the most effective strategy for restricting tumor growth.

3 etency in the brain, with reduced orthotopic tumor growth.

4 of effector functions, and better control of tumor growth.

5 ggers a regenerative response and stimulates tumor growth.

6 is overcome, and low-avidity T cells control tumor growth.

7 for assessing hypoxia, microvasculature, and tumor growth.

8 nner, causing immune activation and reducing tumor growth.

9 1AP1 KD) in breast cancer cell lines reduced tumor growth.

10 iple negative breast cancer (TNBC) prevented tumor growth.

11 and elimination of a drug and its effect on tumor growth.

12 mma) NSG mice, suggesting its implication in tumor growth.

13 ic T-lymphocyte surveillance, which leads to tumor growth.

14 ironment of the breast alter cancer risk and tumor growth.

15 cient mice resulted in a strong reduction of tumor growth.

16 -dependent cancer cell-colony formation, and tumor growth.

17 epletion of these cells abrogated MI-induced tumor growth.

18 ignaling and that CYP24A1 knockdown inhibits tumor growth.

19 ity in human RCC tumors, and its role in RCC tumor growth.

20 ases, without limiting primary or metastatic tumor growth.

21 SCs can, however, either promote or suppress tumor growth.

22 both in vitro and in vivo, and thus promote tumor growth.

23 ng that alpha3beta1 is essential to maintain tumor growth.

24 dgehog inhibitor (GDC-0449) displays reduced tumor growth.

25 ty to form tumorspheres and severely affects tumor growth.

26 st tumors in mice, and significantly reduced tumor growth.

27 mor growth while minimally impacting mammary tumor growth.

28 s via VEGF signaling and enhance the rate of tumor growth.

29 eloid-lineage cells, including TAMs, delayed tumor growth.

30 increased sensitivity to anoikis and reduced tumor growth.

31 nd how bacterial sepsis may impact malignant tumor growth.

32 n the context of both normal development and tumor growth.

33 of EPAC-RAP1 and MAPK, ultimately modulating tumor growth.

34 d survival from 37 to 47 d but did not delay tumor growth.

35 odels, postseptic mice exhibited accelerated tumor growth.

36 and antigen presentation in Gpr81-dependent tumor growth.

37 ctions for (177)Lu-DOTA-JR11 despite further tumor growth.

38 tudies demonstrated that complement promotes tumor growth.

39 have a profound effect on carcinogenesis and tumor growth.

40 vivo without significantly altering primary tumor growth.

41 ated inside the tumor, where they can arrest tumor growth.

42 induced cell death and significantly slowed tumor growth.

43 in T-cell homing to tumors and inhibition of tumor growth.

44 ession of both SEMA5B expression and in vivo tumor growth.

45 formation alters lipid metabolism to sustain tumor growth.

46 t (TDT > 365 days) and rapid (TDT < 90 days) tumor growth.

47 raming of proline metabolism is critical for tumor growth.

48 astasis, despite having no effect on primary tumor growth.

49 urine OX40+ pDC-rich tumor model accelerated tumor growth.

50 -bisphosphatase (FBP1), was found to inhibit tumor growth.

51 expression, proline synthesis, fibrosis and tumor growth.

52 s of debris, resulting in suppression of HCC tumor growth.

53 ation with JNK activation and Hippo-mediated tumor growth.

54 y decreased tumor numbers and did not reduce tumor growth.

55 or microenvironment (TME) for the support of tumor growth.

56 inclusion in mutant KRAS/p53 PDACs decreases tumor growth.

57 icant interest for their potential to combat tumor growth.

58 ized by mitochondrial glutaminase to support tumor growth.

59 in CAFs acts to stimulate stromagenesis and tumor growth.

60 ls present in tumor microenvironment to help tumor growth.

61 VA (17/32, 53%), good final VA (11/32, 34%), tumor growth (12/25, 48%), and need for enucleation (7/5

62 CC tumor sites and efficiently inhibited the tumor growth after multiple IV injection.

63 vo, while AZD2014 and dasatinib each inhibit tumor growth alone, the effect of combination therapy ex

64 f traumatic injury, cell transplantation, or tumor growth, among many others.

65 Dox + Val ISFIs showed a 2-fold reduction in tumor growth and a 27.69% increase in necrosis 20 days p

66 cell cycle-associated genes, indicating that tumor growth and cell proliferation were hormone depende

67 g mice with the PGR antagonist RU486 stalled tumor growth and decreased the expression of cell cycle-

68 1-DD-deficient mice were more susceptible to tumor growth and deficiency of DAPK1 activity significan

69 munosuppressive functions, further fostering tumor growth and dissemination.

70 all mouse survival by controlling both local tumor growth and distant tumor metastasis.

71 D8 T cell migration to the tumor site, delay tumor growth and enhance survival in murine tumor models

72 PC cell growth, migration, invasion, in vivo tumor growth and enhances GEM sensitivity.

73 directly interact with MM cells to increase tumor growth and expression of Ocy-derived factors that

74 with deletion of P2rx7 significantly reduced tumor growth and extended survival.

75 New drugs that control tumor growth and favorably modulate the immune environme

76 roach showed higher blood life span, reduced tumor growth and higher tolerance in a murine carcinoma

77 that Gal2 plays a suppressive role in colon tumor growth and highlights the therapeutic potential of

78 d-derived suppressor cells (G-MDSCs) promote tumor growth and immunosuppression in multiple myeloma (

79 SERBP1 knockdown causes delay in tumor growth and impacts cancer-relevant phenotypes in G

80 C, obesity and excess fatty acids accelerate tumor growth and increase metastasis.

81 Platelets significantly reduced tumor growth and increased intratumoral macrophages.

82 pressed OCSC survival in vitro and inhibited tumor growth and increased platinum sensitivity in vivo.

83 given orally effectively inhibits xenograft tumor growth and induces survivin loss in tumors.

84 Consistently, GBP2 dramatically promotes GBM tumor growth and invasion in mice and significantly redu

85 R2 in the PyVmT mammary epithelium inhibited tumor growth and invasion, elevated CD8+ T cells, decrea

86 tumor-associated macrophages (TAMs) promote tumor growth and invasion.

87 Ultraselective HDAC6 inhibitors can reduce tumor growth and invasiveness of breast cancer by noncan

88 with an immune checkpoint inhibitor, reduces tumor growth and is a potential future treatment option

89 targeted inhibition of RAS pathway-dependent tumor growth and liberation of antitumor immune response

90 t constitutes a major factor responsible for tumor growth and malignancy.

91 e canonical Hh signaling pathway to suppress tumor growth and metastases, in part, by limiting ROS ac

92 show that early cardiac remodeling nurtures tumor growth and metastasis and therefore promotes cance

93 Here we studied tumor growth and metastasis in Cyp2c44(-/-) mice crossed

94 nical outcomes, but also facilitated primary tumor growth and metastasis in vivo.

95 mor cell migration and invasion in vitro and tumor growth and metastasis in vivo.

96 on and colony formation in vitro, as well as tumor growth and metastasis in vivo.

97 Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppress

98 oint blockade further enhances inhibition of tumor growth and metastasis with low systemic toxicity.

99 (CYP) enzymes have been linked to increased tumor growth and metastasis, largely on the basis of ove

100 In addition to inhibiting tumor growth and metastasis, silencing TRAF3IP2 disrupte

101 silencing Rab27a and TRAF3IP2 each inhibited tumor growth and metastasis, silencing TRAF3IP2 is more

102 Rag1-/-, Il9r-/-, and Il17ra-/- mice altered tumor growth and metastasis.

103 avior of the malignant cells and thus affect tumor growth and metastasis.

104 rovide potential targets for intervention of tumor growth and metastasis.

105 ene YAP has been shown previously to promote tumor growth and metastasis.

106 mic nervous system having a direct effect on tumor growth and metastasis.

107 verexpressed or mutated in cancers and drive tumor growth and metastasis.

108 in colon cancer cell lines decreased primary tumor growth and metastasis.

109 RP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neu

110 expression, and tumor necrosis while slowing tumor growth and modestly increasing mouse survival with

111 itro, its attenuation significantly impaired tumor growth and neovascularization in vivo.

112 Kit inhibitor imatinib significantly reduced tumor growth and phospho-Akt and cyclin D1 expression, a

113 sh/W-sh) (Wsh) mice, showed that MCs promote tumor growth and prevent the development of basal CK5-po

114 ne checkpoint blockade to inhibit metastatic tumor growth and prevent tumor relapse by activating cel

115 functions for CDK4 and CDK6 in facilitating tumor growth and progression in metastatic cancers.

116 erate CR-CSC-based mouse avatars to evaluate tumor growth and progression upon treatment with BMP7v a

117 activation induced by t-ASPP2 contributed to tumor growth and progression while being dispensable for

118 spheroids in ovarian cancer (OC) facilitate tumor growth and progression, and also pose major obstac

119 croenvironment (TME) plays critical roles in tumor growth and progression, however key regulators of

120 changes within their host tissues to support tumor growth and progression.

121 regulated by complex mechanisms that promote tumor growth and proliferation.

122 STICK-NPs significantly inhibit tumor growth and prolong the survival time with limited

123 enger, decreased tumor DNA damage, inhibited tumor growth and prolonged mouse survival.

124 re we demonstrate that phenformin suppresses tumor growth and promotes keratinocyte differentiation i

125 These changes were associated with mitigated tumor growth and reduced metastases.

126 eatic cancer, revealed that sVCAM-1 promotes tumor growth and resistance to gemcitabine treatment in

127 of different cell types in the tumor, drive tumor growth and resistance to therapies.

128 Understanding how obesity impacts early tumor growth and response to macrophage-targeted therapi

129 models of TNBC, CDN administration inhibits tumor growth and substantially improves survival.

130 e of the miR-211-DUSP6-ERK5 axis in melanoma tumor growth and suggest a mechanism for the development

131 g C4-2 tumor-bearing SCID mice by evaluating tumor growth and survival over 6 wk after treatment.

132 receptor (Y5R) in HCC, which correlated with tumor growth and survival.

133 pe in high-risk neuroblastoma that modulated tumor growth and therapy resistance in vivo.

134 of these mutations, including their role in tumor growth and treatment resistance and how they can b

135 hosphoinositide recycling results in reduced tumor growth and tumor angiogenesis.

136 howed that YY1 deletion in ECs inhibited the tumor growth and tumor angiogenesis.

137 ful to define effective treatments that halt tumor growth and tumor progression in NF1.

138 ically injected 4T1 cells, Cl-OCH3 decreased tumor growth and weight and inhibited lung metastasis.

139 at maintain the ability to self-renew, drive tumor growth, and contribute to therapeutic resistance a

140 ng CD8(+) T and natural killer cells, slowed tumor growth, and improved mouse survival.

141 or inhibition decreased migration/invasion, tumor growth, and lung metastasis.

142 colony formation, migration, wound healing, tumor growth, and lung metastasis.

143 an cancer mouse models reduced angiogenesis, tumor growth, and metastasis.

144 ions in tumor microenvironment interactions, tumor growth, and metastasis.

145 d potent cytostatic and cytotoxic effects on tumor growth, and strongly suppressed metastatic capacit

146 echanism by which BRD4 inhibition suppresses tumor growth, and support further development of NHWD-87

147 ages of tumor progression, including primary tumor growth, angiogenesis, invasion and metastasis.

148 es targeting mutant KRAS effectively inhibit tumor growth as well as metastasis in the tumor-bearing

149 monolyso-CL levels but also reduced in vivo tumor growth, as determined by xenograft studies in athy

150 eral mammary gland, evidenced by the lack of tumor growth at MSC-injected site.

151 vation of IKK2 (Sftpc-cRaf-IKK2CA) supported tumor growth; both effects were accompanied by altered e

152 ainly focus on the antiangiogenic effects on tumor growth but do not provide information about host c

153 Furthermore, Pvt1b loss accelerates tumor growth, but not tumor progression, in an autochtho

154 ndicates that vitamins C and D are linked to tumor growth, but the relevance of vitamin B6 remains un

155 metabolism, not only were we able to inhibit tumor growth, but we markedly inhibited the generation a

156 ls (APC), and abrogates local and metastatic tumor growth by a T-cell-related effect.

157 cer agents to inhibit chemotherapy-resistant tumor growth by consuming intracellular glutathione and

158 an cancers and drives aerobic glycolysis and tumor growth by inhibiting pyruvate kinase M2 (PKM2).

159 inhibiting cell proliferation, survival, and tumor growth by suppressing PI3K/mTOR/Akt activities in

160 Tumor-associated macrophages (TAMs) support tumor growth by suppressing the activity of tumor-infilt

161 ancer and plays an autocrine role to promote tumor growth by tumor cell-derived lactate.

162 iple dosing, ALDC1 significantly delayed the tumor growth compared to control treatment arms MMAE, MM

163 r, and therapeutic response characterized by tumor growth curves and histopathology.

164 Tumor growth curves are classically modeled by means of

165 ore vulnerable to radiation, showing delayed tumor growth, decreased proliferation, and increased apo

166 ific differences and ubiquitously suppresses tumor growth, demonstrating the therapeutic utility of t

167 upon implantation in mice, revealed similar tumor growth dynamics and retention of architectural fea

168 with secreted Gaussia luciferase to monitor tumor growth dynamics and tagged with a unique DNA barco

169 In both SCS-groups, levels of tumor growth factor-beta were higher 3 hours post-LT, on

170 ctively, causing a small equivalent delay in tumor growth, followed by regrowth.

171 d, respectively, with a significant delay in tumor growth for all 3 doses.

172 d a syngeneic transplant model by monitoring tumor growth from a mouse breast cancer cell line (AT-3,

173 Nckap1 loss slowed proliferation and tumor growth, highlighting a role in cell-cycle progress

174 cer and implicate GSTO1 in the modulation of tumor growth, immune responses, and expression of F3.

175 miR-15a inhibitor decreases angiogenesis and tumor growth in a CT26 murine colorectal carcinoma model

176 C49 radioimmunotherapy significantly reduced tumor growth in a dose-dependent manner (1.85, 3.7, and

177 s of OLIG2 dimerization and found to inhibit tumor growth in a mouse glioblastoma cell line and in a

178 tivity in a cell-based assay, and can arrest tumor growth in a mouse xenograft BT474 tumor model.

179 imic treatment induces cell death and delays tumor growth in a PEL xenograft model.

180 tte-Guerin, and Citrobacter rodentium and of tumor growth in a syngeneic tumor model.

181 Rab5a suppressed HSC activation and limited tumor growth in a tumor implantation mouse model.

182 xpression of angiogenic markers and promotes tumor growth in a xenograft model.

183 ation in cultured cells and reduced prostate tumor growth in a xenograft model.

184 onjugated ALDC1 also significantly inhibited tumor growth in an immunocompetent syngeneic mouse model

185 tetraxetan synergistically suppressed Raji2R tumor growth in athymic Foxn1(nu) mice.

186 dent activation, metabolic deregulation, and tumor growth in BLCA.

187 of the current standard-of-care used to slow tumor growth in both adult and pediatric patients.

188 ned with RT led to a significant decrease in tumor growth in both heterotopic and orthotopic, includi

189 studies, 5FU-SLN(4) significantly inhibited tumor growth in comparison to 5-FU while area-under plas

190 iting protein elongation with SVC112 reduces tumor growth in head and neck squamous cell carcinoma an

191 tic or chemical inhibition of p38alpha halts tumor growth in lung cancer mouse models.

192 ing wild-type p53, and effectively inhibited tumor growth in metastasis in a mouse homograft mode of

193 a bioavailable LDH inhibitor that decreases tumor growth in mice and functions synergistically with

194 Anti-PD-L1 treatment restricts tumor growth in mice bearing ARID2-knockout melanoma cel

195 f HIF1/2alpha abolished CHD4-mediated breast tumor growth in mice.

196 ng CIP, as well as attenuated suppression of tumor growth in mice.

197 ocal irradiation causes strong inhibition of tumor growth in mouse xenografts, compared with MEK5 dep

198 nt as a combination with anti-PD1, SG7 slows tumor growth in multiple syngeneic mouse models.

199 rrying a CpG DNA ligand of TLR9 can suppress tumor growth in several animal models of various cancers

200 ouse embryonic fibroblasts and in aggressive tumor growth in severe combined immunodeficiency mice.

201 Detailed assessments of tumor growth in subtyped experimental models revealed th

202 -trained mice to naive recipients suppressed tumor growth in the latter in a ROS-dependent manner.

203 L2 demonstrated dose-dependent inhibition of tumor growth in the PSMA(+) flank tumor model.

204 d activity-dependent, specific inhibition of tumor growth in the PSMA+ flank tumor model.

205 n addition, miR-181c significantly regressed tumor growth in the xenograft human hepatocellular carci

206 hanced effect of anti-CD47 blockade limiting tumor growth in TMEM30A-knockout models.

207 ignificantly increased MDSC accumulation and tumor growth in tumor-bearing mice in vivo.

208 , and that GRK2 knockdown enhances ABC-DLBCL tumor growth in vitro and in vivo.

209 in an enhanced ability of T cells to inhibit tumor growth in vitro and in vivo.

210 more, knockdown of PTPRF inhibited xenograft tumor growth in vivo and decreased the expression of Wnt

211 ow senescence and the SASP act on endogenous tumor growth in vivo is unknown.

212 criptional activity and is required for TNBC tumor growth in vivo using an orthotopic xenograft model

213 Inhibition of tumor growth in vivo with adjuvant IGFBP-3-Fc with erlot

214 d PTEN-deficient TNBC in vitro and inhibited tumor growth in vivo, but had no effect on the prolifera

215 ll proliferation, and migration in vitro and tumor growth in vivo, while the depletion or inhibition

216 ls increased cell proliferation in vitro and tumor growth in vivo.

217 mor cell proliferation in vitro and enhanced tumor growth in vivo.

218 ell lines in vitro and for optimal xenograft tumor growth in vivo.

219 s of basal-like TNBC and reduces PDX mammary tumor growth in vivo.

220 ion rescued MITF.KO cell growth in vitro and tumor growth in vivo.

221 liferation in vitro and inhibited orthotopic tumor growth in vivo.

222 rowth in vitro and trending toward decreased tumor growth in vivo.

223 gistically promoted ER stress and suppressed tumor growth in vivo.

224 h KURAMOCHI and COV362 cells did not improve tumor growth in vivo.

225 mune cell polarization, we assayed syngeneic tumor growth in wild-type and mirn23a (-/-) mice.

226 ibition of AURKA, a miR-497 target, suppress tumor growth in xenograft mouse models, proposing the TA

227 Candidate models of tumor growth included the exponential, logistic and Gomp

228 inhibition of MTA2 suggested that in primary tumor growth, independent of IKK2, MTA2/NuRD corepressor

229 omote invasion, chemoresistance, and in vivo tumor growth, indicating that it acts as a master regula

230 blocking antibodies with radiation increases tumor growth inhibition and extends the survival of tumo

231 e well tolerated and resulted in significant tumor growth inhibition and prolonged overall survival i

232 aser irradiation provided the most efficient tumor growth inhibition capability without severe system

233 Marked tumor growth inhibition compared with controls was obser

234 SHP2 inhibition has demonstrated tumor growth inhibition in RTK-activated cancers in prec

235 ting of MEK1/2, HDAC3, and G9a sustains PDAC tumor growth inhibition in vivo.

236 oma cell lines promoted tumor cell death and tumor growth inhibition in xenograft mouse models.

237 Moreover, tumor growth inhibition of E.G-7 tumors was closely corr

238 26a was able to induce an 80% tumor growth inhibition of xenografts derived from the e

239 In xenografts, a significant tumor growth inhibition was seen after twice-weekly intr

240 nergetic conditions that provide significant tumor growth inhibition with acceptable host body weight

241 ession of the GSC critical genes, leading to tumor growth inhibition.

242 xenograft tumors resulted in PD-L1-dependent tumor growth inhibition.

243 the RT-induced antitumor immune response and tumor growth inhibition.

244 zfh1 are depleted in the mesenchymal cells, tumor growth is compromised.

245 This disease is characterized by invasive tumor growth, leading to extensive bone destruction, and

246 suggest a prominent role of MTA2 in primary tumor growth, lung metastasis, and NF-kappaB signaling m

247 -terminal domain in blood vessel remodeling, tumor growth, metastasis, integrin binding, and proteoly

248 pivotal role in lung cancer, contributing to tumor growth, microenvironmental changes, and metastasis

249 combined CAP and ICB therapy can inhibit the tumor growth of both primary tumors and distant tumors,

250 Phendione treatment reduces tumor growth of BRAF(V600E)-driven melanoma patient-deri

251 Notably, Norrin mediates enhanced tumor growth of glioblastomas by activating the Notch pa

252 l hemodynamic heterogeneity as a function of tumor growth or therapy affects the development of novel

253 th checkpoint blockade significantly reduced tumor growth over time and, in some cases, cleared the t

254 ytic viruses affect virotherapy outcomes and tumor growth patterns in a tumor microenvironment, we de

255 vasive cells that coordinately drive primary tumor growth, progression, and recurrence after therapy.

256 t doses similar to those reported to inhibit tumor growth, rapidly impaired ventilatory responses to

257 interstitial hydraulic conductivity increase tumor growth rate and contribute to tumor malignancy.

258 tions in this effort included variability in tumor growth rate and tumor size, solid tumors versus tu

259 andard clinical dose of Abraxane reduces the tumor growth rate as effectively as the standard clinica

260 t at baseline was negatively correlated with tumor growth rate.

261 onin 1C in this model increases both primary tumor growth rates and distant metastases.

262 irradiated breast carcinoma cells increases tumor growth rates in mice recipients in comparison with

263 FCW34 was shown to inhibit tumor growth, reduce angiogenesis, and delay cancer cell

264 ll intrinsic oncogenic properties, decreased tumor growth, reduced the incidence of lung metastasis a

265 s promote metastasis, however, their role in tumor growth remains controversial.

266 nd, by in vivo CRISPR led to more aggressive tumor growth suggesting that IHH, rather than SHH, activ

267 ese data show that Rh-PPO inhibits xenograft tumor growth, supporting the strategy of using Rh-PPO as

268 evaluated BCL2 inhibitor, ABT-263, restored tumor growth suppression and induced apoptosis.

269 al effects, bone regeneration potential, and tumor growth suppression under NIR laser radiation are t

270 53 and dinaciclib would be most effective in tumor growth suppression, which we demonstrated in neuro

271 eability, increased T cell infiltration, and tumor growth suppression.

272 ion therapy (RT) more significantly inhibits tumor growth than monotherapies (i.e., PDT or RT).

273 acute and chronic bacterial infection and of tumor growth that the conditional ablation of Irf4 in CD

274 od vessel (BV) formation is thought to drive tumor growth through elevated nutrient delivery.

275 Mitochondria contribute to tumor growth through multiple metabolic pathways, regula

276 nockdown produced substantial suppression of tumor growth upon intracranial implantation, as well as

277 is stimulates hepatocellular carcinoma (HCC) tumor growth via an "eicosanoid and cytokine storm." AFB

278 ator that synergizes with Ras(V12) to induce tumor growth via JNK-mediated Hippo signaling.

279 ased Mn(2+) , and inhibited orthotopic liver tumor growth via synergistic SDT/CDT.

280 were injected along with WT parental cells, tumor growth was enhanced with mutant cells becoming the

281 administration of (67)Cu-CuSarTATE (5 MBq), tumor growth was inhibited by 75% compared with vehicle

282 n intraperitoneal injections of simvastatin; tumor growth was monitored and tumors were collected and

283 mall molecule inhibitor of CDH11 (SD133) and tumor growth was monitored.

284 mitogen-activated protein kinase inhibition, tumor growth was significantly blunted and corresponded

285 Results: At 13 d after injection, tumor growth was similarly inhibited by the 2 tracers in

286 Tumor growth was suppressed in Gpr81-null mice compared

287 sculature and tumor tissue that occur during tumor growth, we used a computational model to develop a

288 duction of cellular damage and the effect on tumor growth were analyzed to determine treatment effica

289 that during early oncogenesis IL-17 supports tumor growth, whereas in established tumors IL-17 produc

290 negatively regulates NF-kappaB signaling and tumor growth, whereas later dissociation of MTA2/NuRD co

291 t1 or Glut3, in cancer cells does not impair tumor growth, whereas their combined loss diminishes tum

292 ion of CDK7 reduced organ size and inhibited tumor growth, which could be reversed by restoring Yki/Y

293 s) was impaired and associated with enhanced tumor growth, which were inhibited by metformin.

294 lycolytic pathways selectively impairs brain tumor growth while minimally impacting mammary tumor gro

295 PARP-1/PARP-2-deficiency in T cells promotes tumor growth while single deficiency of each protein lim

296 The model combines Gompertzian tumor growth with antibody-mediated pharmacokinetics and

297 model, we showed that FN3-PARs can suppress tumor growth with no adverse effects and FN3-PARs reduce

298 M results in a potent reduction of xenograft tumor growth without any obvious side effects in normal

299 ly limits the synthesis of mRNAs involved in tumor growth without causing an outage of transcription

300 expressed Angpt2 was dispensable for primary tumor growth, yet in-depth analysis of primary tumors re