ライフサイエンスコーパス: tumor development

1 ence in primary cells, an initial barrier to tumor development.

2 involved in eubiology and pathology, such as tumor development.

3 t role in immune surveillance and control of tumor development.

4 o escape immune recognition is important for tumor development.

5 igated the role of calcineurin in intestinal tumor development.

6 blishing a positive feedback loop to support tumor development.

7 nduced epidermal hyperproliferation and skin tumor development.

8 atopoietic stem cells (HSCs) and may promote tumor development.

9 iples underlie the responses observed during tumor development.

10 n by random mutations that accumulate during tumor development.

11 anistic link between periodontal disease and tumor development.

12 ulation of angiogenesis during embryonic and tumor development.

13 y unidentified signaling pathway involved in tumor development.

14 sets, and the balance among subtypes impacts tumor development.

15 into account its kinase-independent role in tumor development.

16 Ikk-related kinase Ikkepsilon in Wnt-driven tumor development.

17 s from immune attack are hijacked to license tumor development.

18 ific functions and contribute differently to tumor development.

19 nocytes and to molecular cascades leading to tumor development.

20 at may contribute to disease progression and tumor development.

21 g of the alterations of this biofluid during tumor development.

22 owth only when initiated at an early time of tumor development.

23 on and the occurrence of M2-type TAMs during tumor development.

24 malignancy and liver fibrosis, and prevented tumor development.

25 growth and development is established during tumor development.

26 e commensal microbiota to promote intestinal tumor development.

27 n-specific cytotoxic T-cell responses during tumor development.

28 ling, phorbol ester-induced hyperplasia, and tumor development.

29 ing system is progressively disrupted during tumor development.

30 a inhibits the earliest stages of intestinal tumor development.

31 cell proliferation, organ size control, and tumor development.

32 vate repair pathways, which can help prevent tumor development.

33 he cell transfer on immune cell activity and tumor development.

34 ased hepatic lipid metabolism prior to overt tumor development.

35 sponse to tissue damage, transplantation, or tumor development.

36 oring oncogenic mutations, thereby promoting tumor development.

37 ons of Foxa1 and Foxa2 in both embryonic and tumor development.

38 to selectively promote BRAF V600E-dependent tumor development.

39 the tumor stroma, play an important role in tumor development.

40 numerary centrosomes are sufficient to drive tumor development.

41 cific metabolic alterations are required for tumor development.

42 pproach for prediction of local and systemic tumor development.

43 g cells, which may potentially contribute to tumor development.

44 infection, wound healing, tissue repair, and tumor development.

45 MT2D, suggesting a role in driving phyllodes tumor development.

46 tion, based on Ki67 staining, and suppressed tumor development.

47 icient mice were hypersusceptible to colonic tumor development.

48 s DNA-PK and CHK1 during the later stages of tumor development.

49 tinoblastoma can occur at the early stage of tumor development.

50 nt for angiogenesis during embryogenesis and tumor development.

51 eIF4E must be phosphorylated to promote tumor development.

52 0 weeks during the 'risk window' for mammary tumor development.

53 erexpressing tissues and could contribute to tumor development.

54 tenuation of the p53 pathway and accelerated tumor development.

55 genetic regions frequently gained or lost in tumor development.

56 epithelial to mesenchymal transition during tumor development.

57 y promote DNA repair with the suppression of tumor development.

58 irect evidence for the impact of this SNP in tumor development.

59 the potential role of p53 status in MSCs in tumor development.

60 on representing an avenue of deregulation in tumor development.

61 ve immunosuppressive microenvironment during tumor development.

62 mor volume and quantitative follow-up of the tumor development.

63 onstruct induce necrosis and completely lack tumor development.

64 e chronic inflammation, promoting intestinal tumor development.

65 fines mutational signatures occurring during tumor development.

66 ral microenvironment plays a role in oral KS tumor development.

67 e constraints encountered over the course of tumor development.

68 ell proliferation, providing a mechanism for tumor development.

69 aling in physiologic processes as well as in tumor development.

70 pathways that are indicative of early-stage tumor development.

71 elopment of cancer and are often lost during tumor development.

72 liferation and migration of cancer cells and tumor development.

73 titumor response but instead further boosted tumor development.

74 plore heparanase function at early stages of tumor development.

75 t for augmented oncogenic HRAS signaling for tumor development.

76 actor in the observed overall enhancement of tumor development.

77 liferation, and leads to spontaneous luminal tumor development.

78 axis in bladder whose disruption can promote tumor development.

79 optosis signaling pathways thought to govern tumor development.

80 ombinase and sgRNAs, which caused rapid lung tumor development.

81 that plays pivotal roles in angiogenesis and tumor development.

82 fects seen in the single mutants, but led to tumor development.

83 some amplification, genomic instability, and tumor development.

84 eutrophil function during mouse versus human tumor development.

85 d to p62(-/-) mice were protected from renal tumor development.

86 nd lipid synthesis, leading to steatosis and tumor development.

87 erations that are clonally selected to drive tumor development.

88 nduced apoptosis and markedly promotes renal tumor development.

89 ted the formation and reduced the latency in tumor development.

90 riters/erasers and PcG complexes to restrict tumor development.

91 ts that cooperate with Hras(G12V) in thyroid tumor development.

92 kaca fusion and monitored the mice for liver tumor development.

93 thylcellulose or polysorbate-80, exacerbated tumor development.

94 the cancer cells themselves, contributes to tumor development.

95 aling and expression of proteins relevant to tumor development.

96 le of tumor-associated macrophages (TAMs) in tumor development.

97 ho show increased susceptibility to squamous tumor development.

98 toms are not specific during early stages of tumor development.

99 Smarcal1 in hematopoietic cell survival and tumor development.

100 erates with ionizing radiation to exacerbate tumor development.

101 metabolic changes as a novel GOF to promote tumor development.

102 point modification contributes to esophageal tumor development.

103 tylation in maintaining cell homeostasis and tumor development.

104 could have protumor or antitumor effects on tumor development.

105 rthotopic model of pancreatic cancer delayed tumor development.

106 A damage, widespread aneuploidy, spontaneous tumor development, accelerated Emu-Myc-induced lymphomag

107 We observed accelerated tumor development, aggressive tumor invasion and a decre

108 s of specific microRNAs (miRNAs) involved in tumor development and aggressiveness.

109 the DDR factor p53 takes center stage during tumor development and also plays an important role in th

110 The miR-17-92 cluster has been linked to tumor development and angiogenesis, but its role in vasc

111 t inflammatory cells that play a key role in tumor development and are considered therapeutic targets

112 s, such as HIV infection/AIDS, tuberculosis, tumor development and atherosclerosis.

113 cation, and such mechanism may contribute to tumor development and drug resistance.

114 as a potential therapy for ADAM10-dependent tumor development and drug resistance.

115 creases microtubule dynamics, and results in tumor development and drug resistance.

116 s a (previously unrecognized) contributor to tumor development and establish a novel paradigm of tumo

117 dentified pleiotropic roles for DeltaNp63 in tumor development and found that its regulation of Lef1

118 Tumor development and growth, as well as metastatic spre

119 autocrine VEGF signaling abolished vascular tumor development and growth.

120 lls, and these alterations play key roles in tumor development and growth.

121 ts into the role and mechanism of PPP1R1A in tumor development and identified an important kinase and

122 Tumor development and inflammation were determined by en

123 d3 signaling pathways that may contribute to tumor development and inflammation.

124 potent angiogenic factor in the settings of tumor development and inflammation.

125 Macrophages have key roles in tumor development and invasion in several human cancers,

126 (EGF) receptor (EGFR) has been implicated in tumor development and invasion.

127 ival and proliferation pathways important in tumor development and maintenance, are becoming promisin

128 investigating novel genetic interactions in tumor development and maintenance.

129 cription factors play key roles in mediating tumor development and metastasis in addition to their we

130 ondrial process as a basis for understanding tumor development and metastasis in individual subjects.

131 pigenetic events function in tandem to drive tumor development and metastasis.

132 tion of HIF protein activity correlates with tumor development and metastasis.

133 as shown that FOXC1 plays a critical role in tumor development and metastasis.

134 ned with Th1 or Th17 lymphocytes to suppress tumor development and metastatic disease.

135 ut the signaling pathways that contribute to tumor development and metastatic progression are not com

136 ssion of AKT and c-Met triggered rapid liver tumor development and mice required to be euthanized wit

137 ated the effect of LIMK inhibition on breast tumor development and on paclitaxel-resistant tumors, us

138 pressed genes, but have an essential role in tumor development and patient outcome.

139 esearch and is a platform for mining data on tumor development and patterns of metastases.

140 The contributions of intracellular IGFBP2 to tumor development and progression are also unclear.

141 iptionally regulates numerous key aspects of tumor development and progression by promoting a more ag

142 (HDACs) have been associated with malignant tumor development and progression in humans.

143 e on the function and regulation of FOXC1 in tumor development and progression with a focus on BLBC,

144 ng of the roles of complement and the MAC in tumor development and progression, which in turn will in

145 d by distinct genotypic subgroups that drive tumor development and progression.

146 ancer cells correlates with their potency of tumor development and progression.

147 aberrations that likely drive nasopharyngeal tumor development and progression.

148 transcription factors are integral to HER2+ tumor development and progression.

149 Cancer stroma has a profound influence on tumor development and progression.

150 gammadelta) T cells as unexpected drivers of tumor development and progression.

151 nd determine the impact of KLF10 deletion on tumor development and progression.

152 ne responses, and can be dysregulated during tumor development and progression.

153 upregulation of genes that are critical for tumor development and progression.

154 e a variety of activities that promote colon tumor development and progression; these include regulat

155 ency significantly repressed MET/CAT-induced tumor development and prolonged survival of animals with

156 en historically associated with experimental tumor development and recently described in association

157 anti-apoptotic BCL-2 proteins contributes to tumor development and resistance to therapy by suppressi

158 ecruit and reprogram immune cells to support tumor development and spread, the most prominent among t

159 hat Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequest

160 somatic point mutations thought to initiate tumor development and sustain cancer growth.

161 nt review, we discuss the role of hypoxia in tumor development and the clinical outcome of hypoxia-ta

162 rophils that might have a profound impact on tumor development and the function of these cells.

163 Tumor development and therapeutic resistance are linked

164 the importance of GC formation in TLS during tumor development and treatment.Significance: Corticoste

165 strate increased sphere formation, xenograft tumor development, and invasion.

166 tion and dynamics in models of inflammation, tumor development, and other lymphatic diseases.

167 o, the mechanisms by which PAX3-FOXO1 drives tumor development are not well characterized.

168 identified, the subsequent steps leading to tumor development are poorly defined.

169 Apart from being prone to tumor development, Arf-null mice are blind, and their ma

170 iated with tyrosine phosphorylation, support tumor development as transcription factors, but alternat

171 cific CD8(+) T cells were not deleted during tumor development, as revealed by pentamer staining in t

172 : a) mechanisms resulting in fibrosis and/or tumor development; b) relative toxicity of different for

173 VEGF-A was essential for initiation of skin tumor development, both spontaneously and UV-light trigg

174 eletion in mice not only exacerbates mammary tumor development but also impairs the anti-tumor effect

175 homozygous deletion of SIRT1 suppresses skin tumor development but sensitizes the B6 mice to chronic

176 atic progression.Stromal cells contribute to tumor development but the mechanisms regulating this pro

177 at bad luck has an important role to play in tumor development, but the full extent of this contribut

178 pancreatic cancer (PC) that not only impacts tumor development, but therapeutic outcome as well.

179 organoids recapitulate the full spectrum of tumor development by forming early-grade neoplasms that

180 ild-type p53-induced phosphatase 1, promotes tumor development by inactivating the p53 tumor suppress

181 clusion, angiogenin secretion by HCCs favors tumor development by inducing HSC activation and ECM rem

182 TGF-beta1 signaling can impair tumor development by its anti-proliferative and pro-apop

183 tus in tumor stromal cells has a key role in tumor development by modulating immune responses.

184 been used to study mechanisms of epithelial tumor development by oncogenic Hras.

185 Inasmuch, GdX suppresses tumorigenesis and tumor development by reducing the level of phospho-STAT3

186 idence suggesting that ARG1 secretion drives tumor development by stimulating epidermal cell prolifer

187 oteinase-activated receptor 2 (PAR2) promote tumor development by stimulating invasion and metastasis

188 we found that monocyte-derived TAMs advance tumor development by the remodeling of its extracellular

189 on mouse model led to a significant delay in tumor development, characterized by decreased cell proli

190 During tumor development, constant interplay occurs between tum

191 this study show that the effect of ZBED6 on tumor development depends on the genetic background and

192 Tumor development driven by inflammation is now an estab

193 isparate impacts of Setd2 and Arid1a loss on tumor development, each resulted in a gene expression pr

194 human CAFs at different stages of xenograft tumor development, effectively circumventing the challen

195 Chromosomal instability enables tumor development, enabled in part by aberrant expressio

196 and linearization of collagen fibers during tumor development, especially at areas of tumor invasive

197 Over the course of human tumor development, FA genes perform critical tumor-suppr

198 These results suggest that early in tumor development following Pten deletion, cells are pri

199 coding RNAs to control energy metabolism and tumor development.FoxO are commonly down-regulated trans

200 and reactive oxygen species (ROS) influence tumor development from early stages to the metastasis ph

201 ations in non-tumor stromal cells can affect tumor development has received very little attention.

202 number of causative genetic backgrounds for tumor development have been discovered, the initial step

203 e PI3K p110alpha subunit mediates RAS-driven tumor development: however, it is not clear how p110alph

204 hways that regulate regeneration can lead to tumor development; however, the negative regulators of o

205 or cells have the potential to contribute to tumor development; however, there is little experimental

206 nce suppression by MYC is a discrete step in tumor development important for sustained tumor growth b

207 exhibited increased susceptibility to colon tumor development in a manner associated with higher abu

208 lung adenocarcinoma, ASM deficiency reduced tumor development in a manner associated with significan

209 use embryo fibroblasts and for primary brain tumor development in a rat model of neurocarcinogenesis.

210 analyses showed that the role of thrombin in tumor development in CAC was temporally associated with

211 t with immune cell recruitment is augmenting tumor development in Cdh1(d/d)Trp53(d/d) uteri.

212 f Hh signaling, providing an explanation for tumor development in CJS.

213 e hypothesis that prothrombin contributes to tumor development in colitis-associated colon cancer (CA

214 of the complement (C) cascade may influence tumor development in disparate ways; however, little att

215 n, accelerated mPanIN progression, and early tumor development in K-ras(G12D) mice.

216 Pancreatic Ngf overexpression accelerated tumor development in LSL-Kras(+/G12D);Pdx1-Cre (KC) mice

217 Paradoxically, during early tumor development in many cancer types, TGF-beta acts as

218 he lymphotoxin-beta receptor markedly delays tumor development in mice with chronic liver injury.

219 Here, we studied the impact of host FasL on tumor development in mice.

220 d cells and acts to inhibit inflammation and tumor development in mice.

221 C accumulation and hedgehog signaling-driven tumor development in mice.

222 revealed that Tgif1 ablation impeded mammary tumor development in MMTV-Wnt1 mice, further underscorin

223 delta-Catenin mutations promote tumor development in mouse prostate with probasin promot

224 the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with m

225 ells, underlying the increased risk of liver tumor development in obese individuals.

226 ls, but not T cells, was sufficient to allow tumor development in ogr1(-/-) mice.

227 ografts, which may be less representative of tumor development in patients, showed higher liposomal a

228 nd might represent important progenitors for tumor development in prostate epithelium.

229 ichloropyridyloxy)] benzene yielded profound tumor development in RB-deficient livers that was princi

230 roliferators that can drive hepatomegaly and tumor development in rodents.

231 nclusion, elevated IL-33 signaling increases tumor development in the Apc (Min/+) mice.

232 Analysis of tumor development in the Plk1-overexpressing mice indica

233 mouse model of two NB cell lines and blocked tumor development in the TH-MYCN transgenic NB mouse mod

234 d skin, but this did not promote spontaneous tumor development in these tissues or enhance the growth

235 a tumor suppressor, we monitored spontaneous tumor development in three different mouse models with g

236 Loss of BID significantly delayed tumor development in two mouse models of Fah-mediated an

237 of reprogramming factors in vivo results in tumor development in various tissues consisting of undif

238 man cholangiocytes but it likely facilitated tumor development in vivo by an IL-6-sensitive process a

239 in vitro cellular proliferation and promoted tumor development in vivo in mice.

240 uclear SREBP-1a was also critical for breast tumor development in vivo.

241 tly increased anoikis in vitro and inhibited tumor development in vivo.

242 unclear whether MYC has the same role during tumor development in vivo.

243 ructs for their abilities to track and treat tumor development in vivo.

244 induced EOMA cell proliferation in vitro and tumor development in vivo.

245 reveals that alphavbeta8 integrin regulates tumor development, in part, by driving TGFbeta1-induced

246 to play important roles in various stages of tumor development including initiation, growth, and meta

247 tty acid or sphingolipid synthesis prevented tumor development, indicating a causal effect in tumorig

248 73 loss cooperate in genomic instability and tumor development, indicating that the oncogenic functio

249 Tumor-associated macrophages (TAMs) promote tumor development, invasion, and dissemination by variou

250 Tumor development is a Darwinian evolutionary process, i

251 nsion of myeloid cells associated with solid tumor development is a key contributor to neoplastic pro

252 Tumor development is associated with increased cell prol

253 Tumor development is etiologically associated with tobac

254 tase 1 (PP1) inhibitor; however, its role in tumor development is largely undefined.

255 minant negative impaired function of PKM2 in tumor development is not known; this study demonstrates

256 Tumor development is preceded by chronic liver disease w

257 Thus, Notch-induced mammary tumor development is Rbpj-independent.

258 g of the alterations of this biofluid during tumor development.-Katsiougiannis, S., Chia, D., Kim, Y.

259 ions of the reported technique, implantation tumor development, local tumor recurrence, presence of m

260 esented here suggested that Vps34 stimulates tumor development mainly through PKC-delta- activation o

261 a subset of cancer cells is responsible for tumor development, metastasis, and recurrence, and targe

262 4L1 inhibited angiogenesis but also affected tumor development more directly, depending on the tumor

263 At different times during tumor development, optical imaging was performed using a

264 ar phenotypic consequences, impairing either tumor development or maintenance, and suppressing ST18 e

265 Naive CD8(+) T cell priming during tumor development or many primary infections requires cr

266 ion in allergy, asthma, autoimmune diseases, tumor development, organ transplantation, and chronic in

267 s that are implicated in immune function and tumor development pathways.

268 Tumor development progresses through a complex path of b

269 Since acidosis is a hallmark of tumor development, progression, and aggressiveness, the

270 Chronic inflammation promotes tumor development, progression, and metastatic dissemina

271 plays an important role in inflammation and tumor development, progression, and responses to therapy

272 pathologic evolution of HCC during advanced tumor development, providing the first evidence that tum

273 controlling gene expression and suppressing tumor development, providing valuable insights into the

274 The mechanisms leading to kidney tumor development remain uncharacterized and effective t

275 and inflammatory pathways, but their role in tumor development remains largely unexplored.

276 cond, metastatic lineages can arise early in tumor development, sometimes long before diagnosis.

277 significantly worse prognosis regardless of tumor development subtype (i.e., classical, mesenchymal,

278 ges leads to reduction of Wnt and suppresses tumor development, suggesting infiltrating macrophages a

279 ell-cell contact seems a better predictor of tumor development than the response to ectopic RAS(V12)

280 3 (SOCS3); therefore, absence of CD37 drives tumor development through constitutive activation of the

281 Ras in mouse liver (AKT/Ras) leads to rapid tumor development through strong activation of the mamma

282 have attempted to clarify the intricacies of tumor development to propose effective approaches for ca

283 lular behaviors from the earliest moments of tumor development to the final steps of metastasis.

284 cells in immunocompromised mice and compared tumor development using clodronate-containing liposomes

285 otine promotes pancreatic carcinogenesis and tumor development via down-regulation of Gata6 to induce

286 loss of TGFbeta signaling protected against tumor development via inhibition of tumor-associated fib

287 d chronic inflammation increases the risk of tumor development via oncogenic mutations.

288 Enhanced tumor development was associated with an altered microbi

289 nd in oral squamous cell carcinoma patients, tumor development was associated with decreased blood fr

290 Tumor development was monitored through longitudinal mag

291 ment in vivo by an IL-6-sensitive process as tumor development was significantly attenuated in Il-6(-

292 methyltransferase 3a (Dnmt3a) in intestinal tumor development, we analyzed the expression of Dnmt3a

293 stand the extent that ARID3B participates in tumor development, we assessed protein expression of ARI

294 e of the immune system in hepatic injury and tumor development, we comparatively studied the extent o

295 f GRP94 in maintaining liver homeostasis and tumor development, we created two liver-specific knockou

296 o identify the direct role of these cells in tumor development, we used S100A9 transgenic mice to cre

297 Strikingly, chronic liver injury and tumor development were markedly suppressed in alymphoid

298 sgenes, tamoxifen treatment resulted in oral tumor development with increased bioluminescent activity

299 s of preventive or therapeutic strategies on tumor development without killing the animal or requirin

300 o an angiogenic state is a critical event in tumor development, yet few patient characteristics have