ライフサイエンスコーパス: tumor development

1 ivation, telomere fragility, and accelerated tumor development.

2 itical role in normal tissue homeostasis and tumor development.

3 as genes controlled by dTcf/Pan involved in tumor development.

4 more on a mutation that is more integral to tumor development.

5 g has been implicated in different stages of tumor development.

6 tivating stem cell proliferation and fibroid tumor development.

7 t resistant to early changes associated with tumor development.

8 s in lymphatic tissues than mice controlling tumor development.

9 een aberrant mitochondrial Ca(2+) levels and tumor development.

10 ogically normal kidney tissues that preceded tumor development.

11 operation of the hormone and the oncogene in tumor development.

12 2-IL1B mice fed the control diet accelerated tumor development.

13 whether phosphorylated Dicer1 contributed to tumor development.

14 ger an autoantibody response associated with tumor development.

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

16 ho show increased susceptibility to squamous tumor development.

17 nocytes and to molecular cascades leading to tumor development.

18 ing system is progressively disrupted during tumor development.

19 ased hepatic lipid metabolism prior to overt tumor development.

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

21 0 weeks during the 'risk window' for mammary tumor development.

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

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

24 e constraints encountered over the course of tumor development.

25 optosis signaling pathways thought to govern tumor development.

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

27 5 weeks; injections of anti-PD1 did not slow tumor development.

28 that plays pivotal roles in angiogenesis and tumor development.

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

30 some amplification, genomic instability, and tumor development.

31 eutrophil function during mouse versus human tumor development.

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

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

34 owth, whereas their combined loss diminishes tumor development.

35 erations that are clonally selected to drive tumor development.

36 nduced apoptosis and markedly promotes renal tumor development.

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

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

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

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

41 thylcellulose or polysorbate-80, exacerbated tumor development.

42 the cancer cells themselves, contributes to tumor development.

43 aling and expression of proteins relevant to tumor development.

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

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

46 Smarcal1 in hematopoietic cell survival and tumor development.

47 erates with ionizing radiation to exacerbate tumor development.

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

49 point modification contributes to esophageal tumor development.

50 tylation in maintaining cell homeostasis and tumor development.

51 could have protumor or antitumor effects on tumor development.

52 rthotopic model of pancreatic cancer delayed tumor development.

53 ipsis generated recurrent fusions that drove tumor development.

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

55 ment with short telomeres leads to increased tumor development.

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

57 o escape immune recognition is important for tumor development.

58 igated the role of calcineurin in intestinal tumor development.

59 blishing a positive feedback loop to support tumor development.

60 nduced epidermal hyperproliferation and skin tumor development.

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

62 iples underlie the responses observed during tumor development.

63 n by random mutations that accumulate during tumor development.

64 anistic link between periodontal disease and tumor development.

65 flicting roles of SIRT6 in processes such as tumor development.

66 ulation of angiogenesis during embryonic and tumor development.

67 y unidentified signaling pathway involved in tumor development.

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

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

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

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

72 ific functions and contribute differently to tumor development.

73 at may contribute to disease progression and tumor development.

74 ts related metabolic products play a role in tumor development.

75 rovide another mechanism for decreased solid tumor development.

76 response to TBT exposure and preceded liver tumor development.

77 anscription factor, are predicted to promote tumor development.

78 driver' genes, which have essential roles in tumor development.

79 by Arid1a and have an impact on endometrial tumor development.

80 iota-induced intestinal inflammation but not tumor development.

81 tiated cell states are often dysregulated in tumor development.

82 a-catenin target gene expression and delayed tumor development.

83 ught to contribute to colon inflammation and tumor development.

84 e receptors) into skin can positively affect tumor development.

85 totoxic (CD8(+)) T cells as risk factors for tumor development.

86 c mutations but few of these mutations drive tumor development.

87 tic variants acting in networks can exert on tumor development.

88 ltration plays an active role in controlling tumor development.

89 atially-heterogeneous lipids associated with tumor development.

90 ly little is known about its relationship to tumor development.

91 bsets is poorly understood in the context of tumor development.

92 cy of chemotherapy and decreased spontaneous tumor development.

93 ents a new regulatory pathway in suppressing tumor development.

94 e mechanisms underlying MDSC contribution to tumor development.

95 eritable cancers has provided insights about tumor development.

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

97 the systemic immune landscape in response to tumor development across five tissues in eight mouse tum

98 riptional oncogenic driver of angiomyolipoma tumor development, acting through regulation of CYR61.

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

100 creata were collected at different stages of tumor development and analyzed by immunohistochemistry,

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

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

103 lease of angiogenic growth factors promoting tumor development and autoreactive immune cells to reach

104 Mito-LND blocks lung tumor development and brain metastasis by inhibiting mit

105 scovered that a phosphomimetic Dicer1 drives tumor development and dissemination in two independent m

106 vance of Dicer1 phosphorylation in mammalian tumor development and dissemination.

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

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

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

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

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

112 l DMPs were located in genes associated with tumor development and glucose metabolism.

113 sound imaging was used to detect and monitor tumor development and growth over time in the lungs of t

114 Tumor development and growth, as well as metastatic spre

115 While not affecting primary tumor development and growth, FAK deletion significantly

116 our understanding of the molecular basis of tumor development and GSL metabolism.

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

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

119 onstrate that phosphomimetic Dicer1 promotes tumor development and invasion.

120 of FASN before oncogenic activation prevents tumor development and invasive growth.

121 al to understand the evolutionary history of tumor development and its association with treatment res

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

123 to mediate oncogenic functions necessary for tumor development and malignant spread.

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

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

126 oenvironment (TME) and play crucial roles in tumor development and metastasis.

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

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

129 after their intra-femoral inoculation blocks tumor development and preserves a normal bone architectu

130 ers, suggesting potential roles for OATPs in tumor development and progression and as novel targets f

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

132 tic tumor development and to be required for tumor development and progression in mice.

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

134 As dogs are an excellent model for human tumor development and progression, we set out to identif

135 uting to our understanding of their roles in tumor development and progression.

136 stress signaling networks directly influence tumor development and progression.

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

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

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

140 into the mechanisms by which PGE(2) promotes tumor development and progression.

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

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

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

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

145 nant arginase BCT-100, significantly delayed tumor development and prolonged murine survival.

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

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

148 rturbations in genomic stability can lead to tumor development and suggest that cell cycle regulators

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

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

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

152 space and time is critical for understanding tumor development and the role of spatial heterogeneity

153 he strong spatiotemporal correlation between tumor development and the T-cell dysfunctional status se

154 Tumor development and therapeutic resistance are linked

155 ighting the importance of nutrient supply to tumor development and therapeutic response.

156 nk local microbiota-immune crosstalk to lung tumor development and thereby define key cellular and mo

157 increased during pancreatitis and pancreatic tumor development and to be required for tumor developme

158 c factor contributing substantively to brain tumor development and to the success of therapy.

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

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

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

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

163 mprehensive longitudinal assessment of human tumor development as governed by molecular subtype mutat

164 ce and had increased gut permeability before tumor development, associated with reduced expression of

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

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

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

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

169 e increasingly recognized to influence solid tumor development, but why their effects are so context

170 l, including the treatment and prevention of tumor development by chronic inflammatory responses.

171 that tumor cell-secreted PLD2 contributes to tumor development by modifying the microenvironment, mak

172 optosis process in cancer cells and promotes tumor development by stabilizing the cystine transporter

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

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

175 infection, which is lifelong and can precede tumor development by years, requires the concerted actio

176 Furthermore, tumor development can be determined by a time course of

177 oved our understanding of the key drivers of tumor development, clonal evolution, and recurrence, and

178 Tumor development driven by inflammation is now an estab

179 These results demonstrate that tumor development dynamically reshapes the composition a

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

181 raphane in colon cancer cells and suppressed tumor development effectively in a preclinical model of

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

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

184 n and puncture-induced sepsis earlier during tumor development exhibited CD8 T cell-dependent attenua

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

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

187 Tumor development frequency after exposure to high-LET p

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

189 oenvironmental and physiological stressor in tumor development, gastric acid-mediated regional micros

190 The extent to which tumor development/growth is affected in sepsis survivors

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

192 that limit the acquisition of mutations and tumor development have not been well defined.

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

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

195 200c potently inhibited TNBC cell growth and tumor development in a mechanism distinct from its abili

196 Loss of IL-17RD also promotes tumor development in a model of colitis-associated color

197 hat ablation of Aldh1b1 completely abrogates tumor development in a mouse model of Kras(G12D)-induced

198 g to oxidative stress, hemolytic anemia, and tumor development in a mouse model.

199 Mutations associated with tumor development in certain tissues can be nontumorigen

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

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

202 id not lead to an increase in fatty liver or tumor development in female offspring.

203 and transgenic expression of LRIG1 inhibits tumor development in Hi-Myc and TRAMP models.

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

205 We provide evidence that tumor development in liver expressing CDK1(AF) is inhibi

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

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

208 d migration, invasion, sphere formation, and tumor development in mice after TGF-beta treatment.

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

210 otease decreases growth factor signaling and tumor development in mice.

211 Natural killer (NK) cells inhibit tumor development in mouse models and their presence in

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

213 tumor suppressor syndrome, characterized by tumor development in multiple organs, including renal an

214 The venom was effective at impairing tumor development in murine xenogeneic model, activating

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

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

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

218 sclerosis complex (TSC) is characterized by tumor development in the brain, heart, kidney, and lungs

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

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

221 genetic loss of GPER1 significantly reduced tumor development in the zebrafish.

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

223 th in human melanoma cell lines in vitro and tumor development in vivo in immune-deficient xenografts

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

225 relevant to establish the effects of PnV on tumor development in vivo, considering the complex neopl

226 nd migration in vitro as well as xenografted tumor development in vivo.

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

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

229 ne expression profile that supports enhanced tumor development in vivo.

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

231 on of the H19 locus, a known driver of Wilms tumor development, in 58% of the expansions.

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

233 as, and that deletion of Bap1 contributes to tumor development, in part, by loss of PRC2-mediated rep

234 mbination of p53 deficiency and AOM promotes tumor development, including growth of invasive cancers

235 influencing sporadic or inflammation-driven tumor development, including the analysis of local invas

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

237 in alone does not predispose mice to mammary tumor development, indicating that additional perturbati

238 73 loss cooperate in genomic instability and tumor development, indicating that the oncogenic functio

239 Tumor development is a Darwinian evolutionary process, i

240 The accelerated tumor development is accompanied by increased Polycomb r

241 unction of monocytic MDSC (M-MDSC), although tumor development is delayed in E0771 tumor-bearing mice

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

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

244 Tumor development is restricted to a subset of alveolar

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

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

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

248 ion and these mucins play important roles in tumor development, metastasis and chemo-resistance.

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

250 cell-cycle gene expression that occur during tumor development might help identify new targets and im

251 4L1 inhibited angiogenesis but also affected tumor development more directly, depending on the tumor

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

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

254 cer, there is little evidence that it alters tumor development or progression.

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

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

257 Tumor development progresses through a complex path of b

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

259 oids are increasingly enabling insights into tumor development, progression, and treatment.

260 The role of the physical microenvironment in tumor development, progression, metastasis, and treatmen

261 sults highlight the importance of TOP1MT for tumor development, providing a potential rationale to de

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

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

264 r cachexia, the MasR agonist AVE 0991 slowed tumor development, reduced weight loss, improved locomot

265 SCs) are rare types of cells responsible for tumor development, relapse, and metastasis.

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

267 p110gamma ablation failed to protect against tumor development, showing increased activation of pAKT

268 ing cells in athymic nude mice induced rapid tumor development, showing their driving oncogenicity.

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

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

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

272 ment by a more realistic model of continuous tumor development that includes mixtures of subclones, a

273 Hypermethylation may be an early event in tumor development that progress along a common pathway w

274 insignificant role for classic oncogenes in tumor development, the release of bioactive amines, and

275 acrophage proliferation to support malignant tumor development, thereby strengthening the value of ER

276 Widely assumed to be an early event in tumor development, this phenomenon plays a prominent rol

277 siological function, AID also contributes to tumor development through its mutagenic activity.

278 that mutations alone are not sufficient for tumor development, thus prompting the question of how si

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

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

281 nce that strength of immune selection during tumor development varies with sex and age, and may influ

282 The tumor microenvironment (TME) promotes tumor development via complex intercellular signaling, a

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

284 Enhanced tumor development was associated with an altered microbi

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

286 than mice fed the control diet; the speed of tumor development was independent of body weight.

287 ithout knockdown of PRLR, into pancreas, and tumor development was monitored for 4 weeks, with some m

288 Tumor development was monitored through longitudinal mag

289 cted into C57BL/6 mice or Il22(-/-)mice, and tumor development was monitored.

290 Maximal protection against tumor development was observed when the tumor and host w

291 , miR-200c-led inhibition in cell growth and tumor development was prevented by forcing PDE7B transge

292 The role of the TLR4-shaped microbiota in tumor development was tested in wild-type germ-free mice

293 However, whether ZAP has an impact on tumor development was unknown.

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

295 ect involvement of Dicer1 phosphorylation in tumor development, we studied mice with phosphomimetic a

296 In the present work, the effects of PnV on tumor development were established in vivo using a xenog

297 of Atg5 and reduced protein levels promotes tumor development, whereas homozygous disruption of Atg5

298 al mechanism underlying aggressive prostatic tumor development, which has been frequently observed in

299 cancer mouse model exhibits enhanced mammary tumor development with deficient ERalpha expression that

300 protein with regulatory roles in hemostasis, tumor development, wound healing, and atherogenesis.