ライフサイエンスコーパス: malignant progression

1 prostate cancer, SIN3B provides a barrier to malignant progression.

2 ivator to drive podoplanin expression in the malignant progression.

3 promotes tumor initiation and contributes to malignant progression.

4 gained functions that help to contribute to malignant progression.

5 nction, a Krtap can serve as a switch toward malignant progression.

6 ts a strong barrier against tumor growth and malignant progression.

7 ression and signaling paradoxically promotes malignant progression.

8 tiating a feed-forward loop that can sustain malignant progression.

9 in vivo, defining a new function for DDB2 in malignant progression.

10 f-stimulation of tumor growth and presumably malignant progression.

11 ir association with epigenetic silencing and malignant progression.

12 2f7/8 enhanced tumorigenesis and accelerated malignant progression.

13 ing CSCs may be a useful strategy to inhibit malignant progression.

14 tervention and likely also the mechanisms of malignant progression.

15 cial during wound healing, inflammation, and malignant progression.

16 ing that stimulates their in vivo growth and malignant progression.

17 is important in breast cancer initiation and malignant progression.

18 gs or contrast-enhanced MR imaging suggested malignant progression.

19 berrations leading to disease relapse and/or malignant progression.

20 ngly exacerbates pancreatic inflammation and malignant progression.

21 anisms involved in both tumor initiation and malignant progression.

22 t likely contribute to viral persistence and malignant progression.

23 e between hepatocyte loss, regeneration, and malignant progression.

24 cer where it contributes to inflammation and malignant progression.

25 whose mutational attenuation contributes to malignant progression.

26 anced stages significantly delays aggressive malignant progression.

27 related inflammation, immunosuppression, and malignant progression.

28 nd invasion (D) are not always necessary for malignant progression.

29 ed fibroblasts (CAF) play a critical role in malignant progression.

30 ssociated macrophages (TAM) that can promote malignant progression.

31 butions from the microenvironment to undergo malignant progression.

32 udy suggests that these are not required for malignant progression.

33 Ttf-1 or Titf1) as a candidate suppressor of malignant progression.

34 , mammary tumors, and lung metastases during malignant progression.

35 resents an opportunity to intervene prior to malignant progression.

36 scularization to facilitate tumor growth and malignant progression.

37 ical HSC numbers in check and interfere with malignant progression.

38 ccompanying activation and a strong drive to malignant progression.

39 necessary and sufficient for EMT during PDA malignant progression.

40 omatic alterations at this locus, leading to malignant progression.

41 ing an axis for either tissue homeostasis or malignant progression.

42 g tumors cleverly find alternative routes to malignant progression.

43 trates how deregulated ROS may contribute to malignant progression.

44 cells and the tumor microenvironment and for malignant progression.

45 ing model with two distinct trajectories for malignant progression.

46 types is the single greatest risk factor for malignant progression.

47 at macrophages promote cancer initiation and malignant progression.

48 ting tumor-associated myeloid cells to drive malignant progression.

49 been implicated in tumor cell metastasis and malignant progression.

50 commonly occurs in solid tumors and promotes malignant progression.

51 and its loss of function is associated with malignant progression.

52 tance of tissue architecture and polarity in malignant progression.

53 ar association of the "T-pro phenotype" with malignant progression.

54 tumor-associated macrophages (TAMs) promote malignant progression.

55 ion, thus sustaining a feed-forward loop for malignant progression.

56 ents may directly link Tax to early steps in malignant progression.

57 facilitates either inflammatory diseases or malignant progression.

58 important in cancer-related inflammation and malignant progression.

59 , multiplicity, growth rate, and the rate of malignant progression.

60 very high levels in tumors, contributing to malignant progression.

61 ng how phenotypic shifting can contribute to malignant progression.

62 ial link between inflammatory activation and malignant progression.

63 uman tumors, suggesting its participation in malignant progression.

64 tumors showing shortened incubation time and malignant progression.

65 in three stages: initiation, promotion, and malignant progression.

66 genic roles at different stages of mammalian malignant progression.

67 revealed a novel aspect of SnoN function in malignant progression.

68 ining 22% (n = 26) had little or no risk for malignant progression.

69 evelopment by secreting factors that promote malignant progression.

70 f (p16(Ink4a)/p19(Arf)) or p53 enables their malignant progression.

71 sitive proliferative cell compartment during malignant progression.

72 , characteristics frequently associated with malignant progression.

73 the tumor suppressor activity of p53 during malignant progression.

74 lts in an increased number of papillomas and malignant progression.

75 clin D2 results in reduced tumorigenesis and malignant progression.

76 a selection mechanism for immune escape and malignant progression.

77 invasion and proliferation can contribute to malignant progression.

78 ypoxic stress is an important determinant of malignant progression.

79 hile decreasing benign tumor development and malignant progression.

80 ociated with abnormal differentiation and/or malignant progression.

81 g tool in HPV-positive populations to detect malignant progression.

82 own about the genetic events responsible for malignant progression.

83 feed-forward signaling mechanism involved in malignant progression.

84 t losses of Rb or its regulators can enhance malignant progression.

85 nce of metabolic rewiring during lung cancer malignant progression.

86 alignant growth rather than a consequence of malignant progression.

87 e potentially serve as genomic biomarkers of malignant progression.

88 utic strategy for targeting c-MYC-associated malignant progression.

89 expression in human glioma decreases during malignant progression.

90 -small cell lung cancer (NSCLC) cells during malignant progression.

91 ate tumor-associated macrophages that enable malignant progression.

92 e gastric epithelial differentiation but not malignant progression.

93 e ligand guanylin contributes universally to malignant progression.

94 d other immunosuppressive cells that promote malignant progression.

95 ment of the B-cell receptor is important for malignant progression.

96 mpeded early-stage tumor growth and retarded malignant progression.

97 n human prostate cancers and associated with malignant progression.

98 RAF(V600E)-induced lung adenomas, leading to malignant progression.

99 elial-to-mesenchymal transition (EMT) during malignant progression.

100 ted to a proinflammatory state that supports malignant progression.

101 t cancer stem-like cells (CSC) that promotes malignant progression.

102 enhances transport kinetics, which promotes malignant progression.

103 ampening antitumor immunity and accelerating malignant progression.

104 matin landscape and unveil its importance in malignant progression.

105 (mTOR) functions, which is important for the malignant progression.

106 There is a strong link between TANs and malignant progression.

107 s and their microenvironment is critical for malignant progression.

108 tophagy in HNSCC stromal cells that promotes malignant progression.

109 otypes, suggesting inhibition of early-stage malignant progression.

110 d are coupled with the angiogenic switch and malignant progression.

111 transformation (11/20) than in those without malignant progression (3.2 +/- 0.9 vs. 1.9 +/- 0.5; P =

112 cancer, but it is unclear whether it affects malignant progression after diagnosis.

113 arcinomas where it appears to be involved in malignant progression, although the biology of this inte

114 MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumou

115 ance of the ATR pathway both as a barrier to malignant progression and as a potential target for canc

116 transition program becomes activated during malignant progression and can enrich for cancer stem cel

117 ress the question whether ITH increases with malignant progression and can hence be exploited as a pr

118 already established tumors markedly impaired malignant progression and caused regression of individua

119 may diminish tumor cell invasiveness during malignant progression and following antivascular therapi

120 because it is frequently inactivated during malignant progression and has recently been shown to fun

121 specific changes and processes required for malignant progression and identification of prognostic i

122 ow result in positive roles for autophagy in malignant progression and in subsequent tumor maintenanc

123 RAS expression provides an early barrier to malignant progression and is mediated by TGF-beta recept

124 cells to migrate is strongly correlated with malignant progression and metastasis.

125 clinical severity, play an important role in malignant progression and metastatic dissemination of PC

126 rf or p53 tumor suppressor genes accelerates malignant progression and metastatic spread of 7,12-dime

127 olic phenotype has long been correlated with malignant progression and poor clinical outcome.

128 expression and activity are associated with malignant progression and poor patient prognosis in a nu

129 2 in breast cancer specimens correlated with malignant progression and poor patient survival.

130 ium cooperates with PTEN deletion to augment malignant progression and produce an aggressive metastas

131 periencing telomere dysfunction enables full malignant progression and provides a mechanism for acqui

132 er, our findings indicated that AK4 promotes malignant progression and recurrence by promoting metast

133 vates multiple signaling cascades to promote malignant progression and resistance to PLX4720 treatmen

134 ased beta1 integrin signaling is involved in malignant progression and that inhibitory antibody to be

135 er, p21-associated inhibition of early-stage malignant progression and the intense expression in papi

136 elp identify cellular processes critical for malignant progression and therapeutic intervention.

137 new mechanism on how hypoxia can affect the malignant progression and therapeutic response of solid

138 nk4a) epimutation drives tumor formation and malignant progression and validate a targeted methylatio

139 intervention with respect to inhibiting the malignant progression and/or reducing the treatment resi

140 molecular mechanism of p62/Sqstm1-dependent malignant progression, and suggest that molecular target

141 in neuroblastoma, we serially characterized malignant progression, angiogenesis, and sensitivity to

142 However, cancer development and malignant progression are also associated with accumulat

143 echanisms by which galectin-3 contributes to malignant progression are not fully understood.

144 nitrosamine-induced hepatocarcinogenesis and malignant progression are suppressed.

145 Unresected tumor causes recurrence and malignant progression, as observed within a year in one

146 g the most neovascularised neoplasms and its malignant progression associates with striking neovascul

147 that TLR5-dependent commensal bacteria drive malignant progression at extramucosal locations by incre

148 own-regulation of Fas and ICAM-1 intensified malignant progression at the level of colonization.

149 Commensal microorganisms influence malignant progression by altering systemic inflammation.

150 sms that block or reverse stromal support of malignant progression by isolating the HER family from a

151 transition (EMT) in carcinoma cells enhances malignant progression by promoting invasion and survival

152 myeloid cells to oncogenic transformation or malignant progression by promoting whole chromosome inst

153 d the role of constitutive EGFR signaling in malignant progression by stably transfecting colon cance

154 We propose that p53 not only limits malignant progression by suppressing the acquisition of

155 nses, but these responses are limited during malignant progression by the development of immunosuppre

156 , however, information on tumor activity and malignant progression cannot be obtained on the basis of

157 These cancers exhibit a relentless malignant progression characterized by widespread invasi

158 horylation (OXPHOS) toward glycolysis during malignant progression, even when aerobic metabolism is a

159 .007; 95% CI, 1.001 to 1.014; P = .035), and malignant progression-free survival was predicted by EOR

160 At a median follow-up of 15 years, malignant progression had occurred in 87 (7.6%) patients

161 c balance of the mammary epithelium to drive malignant progression; however, complexities of Wnt path

162 associated macrophages (TAM) correlates with malignant progression, immune suppression, and poor prog

163 hether acid suppression alone can impact the malignant progression in Barrett esophagus patients.

164 relevance in the context of premalignant to malignant progression in Barrett's esophagus.

165 Malignant progression in cancer requires populations of

166 ssociated macrophages (TAMs) associates with malignant progression in cancer.

167 endogenous wild-type Ras and predisposes to malignant progression in cooperation with Ras oncogenic

168 h deregulated kinase pathways are drivers of malignant progression in glioblastoma multiforme, glioma

169 paB), a transcription factor, which promotes malignant progression in HNSCC.

170 ivated oncogenes are the dominant drivers of malignant progression in human cancer, yet little is kno

171 sive tumor-bearing mice but only accelerates malignant progression in IL-6-unresponsive tumors.

172 at the hMENA splicing program is relevant to malignant progression in invasive disease.

173 is study, TANs were strongly associated with malignant progression in IPMNs.

174 Here, we report that mTOR inhibition blocked malignant progression in K-ras(LA1) mice, which undergo

175 We conclude that fibulin-2 is a driver of malignant progression in lung adenocarcinoma and plays a

176 l adhesion molecule that may impact risks of malignant progression in many cancers.

177 Persistent STAT3 signaling contributes to malignant progression in many diverse types of human can

178 sponses may underlie genetic instability and malignant progression in melanoma.

179 t as a lesion driving MDS or contributing to malignant progression in MPN.

180 ent a model in which SPR drives ODC-mediated malignant progression in NB.

181 Hypoxia drives malignant progression in part by promoting accumulation

182 sine ((18)F-FET) PET to noninvasively detect malignant progression in patients with LGG.

183 on, activation of CDK2 alone does not induce malignant progression in Ras-mediated tumorigenesis.

184 Expression increased during malignant progression in RIP-Tag2 mice.

185 vide new insight into the mechanisms driving malignant progression in squamous cancer.

186 ses tumor incidence, tumor multiplicity, and malignant progression in the chemically induced mouse mo

187 epigenetic modifications that contribute to malignant progression in the GC remain poorly defined.

188 Myeloid cells that orchestrate malignant progression in the tumor microenvironment offe

189 meres also may cause genomic instability and malignant progression in these marrow failure syndromes.

190 t occur in the tumor microenvironment during malignant progression in this disease.

191 is persistently activated and contributes to malignant progression in various cancers.

192 quisition of many phenotypes associated with malignant progression, including accelerated growth rate

193 completely prevented matriptase-induced pre-malignant progression, including inflammatory cytokine p

194 cells did not prevent matriptase-driven pre-malignant progression, indicating that matriptase activa

195 tion in colonic inflammation and its related malignant progression, indicating that targeting ubiquit

196 nic gain-of-function activities that promote malignant progression, invasion, metastasis and chemores

197 esponses to p53 contributes to inhibition of malignant progression is beginning to be clarified, with

198 y of targeting CDK2 in tumor development and malignant progression is dependent on the oncogenic path

199 d suggest that subgroups of patients in whom malignant progression is driven by EMT activators may re

200 An important aspect of malignant progression is the acquired ability of tumor c

201 g because this tissue may have potential for malignant progression, is not visible by conventional en

202 wever, study of stromal or immune drivers of malignant progression may be limited.

203 ly reserved for patients that have undergone malignant progression (MP) to an anaplastic glioma or se

204 cient to overcome a p53-regulated barrier to malignant progression, nor establish the prometastatic c

205 downstream mediator of mTOR, increased with malignant progression (normal alveolar epithelial cells

206 hed that ECM stiffness, per se, promotes the malignant progression of a mammary epithelium by activat

207 tudy, we investigated the role of CYP24A1 on malignant progression of a murine model of Braf(V600E) -

208 of the ER stress response is associated with malignant progression of B cell chronic lymphocytic leuk

209 The treatment of choice to prevent the malignant progression of BE remains controversial.

210 a recently discovered oncogene implicated in malignant progression of both endocrine and nonendocrine

211 ment, highlighting the mechanisms that limit malignant progression of BRAF(V600E)-initiated tumors.

212 ing SnoN decreases TAZ expression as well as malignant progression of breast cancer cells.

213 wever, the precise role of heparanase in the malignant progression of breast cancer is unknown.

214 The myriad changes that occur during the malignant progression of cancer cells present challenges

215 growth factor (HGF), has been implicated in malignant progression of cancer involving stimulation of

216 mplicated in the survival, proliferation and malignant progression of cancers.

217 xtracellular matrix plays a decisive role in malignant progression of carcinomas.

218 deletion exhibited accelerated formation and malignant progression of chemically induced skin tumors

219 and found that XBP-1 deficiency decelerates malignant progression of CLL-associated disease.

220 vating the ER stress response in support for malignant progression of CLL.

221 could be targeted to prevent the relapse and malignant progression of CML.

222 a pro-inflammatory cytokine linked to rapid malignant progression of colorectal cancer (CRC) and the

223 rvous system and have been implicated in the malignant progression of different tumor types.

224 alloproteinase (TIMP)-4, are associated with malignant progression of ductal carcinoma in situ, a pre

225 xpression of Prdx6 led to an acceleration of malignant progression of existing tumors, revealing a du

226 en shown to promote mesenchymal features and malignant progression of glioblastoma.

227 n a myeloid cell sublineage is necessary for malignant progression of gliomas in transgenic murine mo

228 tes in vivo contributes to the formation and malignant progression of gliomas.

229 onally, we found that ZEB1 causally promotes malignant progression of HBECs and tumorigenicity, invas

230 FR3 variants exhibit specific effects in the malignant progression of HCC cells.

231 nce of the epithelial-stromal compartment in malignant progression of HCC in cirrhosis.

232 of viral persistence, which is requisite for malignant progression of HPV-infected lesions.

233 type that could be linked to the etiology or malignant progression of human cancer.

234 and is a critical contributing factor to the malignant progression of human prostate tumors.

235 in the intestine, deletion of Cnnm4 promoted malignant progression of intestinal polyps to adenocarci

236 at p27 is a potent barrier to the growth and malignant progression of Kras-initiated lung tumors.

237 information for the noninvasive detection of malignant progression of LGG.

238 tand the molecular mechanisms underlying the malignant progression of low-grade gliomas with mutation

239 nhibited the angiogenic switch necessary for malignant progression of low-grade to high-grade tumors.

240 is a common critical contributing factor to malignant progression of many solid tumors and its expre

241 sine kinase c-Met promotes the formation and malignant progression of multiple cancers.

242 Malignant progression of normal alveolar epithelial cell

243 and pattern of FGF-BP1 expression during the malignant progression of pancreas and colorectal carcino

244 ome epithelial tumors, but their role in the malignant progression of pancreatic ductal adenocarcinom

245 The malignant progression of pancreatic ductal adenocarcinom

246 Furthermore, tumor multiplicity and malignant progression of papillomas after chemical skin

247 rogen-dependent cells and might thus promote malignant progression of prostate cancer.

248 gly implicate Aurora-A overexpression in the malignant progression of skin tumors and suggest that Au

249 dy reveals a novel role for Stat3 in driving malignant progression of skin tumors in vivo.

250 embrane glycoprotein closely associated with malignant progression of squamous cell carcinomas (SCCs)

251 -tumor cells and their surrounding stroma in malignant progression of the cerebellar tumor medullobla

252 ventually causing resistance to imatinib and malignant progression of the disease.

253 to inhibitors such as imatinib mesylate and malignant progression of the disease.

254 ion of hepatic neoplasias yet constrain full malignant progression of these neoplasms possibly due to

255 uate their involvement in transformation and malignant progression of these tumor types.

256 that are important for the pathogenesis and malignant progression of these tumors.

257 into the mechanism by which p53 prevents the malignant progression of transformed cells.

258 , is an important mechanism to constrain the malignant progression of tumour cells.

259 7 deficiency accelerated both the growth and malignant progression of urethane-induced lung tumors, a

260 Malignant progression phenotypes were also affected at t

261 precise roles in cancer stem cells (CSC) and malignant progression remain uncertain.

262 ins and relative functional contributions to malignant progression remain uncertain.

263 to promote lung tumour formation in mice but malignant progression requires additional genetic altera

264 Malignant progression requires these genes, whose knockd

265 Malignant progression results from a dynamic cross-talk

266 sis leads to inappropriate cell survival and malignant progression, selective induction of apoptosis

267 via reexpression of HoxD10, which is lost in malignant progression, significantly attenuated VEGF exp

268 tanding of the contributions of microRNAs to malignant progression, specifically their functions in m

269 of this mutation in tumors at all stages of malignant progression suggests that it is an early event

270 her diagnostic accuracy for the detection of malignant progression than changes of contrast enhanceme

271 nd the mechanisms of cell transformation and malignant progression that are reinforced by mouse model

272 ve broad activity in tissue inflammation and malignant progression that depends on the expression of

273 erexpressed in EOC and play key roles in its malignant progression though their contribution in devel

274 cessively by many solid tumors and can drive malignant progression through multiple effects on the tu

275 stability, leading to disease relapse and/or malignant progression to a fatal blast phase.

276 acytidine (5-AzaC), have been shown to lower malignant progression to acute myeloid leukemia and to p

277 ated through promoter hypomethylation during malignant progression to high-grade glioblastoma were en

278 s and multiplicity of skin tumors as well as malignant progression to SCC.

279 y expressed, particularly at early stages of malignant progression to squamous cell carcinoma (SCC),

280 pment of epidermal hyperplasia and increased malignant progression to squamous cell carcinoma.

281 D3 results in reduced tumor development and malignant progression to squamous cell carcinomas (SCC).

282 l vascular invasion is a crucial step in the malignant progression toward metastasis.

283 In patients with histologically proven malignant progression toward WHO grade III or IV (n = 18

284 its dependence on IGF-II and by accelerated malignant progression upon IGF-1R overexpression.

285 n possessed the potency to limit early-stage malignant progression via cyclin D1/E2 inhibition.

286 sential role in mediating hypoxic effects on malignant progression via genetic alterations, resulting

287 ll and -wild-type littermates, implying that malignant progression was dependent specifically upon tu

288 y of imaging parameters for the detection of malignant progression was evaluated by receiver-operatin

289 The influence of p53 loss on malignant progression was observed as early as 6 weeks a

290 To better understand its role in malignant progression, we deleted Shh in a well-defined

291 Dissecting TGF-beta's impact on malignant progression, we demonstrate that TGF-beta conc

292 rominent role for p16(Ink4a) in constraining malignant progression, we sought to assess the pathologi

293 Progression and malignant progression were identified in 95 (44%) and 44

294 quirement of the HIF-alpha-c-Myc pathway for malignant progression, whereas the canonical transcripti

295 The common CSC signature was associated with malignant progression, which is enriched in poorly diffe

296 erexpressing mice increased tumor burden and malignant progression, while Loxl2-deficient mice exhibi

297 setting of telomere dysfunction enabled full malignant progression with alleviation of telomere dysfu

298 ng an adaptive immune response that promotes malignant progression, with implications for cancer prev

299 systemic inflammatory pathways that promote malignant progression, with implications for how to prev

300 proliferation and invasion are critical for malignant progression, yet how these processes relate to