ライフサイエンスコーパス: progression

1 integrin beta(3)-KRAS signaling drives tumor progression.

2 gle deficiency of each protein limited tumor progression.

3 s were not associated with KS development or progression.

4 part explain how obesity drives colon cancer progression.

5 se, inextricably linked to disease onset and progression.

6 ostate cancer cell proliferation and disease progression.

7 the molecular interactions governing disease progression.

8 may contribute to MYC-driven development and progression.

9 r stress but, paradoxically, it favors tumor progression.

10 deficiency is associated with liver fibrosis progression.

11 d as key regulators of tumor maintenance and progression.

12 detrimental and beneficial effects on tumor progression.

13 ive drugs are clearly needed to slow disease progression.

14 for scanning, and patients with and without progression.

15 ogy when comparing regression vs persistence/progression.

16 laparib led to better suppression of the HCC progression.

17 their phenotype differed by rate of disease progression.

18 Age affects its onset and progression.

19 r maintaining stem cell phenotype and cancer progression.

20 icantly (P < 0.05) inversely associated with progression.

21 fying TF GATA6 in lung adenocarcinoma (LUAD) progression.

22 ins stably elevated with Parkinson's disease progression.

23 cilitate myofibroblast survival and fibrotic progression.

24 ntitative trait locus (QTL) mapping for rust progression.

25 ients and might have a role in liver disease progression.

26 transcriptome as a whole to predict disease progression.

27 nce to understand driving factors of disease progression.

28 sponses) and 14 (33%; 20-50) had 6-month non-progression.

29 the rate of SIV oral transmission or disease progression.

30 e pharmacologic treatment to prevent disease progression.

31 ages and increased in abundance with disease progression.

32 a progressive disease with variable rates of progression.

33 ng its transcriptional activation to meiotic progression.

34 how nutrient depletion might influence PDAC progression.

35 autoreactive CD8+ T cells influence disease progression.

36 itive advantage of MDS HSPCs and for disease progression.

37 lays an active role in cancer initiation and progression.

38 t have no significant favorable effect on VC progression.

39 our fitness maintained throughout the tumour progression.

40 esulted in inhibition of RMS development and progression.

41 ition and serum C3M, a marker of IPF disease progression.

42 most common cause of death is due to disease progression.

43 odegeneration as well as in cancer onset and progression.

44 at can reinitiate growth and promote disease progression.

45 patients at high risk for near-term clinical progression.

46 to SARS-CoV-2 and the predictors of disease progression.

47 ameliorate synaptic dysfunction and disease progression.

48 ommunications in CCA and their role in tumor progression.

49 ically with CCT as risk factors for glaucoma progression.

50 continue to benefit from enzalutamide beyond progression.

51 E) can dampen their ability to control tumor progression.

52 FLT change became a stronger predictor of VF progression.

53 s disease and can be used to monitor disease progression.

54 eliorate signs of disease, and delay disease progression.

55 talk surfaced as a key contributor to cancer progression.

56 of ST6Gal-I is associated with premalignant progression.

57 ential autophagy regulators during carcinoma progression.

58 is also ubiquitinated during normal S-phase progression.

59 activates serine synthesis to promote cancer progression.

60 ere neuroinflammation contributes to disease progression.

61 ts and a tumor may promote or prevent cancer progression.

62 option of on-study retreatment after disease progression (1-year fixed duration).

63 Perfusion increased from cycle 4 to disease progression (51% +/- 11; P < .001).

64 ation (6-month cumulative incidence of local progression, 56% [range, 19%-91%] vs 22% [range, 12%-34%

65 pathway mutation had a shorter time to local progression after TAE compared to those without mutation

66 n using naive CD4+ T-cells was predictive of progression along the whole IA-continuum.

67 OPG expression and consequently drive lesion progression, along with pro-osteoclastogenic support pro

68 reduce adverse clinical outcomes and disease progression among patients with stage C HF) and preventi

69 et reached, with only 1 patient experiencing progression and 1 death.

70 as a useful diagnostic indicator of disease progression and as a therapeutic outcome measure in resp

71 roves the model's ability to assess glaucoma progression and better reflects the way clinicians manag

72 extent of expansion correlates with disease progression and formation of amyloid-like protein deposi

73 essenger RNAs (mRNAs) that associate with BE progression and identified one that affects the stabiliz

74 The 4-year cumulative risk of disease progression and intervention after uncomplicated catarac

75 d miR-497 as major players that can suppress progression and metastasis of mouse and human cutaneous

76 critical role in lung cancer control versus progression and metastasis.

77 sion, generally referred to as dormancy, and progression and metastasis.

78 How pluripotency progression and morphogenesis are linked and whether int

79 diate whereby control over both pluripotency progression and morphogenesis pivots from WNT to MEK sig

80 t upon progression, or they were screened at progression and received their substudy assignment upon

81 Prevention of progression and reduction in fibrosis are the main aims

82 le variation exists in disease presentation, progression and response to therapy, highlighting hetero

83 ated, may provide useful measures of disease progression and response to therapy.

84 pre-existing hereditary genetics can impact progression and survival outcomes of a future malignancy

85 tions perturb its function to dictate cancer progression and therapeutic response.

86 ent (TME) plays a significant role in cancer progression and thus modeling it will advance our unders

87 the ER, its function, and its role in cancer progression and treatment.

88 stigation of cell states throughout melanoma progression and treatment.

89 chaperone protein SmgGDS promotes cell-cycle progression and tumorigenesis in human breast and nonsma

90 t the degree of their enactment during tumor progression and under the selective pressures of immune

91 rian cancer (OC) facilitate tumor growth and progression, and also pose major obstacles for cancer th

92 cantly (P < 0.05) positively associated with progression, and from 0.77 to 0.82 for those statistical

93 with which to understand disease aetiology, progression, and heterogeneity and to target future trea

94 roles in cell differentiation and cell-cycle progression, and kinase dysregulation is associated with

95 therapies to reduce CKD incidence, slow CKD progression, and lower hospitalization risk are needed t

96 aling modulator, promotes cancer initiation, progression, and metastasis by regulating cell prolifera

97 ow sKlotho in CKD is associated with disease progression, and sKlotho supplementation has emerged as

98 herapy is available to block or slow down AD progression, and the mechanisms of the disease are not f

99 , effects on pulmonary pathology and disease progression are monitored by using histopathology images

100 eruricemia or uric acid (UA) crystals in CKD progression are unknown.

101 cells, but not CD8(+) T cells, halts cancer progression as a result of tissue healing and remodellin

102 also affected networks related to cell cycle progression as well as connective tissue development and

103 The disease progression associated with the proinflammatory host res

104 dy endpoints included AR progression, asthma progression, asthma occurrence, and therapy adherence.

105 Study endpoints included AR progression, asthma progression, asthma occurrence, and

106 lternative strategy to control ovarian tumor progression based on selectively disrupting a previously

107 ants were excluded because they had clinical progression before imaging showed PD, and one participan

108 cript defines a novel role of E2F2 in cancer progression beyond cell cycle and could impact patient t

109 lated macular degeneration (AMD) and disease progression, but the precise biological function of HtrA

110 knockdown is a powerful means to prevent LD progression, but this approach did not reduce brain glyc

111 t type 2 immunity is associated with disease progression by promoting fungal growth and dissemination

112 ntial for multiple myeloma cell survival and progression by protecting multiple myeloma cells from ox

113 ation is an effective means of slowing ADPKD progression caused by inactivation of Pkd1.

114 d progression in 100% of patients with tumor progression, compared with 71% for only ctDNA detection

115 ession in this mouse model, and that disease progression could be ameliorated by inhibition of PTP1B.

116 tissue, raising the possibility that disease progression could potentially be slowed by disrupting th

117 mmunity exerts a mechanistic role in disease progression, determining the clinical outcomes.

118 stinct biological and disease initiation and progression events associated with Chr1- and Chr10-direc

119 patients aged 18 years or older with disease progression following at least one previous treatment an

120 Differences in progression-free (PFS) and overall survival (OS) were ev

121 y higher objective response rates and longer progression-free and overall survival than those with NM

122 relapsed or refractory patients, the median progression-free and overall survival times were not yet

123 the primary analysis and subsequent reports, progression-free and overall survival were significantly

124 verse TME associated with 17 fewer months of progression-free survival (PFS) (95% confidence interval

125 algorithm were applied to predict patients' progression-free survival (PFS) and overall survival (OS

126 x plus rituximab (VenR) resulted in improved progression-free survival (PFS) compared with bendamusti

127 Progression-free survival (PFS), OS, and adverse events

128 linical or radiographic characteristics with progression-free survival (PFS; by RECIST) were evaluate

129 At the time of final progression-free survival analysis and interim overall s

130 e overall survival, event-free survival, and progression-free survival and safety.

131 The primary endpoint was progression-free survival assessed by intention to treat

132 ensitivity analysis of investigator-assessed progression-free survival at the overall survival databa

133 s with glioblastoma is controversial because progression-free survival benefit did not translate into

134 Taken together with the lack of progression-free survival benefit, these findings do not

135 The primary endpoint was progression-free survival by independent review in the i

136 e first-line setting significantly prolonged progression-free survival compared with a fixed-duration

137 pathways may postpone resistance and extend progression-free survival in many cancer indications.

138 all survival analysis (May 31, 2019), median progression-free survival in the intention-to-treat popu

139 translocations and associated with divergent progression-free survival patterns.

140 Objective response rate and progression-free survival per investigator assessment we

141 t the overall survival database lock, median progression-free survival remained significantly improve

142 nths (5.6-NE) in the EZH2(WT) cohort; median progression-free survival was 13.8 months (10.7-22.0) an

143 Median progression-free survival was 13.93 months (95% CI 11.73

144 Median progression-free survival was 14.5 months (95% CI 12.5-1

145 One-, 2-, and 3-year progression-free survival was 98%, 93%, and 91% for the

146 Progression-free survival was longer in the BEV group (3

147 We report on biochemical progression-free survival, freedom from non-protocol hor

148 Progression-free survival, the primary endpoint, remaine

149 y reflecting its effectiveness for extending progression-free survival; however, these parameters wer

150 ation between self-identified black race and progression from AD to asthma.

151 patients along a trajectory of LOAD disease progression from brain transcriptomic data.

152 also be useful in deciphering the malignant progression from leiomyoma to leiomyosarcoma.

153 spectively reviewed to longitudinally assess progression from the initial lesion to the final fibrosi

154 prognostic ordinality: grade 1 = no disease progression; grade 2 = development of varices; grade 3 =

155 association between dietary patterns and KOA progression has received little research attention.

156 f the ERK isoforms (ERK1 and ERK2) in cancer progression have not been well defined.

157 chemoradiotherapy was associated with tumor progression (hazard ratio, 18.7; P < .0001), formation o

158 h lower risk of chronic kidney disease (CKD) progression, implicating mechanisms beyond renal clearan

159 DNA and metabolic imaging analysis predicted progression in 100% of patients with tumor progression,

160 ndpoint of reduction in confirmed disability progression in a phase 3 trial of patients with relapsin

161 n in cells and dramatically accelerates SCLC progression in an Rb1/Trp53-deleted mouse model.

162 otein periostin has been associated with CKD progression in animal models and human biopsy specimens.

163 ing antidopaminergic medication had a slower progression in chorea and irritability compared with tho

164 uginosa and Aspergillus were associated with progression in CT scores in the year after an infection

165 severe pancreatic atrophy accompanied tumor progression in Ddr1(-/-); KPC mice.

166 Risk factors for visual field progression in glaucoma can affect both eyes, meaning th

167 s to determine MA prevalence, incidence, and progression in HARBOR.

168 Cxcl1 and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed mice by inducing liver inflammati

169 tivated in the intermediate phase of disease progression in high-risk MM.

170 on variant is associated with kidney disease progression in human cohorts: the African American Study

171 th BrM represents a new strategy to slow AMD progression in humans.

172 An analysis of a >=2-stage progression in MiToS stage showed no difference between

173 The identification of progression in multiple sclerosis is typically retrospec

174 rease in liver stiffness on MRE and fibrosis progression in NAFLD.

175 Thus, we recapitulated nerve tumor progression in NF1 and provided preclinical platforms fo

176 gramming occurs during tumour initiation and progression in renal cell carcinoma (RCC) and three onco

177 been associated with disease initiation and progression in the gastrointestinal (GI) tract and assoc

178 Although disease progression in the mouse does not perfectly model the hu

179 orts to investigate mechanisms driving tumor progression in this deadly disease.

180 rather than inflammation was critical for AD progression in this mouse model, and that disease progre

181 etween appressorium formation and cell cycle progression in U. maydis, which serves as a "toggle swit

182 iption factor NF-Y is crucial for cell-cycle progression in various types of cells.

183 nhancer modulates TAL1 expression and cancer progression in xenotransplants.

184 cardiac injury, namely arrhythmogenesis and progression into heart failure.

185 cycle, suppresses S-phase entry and promotes progression into mitosis.

186 during both the acute pneumonitis stage and progression into the chronic fibroproliferative phase, l

187 nding of the role of this organism in cancer progression is limited, in part due to challenges in mai

188 yet how and when obesity contributes to PDAC progression is not well understood.

189 n inflammatory phenotype associated with CAD progression is unknown.

190 allows the study of human tumor initiation, progression, manifestation, and tumor-immune-system inte

191 se results highlight the potential of IL6 as progression marker in Parkinson's disease due to PRKN/PI

192 stromal cells to promote the initiation and progression of a variety of solid and haematological mal

193 was to determine whether recAP prevents the progression of acute and acute-on-chronic liver failure

194 therapeutic approaches for slowing clinical progression of AD.

195 tify sepsis patients with differing risk for progression of AKI.

196 ction between sex and weight gain alters the progression of allergic asthma in mice with females deve

197 be a key pathogenic factor in the onset and progression of Alzheimer's disease (AD).

198 play a central role in the pathogenesis and progression of Alzheimer's disease.

199 t HtrA1 protease activity is involved in the progression of AMD.

200 ricemia alone did not cause CKD or drive the progression of aristolochic acid I-induced CKD.

201 ting and morphological methods to detail the progression of basal ganglia neuron type-specific pathol

202 st-specific deletion of Txndc5 mitigates the progression of BLM-induced PF and lung function deterior

203 18)F-fluoride uptake demonstrated more rapid progression of calcification compared with those without

204 nction of PDE10A in cardiac cells and in the progression of cardiac remodeling and dysfunction.

205 ysiology and their damage contributes to the progression of chronic kidney diseases.

206 eatment with BIO for only 4 weeks attenuates progression of CKD beyond MRE therapy in mice with type

207 tanding the functional (i.e., fitness-based) progression of co-evolving STM strains.

208 Our study may point to distinct stages of progression of COVID-19 lung disease and highlights the

209 sis in cardiomyocytes, thereby worsening the progression of diabetic cardiomyopathy.

210 utic strategy to prevent the development and progression of diabetic interstitial fibrogenesis.

211 reatment after disease onset potently blocks progression of disease and further alpha-motoneuron dege

212 ment of muscle biogenesis contributes to the progression of Duchenne muscular dystrophy (DMD).

213 to senolytics (n = 9) did not exhibit faster progression of glaucomatous visual field damage compared

214 thetic overactivity in the manifestation and progression of HF is universally accepted.

215 ammation contributes to the pathogenesis and progression of HF.

216 ys before adverse ventricular remodeling and progression of HF.

217 ve a significant impact on the formation and progression of human cancers.

218 particularly those related to the onset and progression of human disease.

219 e led to the fundamentals of development and progression of human diseases, which includes chromosoma

220 tion in kidney tissue, combine to accelerate progression of kidney disease.

221 with high risk of cardiovascular disease and progression of kidney disease.

222 their essential role in the pathogenesis and progression of kidney diseases.

223 ignaling contributes to the pathogenesis and progression of kidney diseases.

224 associated with radiographic and symptomatic progression of KOA.

225 seful for further mechanistic studies in the progression of liver diseases and in the discovery of dr

226 eased liver and as such are important in the progression of liver fibrosis.

227 and potentially monitor the persistence and progression of lung damage.

228 ropose that interrupting the POOR-get-POORer progression of lung injury relies on two principles: 1)

229 the establishment of MSCI permits the timely progression of male meiosis.

230 This technique is of interest to prevent the progression of mild edema and might avoid or reduce the

231 se therapeutic modulation will help slow the progression of motor neuron disease, offering a novel tr

232 rect implications for deducing the molecular progression of neurodegeneration and amyloidogenesis in

233 s and the immune system in the inception and progression of obesity.

234 tructure and mechanics change with onset and progression of POP.

235 This microenvironment develops during the progression of premalignant to malignant disease and bec

236 und healing, epimorphic regeneration and the progression of solid tumors have been uncovered by recen

237 thickness could be better suited to measure progression of structural glaucomatous loss.

238 upregulation of IGF-1 in the initiation and progression of TGFbeta-induced fibrogenesis and IPF have

239 nts with LGMDR3 had a later onset and slower progression of the disease.

240 stimating infection rates and monitoring the progression of the epidemic.

241 dinate axon targeting with the developmental progression of the pharyngeal arches and show that exper

242 rly age and most (67%) have slow-to-moderate progression of their visual field defects.

243 have been implicated in the development and progression of various types of cancer.

244 merous pathological processes such as cancer progression or diabetes.

245 assigned to continue nivolumab until disease progression or unacceptable toxicity or to stop nivoluma

246 reafter as maintenance therapy until disease progression or unacceptable toxicity).

247 orally on days 1 and 3 weekly until disease progression or unacceptable toxicity.

248 dexamethasone in 28-day cycles until disease progression or up to 6 cycles after complete hematologic

249 and received their substudy assignment upon progression, or they were screened at progression and re

250 RI and (1)H MR spectroscopy to track disease progression over a wide range of ages in participants wi

251 eneral health status, odds ratios for 5-year progression ranged from 1.18 to 1.51 (per 1-standard dev

252 gression, sectors with 1 ODH had a faster VF progression rate than those with no ODH (P < 0.017) and

253 glaucoma can affect both eyes, meaning that progression rates (in decibels per year) between eyes li

254 and number of atrophic foci predicted future progression rates with a cross-validated mean absolute e

255 growth is due to perturbation of cell cycle progression rather than induction of apoptosis.

256 nt is necessary to effectively capture these progression-related signatures, and that carcinoma-speci

257 the origins of molecular subtypes and their progression relationships.

258 ar function of STEAP1 and its role in cancer progression remain elusive.

259 he importance of AKT overactivation in tumor progression, results from clinical trials of various AKT

260 Regarding the largest sectoral VF progression, sectors with 1 ODH had a faster VF progress

261 structural outcomes including accelerated OA progression, subchondral insufficiency fracture, complic

262 , was associated with significantly worse VF progression than sectors with moderate or only 1 observe

263 ibroblasts exhibit a marked delay in mitotic progression that can be rescued by lentiviral transducti

264 signaling regulates GI function and disease progression that involve stem/progenitor cells and infla

265 en associated with knee osteoarthritis (KOA) progression, the association between dietary patterns an

266 lation and fuel lipogenesis, enabling tumour progression through metabolic reprogramming.

267 HMR in Saccharomyces cerevisiae, depends on progression through S phase of the cell cycle, but the m

268 is to papilledema documentation, papilledema progression, time to papilledema resolution, treatment i

269 test whether loss of TMPRSS13 impacts tumor progression, TMPRSS13 was genetically ablated in the onc

270 8/A9 mediates neutrophil accumulation during progression to chronic TB.

271 Novel drug development, testing and progression to clinical trials is overwhelmingly expensi

272 erating characteristic curve [AUC] 0.91) and progression to diabetes (AUC 0.92) based on standard cro

273 inuria is an independent risk factor for the progression to end-stage kidney failure, cardiovascular

274 ter the detection of nGA, the probability of progression to GA was 38% (95% CI, 15%-55%) after 24 mon

275 Timely heart valve surgery can mitigate the progression to heart failure, disability, and death.

276 Clinical predictors of BE progression to HGD or EAC are poorly understood, with mu

277 ssessed the kinetics of GBS GI colonization, progression to invasive disease, and the role of GBS-spe

278 Four predictive models for progression to late AMD or atrophic AMD were only develo

279 a positive or negative effect on survival or progression to long-term oxygen therapy in patients with

280 ice were assessed for baseline gastritis and progression to metaplasia.

281 t were associated with an increased risk for progression to PDR.

282 baseline focal hippocampal atrophy predicted progression to syndromal psychosis.

283 r development of islet autoimmunity (IA) and progression to type 1 diabetes in a prospective high-ris

284 f (starting on cycle 1 day 15) until disease progression, unacceptable toxicity, loss to follow-up, o

285 ay cycles from the ninth cycle until disease progression, unacceptable toxicity, or patient withdrawa

286 Evaluating the risk of progression using naive CD4+ T-cells was predictive of p

287 recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, suggested

288 in early stages to prevent or alter disease progression via appropriate interventions.

289 The most robust predictor of PSA progression was change in SUV(hetero) (PET1 to PET3; haz

290 Structural progression was measured by the OCT rate of thinning of

291 but during the open-label period, more rapid progression was noted among patients in the placebo-edar

292 e the role of mesenchymal plasticity in PDAC progression, we generated a PDAC mouse model in which CA

293 to be deriving benefit despite radiographic progression, were randomly assigned to continue nivoluma

294 The initiation of MSCI is required for stage progression, which enables crossover formation, suggesti

295 nisms by which PXN affects cancer growth and progression, which we addressed using cancer patient dat

296 d by t-ASPP2 contributed to tumor growth and progression while being dispensable for tumor initiation

297 ing the causes of immune evasion and disease progression will identify potential immune-mediated targ

298 ed to apply those scores for analysis of S-F progression with a combined vector.

299 ctions in new infections and delayed disease progression, with Atlanta, Baltimore, and Miami projecti

300 mature cardiovascular disease contributed to progression, with dyslipidemia the strongest modifiable