ライフサイエンスコーパス: progressive disease

1 (14 with nonprogressive disease and 15 with progressive disease).

2 response, minor response, stable disease, or progressive disease.

3 response and n=11 stable local disease, one progressive disease.

4 erved kidney function, but not in those with progressive disease.

5 table disease, and three (19%, 4.1-45.7) had progressive disease.

6 ecrease in erythropoiesis in BM in mice with progressive disease.

7 n, 19 mo; interquartile range, 14-26 mo) had progressive disease.

8 ith multiple comorbidities in the setting of progressive disease.

9 Chronic kidney disease (CKD) is a highly progressive disease.

10 rompt treatment can be initiated if there is progressive disease.

11 ts with stable disease than in patients with progressive disease.

12 d stable disease, and two (9%, 1.1-28.0) had progressive disease.

13 ts with EAC to determine L1 activity in this progressive disease.

14 ers of a single node can be used to identify progressive disease.

15 stable disease; the remaining four (9%) had progressive disease.

16 able disease and the remaining two (10%) had progressive disease.

17 eatment of colonized patients with severe or progressive disease.

18 onse, five had stable disease, and seven had progressive disease.

19 achieved partial remission, and 1 of 51 had progressive disease.

20 e domain of ALK, resulting in resistance and progressive disease.

21 esponse, 28 had stable disease, and four had progressive disease.

22 this category than for those with stable or progressive disease.

23 ions that result in ibrutinib resistance and progressive disease.

24 isk of graft loss from recurrent amyloid and progressive disease.

25 derwent HILP, 9 (11.1%) experienced in-field progressive disease.

26 derwent ILI, 43 (32.1%) experienced in-field progressive disease.

27 h low positive margin rates and few cases of progressive disease.

28 partial response, 26 stable disease, and 17 progressive disease.

29 es that IL-17F expression is associated with progressive disease.

30 Complete response or progressive disease.

31 onths for stable disease, and 1.3 months for progressive disease.

32 d chronic pathological process rather than a progressive disease.

33 a, a subset of patients will develop rapidly progressive disease.

34 1 patients were alive and free of documented progressive disease.

35 to 81%); 11 had stable disease, and one had progressive disease.

36 ater in patients with limited as compared to progressive disease.

37 ill provide better options for patients with progressive disease.

38 xtensive cortical pathology that accompanies progressive disease.

39 hocyte depletion (CD4(+) count < 200/muL) or progressive disease.

40 ted with unmutated IGHV gene status and with progressive disease.

41 ed response, 4 had stable disease, and 6 had progressive disease.

42 ng modalities could be of value in detecting progressive disease.

43 tensive cell division in vivo, especially in progressive disease.

44 th those of patients with stable disease and progressive disease.

45 longer than patients with stable disease or progressive disease.

46 amples of 114 patients with either stable or progressive disease.

47 Seven patients died, three of whom due to progressive disease.

48 levels of Dll4 than patients with stable or progressive disease.

49 (84%) had tumor response and one patient had progressive disease.

50 cal improvement, 4 stable disease, and 3 had progressive disease.

51 % (3 of 17) stable disease and 30% (5 of 17) progressive disease.

52 % (4 of 15) stable disease and 20% (2 of 15) progressive disease.

53 mg), 31 showed stable disease, and eight had progressive disease.

54 ransformed cases or accurately predict early progressive disease.

55 ed treatment before study end, mainly due to progressive disease.

56 change in SUV to define partial response and progressive disease.

57 th advanced soft tissue or bone sarcoma with progressive disease.

58 remains a need for effective treatments for progressive disease.

59 se, including 6 of 8 entering the study with progressive disease.

60 ), six with stable disease (13%), eight with progressive disease (18%), and four (9%) who were not ev

61 tients also took longer to develop secondary progressive disease (32 vs 18 years, p=0.0001) and to re

62 inued in 54 (44%) patients, primarily due to progressive disease (39 [31%]) and adverse events (seven

63 98 [39%] of 252; five related to treatment), progressive disease (43 [17%]), sepsis (36 [14%]; two re

64 ) and 20 nonresponders (13 stable disease, 7 progressive disease, 69%).

65 ts who received placebo and who did not have progressive disease, 86 crossed over to lenalidomide.

66 ase after treatment (hazard ratio, 0.017 vs. progressive disease; 95% confidence interval, 0.001-0.35

67 tients) were a priori divided into stable vs progressive disease, according to gross motor and cognit

68 had stable disease, and 8 patients (6%) had progressive disease accounting for an overall response r

69 PED appears to be the primary indicator for progressive disease activity, whereas secondary cystoid

70 ents with metastatic solid malignancies with progressive disease after >/= one line of palliative che

71 d partial response, 49 stable disease, and 6 progressive disease after 6 wk.

72 Two patients developed progressive disease after a complete response for 38 mon

73 e in heavily treated patients with mCRPC and progressive disease after docetaxel and abiraterone and/

74 stage study, we enrolled adult women who had progressive disease after first-line chemotherapy for ad

75 re attained, were not predictors of in-field progressive disease after ILI or HILP.

76 a complete response, patients with in-field progressive disease after ILI were younger (odds ratio,

77 ), 20%-30% of patients experience relapse or progressive disease after initial treatment.

78 clear cell metastatic renal cell carcinoma, progressive disease after one approved systemic treatmen

79 actors are unreliable predictors of in-field progressive disease after regional therapy in patients w

80 with acute myeloid leukaemia (AML) die from progressive disease after relapse, which is associated w

81 resection at diagnosis, or with unresectable progressive disease after surgery alone.

82 ional phase II study; however, she developed progressive disease after two cycles.

83 Patients with progressive disease after two or more HER2-directed regi

84 y of patients with newly diagnosed cancer or progressive disease aimed at identifying patients at ris

85 d stable disease, and six (29%) patients had progressive disease; all responses were across a variety

86 Two patients died as a result of GVHD, 1 of progressive disease and 1 of complications related to a

87 ith multiple sclerosis (seven with secondary progressive disease and 14 with a relapsing remitting di

88 and the second consisting of a patient with progressive disease and a viremic controller.

89 sion pairs: one consisting of a patient with progressive disease and an individual who became an elit

90 erior in detecting patients with biochemical progressive disease and identifying patients with poor s

91 unoregulatory qualities of PD-1 and IL-10 in progressive disease and link exhausted virus-specific CD

92 ial response than among those with stable or progressive disease and those who had received secondary

93 ogical events occur at the earliest stage of progressive disease and which are secondary to the neuro

94 as achieved in 89% of older patients, 3% had progressive disease, and 11% relapsed.

95 ; 180 (36%) had adverse events, 70 (14%) had progressive disease, and 51 (10%) requested to stop trea

96 was markedly suppressed in IPF subjects with progressive disease, and both TGF-beta1 and SHH signalin

97 kinase inhibitors, resistance to inhibitors, progressive disease, and incomplete eradication of Bcr-A

98 ce are normal, Pkd1RC/null mice have rapidly progressive disease, and Pkd1RC/RC animals develop gradu

99 ctive pulmonary disease (COPD) is a chronic, progressive disease, and reversal of COPD diagnosis is t

100 However, many HLA-B*57 patients develop progressive disease, and some studies have suggested tha

101 ML is currently indicated only for recurrent progressive disease, and the acute and long-term toxicit

102 responses that are essential for restricting progressive disease, and the determinants of immunopatho

103 ty with regards to need for therapy, time to progressive disease, and treatment response.

104 combine to define the transition to NASH and progressive disease are complex, and consequently, no ph

105 Amyotrophic lateral sclerosis (ALS) is a progressive disease associated with neuronal cell death

106 ith no need for immediate therapy to rapidly progressive disease associated with therapeutic resistan

107 One patient had progressive disease at 0.4 months.

108 nfidence interval, 65-84) were alive without progressive disease at 6 months (primary end point).

109 Two deaths occurred due to progressive disease at 7 mo.

110 as associated with worse PFS ( P < .001) and progressive disease at first restaging ( P < .001).

111 us, with both patients having no evidence of progressive disease at last follow-up.

112 week 12 (delayed) that was not confirmed as progressive disease at next assessment.

113 of progressive disease or clinical signs of progressive disease at the data cutoff.

114 3 (18%) had stable disease, and 2 (12%) had progressive disease at the final follow-up.

115 eview committee assessed response, including progressive disease, based on imaging using modified Int

116 d be performed in patients with CLL who have progressive disease before starting first-line treatment

117 In the case of progressive disease, bevacizumab was combined with erlot

118 alf of patients with multiple sclerosis have progressive disease characterised by accumulating disabi

119 D1 mice, but not mito-WTSOD1 mice, develop a progressive disease characterized by body weight loss, m

120 Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary

121 Pulmonary fibrosis is a progressive disease characterized by fibroblast prolifer

122 lmonary fibrosis (IPF) is a lethal, chronic, progressive disease characterized by formation of scar t

123 Pulmonary arterial hypertension (PAH) is a progressive disease characterized by lung endothelial ce

124 Pulmonary arterial hypertension (PAH) is a progressive disease characterized by lung endothelial dy

125 arterial hypertension (PAH) is a chronic and progressive disease characterized by pulmonary vasculopa

126 early postnatal development, but resulted in progressive disease characterized by reduced activity an

127 flammatory bowel diseases (IBD) are chronic, progressive diseases characterized by aberrant immune re

128 e elevated MIF and D-DT levels in males with progressive disease compared with relapsing-remitting ma

129 By contrast, rapidly progressive disease correlated with persistent and signi

130 nts who discontinued chemotherapy because of progressive disease could cross over to the ceritinib gr

131 Progressive disease course (P=0.017), thoracic aorta inv

132 Progressive disease course (P=0.018) and carotidynia (P=

133 ith multiple sclerosis who display a rapidly progressive disease course and in whom potent pharmacoth

134 itive decline, behavioural abnormalities and progressive disease course proves negative to the geneti

135 745G>A mutation generally had a less rapidly progressive disease course than the 17 cases with other

136 ever, men with MS tend to demonstrate a more progressive disease course than women, suggesting a disc

137 m HIV-1-infected patients who have the usual progressive disease course.

138 B, treatment continued until development of progressive disease, cumulative toxic effects, or the pa

139 Nine patients with documented progressive disease despite all established therapy unde

140 f patients with plasma cell neoplasms die of progressive disease despite high response rates to novel

141 with median survival of 1 year or less, and progressive disease despite second-line therapy.

142 he second biopsy, abdominal imaging revealed progressive disease despite sorafenib treatment.

143 mplified and RB-expressing WDLS/DDLS who had progressive disease despite systemic therapy.

144 ned positive for HER1/2 and who did not have progressive disease during chemotherapy (four to eight c

145 e aged 18 years or older who had experienced progressive disease during or after one previous platinu

146 Only two patients had progressive disease during the first two vaccine courses

147 median age, 66 years); 28%, 31%, and 41% had progressive disease, early relapse, or late relapse, res

148 atic or recurrent endometrial cancer who had progressive disease following one or two lines of chemot

149 t tuberculosis infection reduces the risk of progressive disease following reexposure and reinfection

150 or response, 48.8% stable disease, and 12.2% progressive disease for nonpancreatic GEP NET.

151 nor response, 18.2% stable disease, and 9.1% progressive disease for pancreatic NET; and 22.0% partia

152 by +/-2 SDs were identified with significant progressive disease for RV, with a decrease in RV-FAC gr

153 or response, 35.1% stable disease, and 10.8% progressive disease for the entire cohort; 54.5% partial

154 Glaucoma is a chronic progressive disease for which ideal treatment would prov

155 ne muscular dystrophy (DMD) is a devastating progressive disease for which there is currently no effe

156 r microRNAs can discriminate patients with a progressive disease from patients with a stable disease.

157 PC2 in the kidney exhibited severe, rapidly progressive disease, illustrating the importance of comp

158 in 11 (20%), stable disease in 15 (27%), and progressive disease in 1 (3%), for an overall response r

159 80%; median time to progression, 34 mo), and progressive disease in 2 patients (10%).

160 n reasons for treatment discontinuation were progressive disease in 34 (24%) patients and adverse eve

161 al remission in 5, stable disease in 13, and progressive disease in 7 patients.

162 al remission in 14, stable disease in 2, and progressive disease in 9 patients.

163 adaptive immunity in driving persistent and progressive disease in acute MPTP-intoxicated mice.

164 nvestigate whether ATXN1[30Q]-D776 curbs the progressive disease in ATXN1[82Q]-S776 mice, we crossed

165 actory diffuse large B-cell lymphoma (due to progressive disease in four patients, infections in thre

166 nt with studies linking T-cell activation to progressive disease in humans and lend support for the u

167 which point 86 (67%) of 128 patients without progressive disease in the placebo group chose to cross

168 , stable disease in nine patients (56%), and progressive disease in two patients (12%).

169 te vigorously in vitro and are able to cause progressive disease in vivo.

170 were enucleated: one at diagnosis, nine with progressive disease including three eyes treated with EB

171 oblastoma patients had no response and 7 had progressive disease, including 6 of 8 entering the study

172 Gauging the risk of developing progressive disease is a major challenge in prostate can

173 Progressive disease is characterized by hepatic leukocyt

174 The transition from stable to progressive disease is unpredictable in patients with bi

175 was an excellent inter-observer agreement in progressive disease (k=0.94, percent agreement=97.1%), s

176 IBM is a slowly progressive disease, leading to wheelchair use, on avera

177 itting disease that transitions to a chronic progressive disease, making the NOD model the only mouse

178 ractory patients with distant metastases and progressive disease (mean age, 71.4 y).

179 trophy and WM abnormalities in patients with progressive disease might indicate a more independent ne

180 Importantly, these experiments establish a progressive disease model that can contribute toward ide

181 For chronic progressive diseases, mortality may not be a feasible en

182 With progressive disease, most patients succumb to death from

183 igible for intermittent sunitinib because of progressive disease (n = 13), toxicity (n = 1), or conse

184 At follow-up, patients who developed progressive disease (n = 18) showed a significantly high

185 +/- 5.1 mL, P = 0.009) than patients without progressive disease (n = 29).

186 response, 36 with stable disease, and 1 with progressive disease (n = 39).

187 s were nonresponders (stable disease, n = 9; progressive disease, n = 2).

188 onders vs stable disease/minimal response vs progressive disease/NE, median PFS was 15.0 months (95%

189 iscontinued nivolumab for reasons other than progressive disease; nine (50%) of those had responses l

190 Biochemical progression or progressive disease occurred in 391 patients (221 [57%]

191 Progressive disease occurred in one patient (2%).

192 12 weeks occurred in four patients (9%), and progressive disease occurred in six patients (14%).

193 Idiopathic pulmonary fibrosis (IPF) is a progressive disease of the middle aged and elderly with

194 ry arterial hypertension (PAH) is a rare and progressive disease of the pulmonary arterial circulatio

195 or stable disease in patients with formerly progressive disease) of up to 95%, with a low incidence

196 Here, we hypothesized that progressive disease on abiraterone may occur secondary t

197 rimary surgery to liver transplantation, and progressive disease on chemotherapy were identified as s

198 ere used to screen patients with and without progressive disease on ibrutinib, and ibrutinib-naive di

199 OS (P = 0.026) than did the 4 patients with progressive disease on PET/CT-2.

200 This method identifies 41% of the later progressive diseases on CT, with no false-positives.

201 s had discontinued study drug as a result of progressive disease or clinical signs of progressive dis

202 ry endpoint was time to progression (time of progressive disease or death from any cause), with inten

203 l, defined as the time from randomisation to progressive disease or death, whichever occurred first.

204 and 44% of patients who received placebo had progressive disease or had died (P<0.001); of the remain

205 mg orally on days 1-21 every 28 days) until progressive disease or intolerability, or single-agent i

206 ients with advanced grades 1 and 2 NETs with progressive disease or other poor prognostic features.

207 DLBCL which, for this study, was defined as progressive disease or stable disease as best response a

208 During BEP, 15 patients died of progressive disease or toxicity, including one patient f

209 ived only a single course of HDCT because of progressive disease or toxicity.

210 t-baseline scans, or discontinued because of progressive disease or treatment-related adverse events

211 Study patients were treated until progressive disease or unacceptable adverse effects occu

212 ntinuous oral ibrutinib (560 mg) daily until progressive disease or unacceptable toxic effects.

213 ory NHL received venetoclax once daily until progressive disease or unacceptable toxicity at target d

214 6 cycles with daily ibrutinib (420 mg) until progressive disease or unacceptable toxicity.

215 ed >75 years) on days 1, 8, 15, and 22 until progressive disease or unacceptable toxicity.

216 eived oral ibrutinib 420 mg once daily until progressive disease or unacceptable toxicity.

217 ed on empirical data derived from studies of progressive disease or whether treatment decisions are b

218 ated with greater brain atrophy in secondary progressive disease over a period of short term follow-u

219 lth states (progression-free survival (PFS), progressive disease (PD) and death) were analyzed in the

220 ging findings during treatment suggestive of progressive disease (PD) despite evidence of clinical be

221 A limitation of this targeted therapy is progressive disease (PD) in some patients.

222 ocal control at 1 year (LC1y), defined as no progressive disease (PD) of irradiated HCC by RECIST (Re

223 nse for mRECIST/mSWOG]), stable disease, and progressive disease (PD) were 28%, 49%, and 24%, respect

224 rtial response (PR), stable disease (SD), or progressive disease (PD).

225 5 showed stable disease (SD), and six showed progressive disease (PD).

226 artial response [PR] v stable disease [SD] v progressive disease [PD]), disease control rate (DCR; CR

227 er irRC (n = 84), and 17.3% in patients with progressive disease per both criteria (n = 177).

228 h criteria (n = 331), 37.5% in patients with progressive disease per RECIST v1.1 but nonprogressive d

229 survived >/= 12 weeks, 84 (14%) experienced progressive disease per RECIST v1.1 but nonprogressive d

230 stages, it tends to have limited effect on a progressive disease, possibly due to adverse effects on

231 d all patients in this group died of rapidly progressive disease postrelapse.

232 ts with multiple sclerosis (MS) have primary progressive disease (PPMS).

233 Patients with MSKCC poor-risk disease or progressive disease prior to surgery had a poor outcome

234 ssible that this gray matter loss reflects a progressive disease process irrespective of medication u

235 cted lesion due to ECD for >/=3 months), and progressive disease (progression or worsening of proven

236 hree with relapsed or refractory CLL (due to progressive disease, pulmonary infection, and pneumonia;

237 It is a progressive disease ranging from mild valve thickening t

238 tus in chronic pancreatitis is likely due to progressive disease rather than individual variables.

239 isease progression (clinical or radiological progressive disease, relapse, or death from any cause).

240 timing for LT in patients with stable versus progressive disease remains unclear.

241 Glaucoma is a progressive disease responsible for the second commonest

242 Type 2 diabetes mellitus (T2DM) is a progressive disease resulting from increasing insulin re

243 Subsequently, four patients experienced progressive disease, seven experienced disease stabiliza

244 Patients with progressive disease show alterations in their serum prot

245 Tumors from patients with progressive disease showed a higher variance of the intr

246 ponders (n = 6) (stable metabolic disease or progressive disease) showed a median OS of 4.4 mo (1-y a

247 Additional criteria are provided for progressive disease, stable disease, and relapse.

248 lysosomal storage was undetectable in iPSCs, progressive disease subtype-specific storage material wa

249 ng T cell-mediated rejection and potentially progressive diseases such as antibody-mediated rejection

250 ) were significantly higher in patients with progressive disease than in patients with stable disease

251 malities was weaker in primary and secondary progressive disease than in relapsing-remitting disease.

252 Rheumatoid arthritis (RA) is a progressive disease that affects both pediatric and adul

253 NASH is a progressive disease that can lead to cirrhosis, cancer,

254 otrophic lateral sclerosis (ALS) is a severe progressive disease that cannot be prevented or cured.

255 Pulmonary arterial hypertension (PAH) is a progressive disease that causes exercise limitation, hea

256 onic obstructive pulmonary disease (COPD), a progressive disease that is characterized by extensive l

257 ia or other forms of cholestasis who develop progressive disease, the postmetamorphosis lampreys grow

258 Seventeen patients (23%) had progressive disease: their PSA level rose by more than 2

259 % to 25%), 25 had stable disease, and 13 had progressive disease; there were no responses among patie

260 espond, and many patients eventually develop progressive disease to daratumumab monotherapy.

261 spectrum from infancy (early onset, rapidly progressive disease) to childhood/adolescence and adulth

262 to-head trials of therapies for this complex progressive disease, to answer issues such as how best t

263 reasing community diversity in patients with progressive disease, total bacterial density remained re

264 has led to several small clinical trials of progressive disease treatment as adjuvant for disease-mo

265 al response (treatment success) or stable or progressive disease (treatment failure)-according to pre

266 least one high-risk feature (aged >40 years, progressive disease, tumour size >5 cm, tumour crossing

267 least one high-risk feature (aged >40 years, progressive disease, tumour size >5 cm, tumour crossing

268 These progressive diseases typically have an insidious onset,

269 nib orally once daily (45 mg or 30 mg) until progressive disease, unacceptable toxicity, or patient w

270 e chief producers of IL-17A in patients with progressive disease undergoing liver transplantation.

271 e median survival for patients with in-field progressive disease was 20.3 months for the ILI cohort a

272 Progressive disease was detected in 2 patients (7.2%) by

273 Progressive disease was detected on week 2 scans in 3 pa

274 longer (5 vs 2.6 years, p=0.04) and primary progressive disease was less common (0.9% vs 8.5%, p=0.0

275 R-CHOP (40% and 34%, respectively; P=0.10), progressive disease was more frequent with R-FC (14%, vs

276 In 15% of tumors (six of 39), progressive disease was seen.

277 rative and procedural predictors of in-field progressive disease were analyzed using logistic regress

278 te and partial response, stable disease, and progressive disease were defined according to the 2014 N

279 sion profiles of MSCs from IPF subjects with progressive disease were enriched for genes regulating l

280 relevant preoperative predictors of in-field progressive disease were identified.

281 th recurrent disease, partial remission, and progressive disease were retreated, with either surgery

282 increased MIF and D-DT levels in males with progressive disease were significantly correlated with t

283 rogression proceeded to HDT/ASCT; those with progressive disease were study failures.

284 Patients with stable/progressive disease were to have radiation before TME, w

285 In general, patients with progressive disease were younger, with advanced-stage me

286 There are 2 forms of this progressive disease: wet and dry.

287 Cholangiopathies are a diverse group of progressive diseases whose primary cell targets are chol

288 ame visible on CT after treatment, mimicking progressive disease with "new" bone lesions, although th

289 y one third of patients experience a rapidly progressive disease with a dismal outcome.

290 Because PD is a progressive disease with a long asymptomatic phase, iden

291 Untreated severe aortic stenosis is a progressive disease with a poor prognosis.

292 Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a prevalence of 1 million perso

293 Calcific aortic stenosis is a progressive disease with no effective medical therapy th

294 Pulmonary fibrosis is a progressive disease with unknown etiology that is charac

295 of blindness in working adults, are chronic, progressive diseases with multifaceted etiologies that a

296 al centres in 12 countries who had confirmed progressive disease within 24 weeks after two or more ip

297 e imaging findings meeting RANO criteria for progressive disease within 6 months of initiating immuno

298 Strikingly, it was also associated with progressive disease within the mutated IGHV gene subset.

299 bevacizumab monotherapy was continued until progressive disease without significant treatment-relate

300 o change in symptoms attributed to ECD), and progressive disease (worsening of symptoms attributed to