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1 (14 with nonprogressive disease and 15 with progressive disease).
2 e response, indeterminate, partial response, progressive disease).
3 t on day 40; the death was deemed related to progressive disease.
4 e determined according to RECIST 1.1 to have progressive disease.
5 response, minor response, stable disease, or progressive disease.
6 % (3 of 17) stable disease and 30% (5 of 17) progressive disease.
7 this category than for those with stable or progressive disease.
8 Seven patients died, three of whom due to progressive disease.
9 % (4 of 15) stable disease and 20% (2 of 15) progressive disease.
10 mg), 31 showed stable disease, and eight had progressive disease.
11 ransformed cases or accurately predict early progressive disease.
12 ed treatment before study end, mainly due to progressive disease.
13 change in SUV to define partial response and progressive disease.
14 th advanced soft tissue or bone sarcoma with progressive disease.
15 remains a need for effective treatments for progressive disease.
16 se, including 6 of 8 entering the study with progressive disease.
17 response and n=11 stable local disease, one progressive disease.
18 erved kidney function, but not in those with progressive disease.
19 table disease, and three (19%, 4.1-45.7) had progressive disease.
20 ecrease in erythropoiesis in BM in mice with progressive disease.
21 n, 19 mo; interquartile range, 14-26 mo) had progressive disease.
22 ith multiple comorbidities in the setting of progressive disease.
23 Chronic kidney disease (CKD) is a highly progressive disease.
24 rompt treatment can be initiated if there is progressive disease.
25 erichia coli sepsis), each in the setting of progressive disease.
26 ts with stable disease than in patients with progressive disease.
27 d stable disease, and two (9%, 1.1-28.0) had progressive disease.
28 ts with EAC to determine L1 activity in this progressive disease.
29 ers of a single node can be used to identify progressive disease.
30 stable disease; the remaining four (9%) had progressive disease.
31 able disease and the remaining two (10%) had progressive disease.
32 eatment of colonized patients with severe or progressive disease.
33 onse, five had stable disease, and seven had progressive disease.
34 achieved partial remission, and 1 of 51 had progressive disease.
35 e domain of ALK, resulting in resistance and progressive disease.
36 esponse, 28 had stable disease, and four had progressive disease.
37 ions that result in ibrutinib resistance and progressive disease.
38 isk of graft loss from recurrent amyloid and progressive disease.
39 xcept in cases of visceral crisis or rapidly progressive disease.
40 in RRMS, making it a potential biomarker of progressive disease.
41 n = 2) after stopping venetoclax because of progressive disease.
42 jority of patients who eventually succumb to progressive disease.
43 criteria, ranging from complete response to progressive disease.
44 Nearly half of the patients presented with progressive disease.
45 tures than patients with partial response or progressive disease.
46 being a potential therapy for patients with progressive disease.
47 eath unrelated to study treatment was due to progressive disease.
48 children with a negative family history and progressive disease.
49 favorable in 3 patients, whereas 4 exhibited progressive disease.
50 drawal of consent, unacceptable toxicity, or progressive disease.
51 ossible exception of a subgroup with rapidly progressive disease.
52 and therapeutic candidate for patients with progressive disease.
53 5% CI, 161-274 Gy; n = 13) and patients with progressive disease (116 Gy; 95% CI, 81-165 Gy; n = 9) (
54 (P = 0.01) and between complete response and progressive disease (117 Gy; 95% CI, 87-159 Gy; n = 21)
56 176 pwMS with relapsing disease than 92 with progressive disease (2124.8 ng/L, SD 3348.9 vs 1121.4 ng
57 inued in 54 (44%) patients, primarily due to progressive disease (39 [31%]) and adverse events (seven
58 98 [39%] of 252; five related to treatment), progressive disease (43 [17%]), sepsis (36 [14%]; two re
60 ase after treatment (hazard ratio, 0.017 vs. progressive disease; 95% confidence interval, 0.001-0.35
63 rmal organ function and centrally documented progressive disease according to Response Evaluation Cri
64 rtial response) and nonresponders (stable or progressive disease) according to PERCIST1 and PERCIST5
65 tients) were a priori divided into stable vs progressive disease, according to gross motor and cognit
66 PED appears to be the primary indicator for progressive disease activity, whereas secondary cystoid
68 ents with metastatic solid malignancies with progressive disease after >/= one line of palliative che
70 e in heavily treated patients with mCRPC and progressive disease after docetaxel and abiraterone and/
71 stage study, we enrolled adult women who had progressive disease after first-line chemotherapy for ad
72 sies; an ECOG performance status of 0-1; and progressive disease after previous treatment with at lea
75 y of patients with newly diagnosed cancer or progressive disease aimed at identifying patients at ris
76 d stable disease, and six (29%) patients had progressive disease; all responses were across a variety
78 Two patients died as a result of GVHD, 1 of progressive disease and 1 of complications related to a
79 ith multiple sclerosis (seven with secondary progressive disease and 14 with a relapsing remitting di
80 ent emphysema at CT were more likely to have progressive disease and increased mortality at 5 years c
81 unoregulatory qualities of PD-1 and IL-10 in progressive disease and link exhausted virus-specific CD
82 ial response than among those with stable or progressive disease and those who had received secondary
83 e opportunity to treat patients with rapidly progressive disease and where autologous CAR-T-cell ther
84 sease, suboptimal myeloma control (active or progressive disease), and 1 or more comorbidities as ris
86 ; 180 (36%) had adverse events, 70 (14%) had progressive disease, and 51 (10%) requested to stop trea
87 was markedly suppressed in IPF subjects with progressive disease, and both TGF-beta1 and SHH signalin
89 ve and disease-free, eight (16%) had died of progressive disease, and one patient (2%) each had died
90 ctive pulmonary disease (COPD) is a chronic, progressive disease, and reversal of COPD diagnosis is t
92 ML is currently indicated only for recurrent progressive disease, and the acute and long-term toxicit
93 combine to define the transition to NASH and progressive disease are complex, and consequently, no ph
94 ess the most common components of radiologic progressive disease as defined by RECIST 1.1 in patients
95 We used Alzheimer's disease (AD), a complex progressive disease, as a model because the well-establi
96 ith no need for immediate therapy to rapidly progressive disease associated with therapeutic resistan
98 nfidence interval, 65-84) were alive without progressive disease at 6 months (primary end point).
99 nivolumab or docetaxel was longer than after progressive disease at 6 months, with hazard ratios for
104 as associated with worse PFS ( P < .001) and progressive disease at first restaging ( P < .001).
109 eview committee assessed response, including progressive disease, based on imaging using modified Int
110 ion Whole-body MRI enabled identification of progressive disease before CT in most participants with
112 (AS) is the prototypic form of SpA in which progressive disease can lead to fusion of the spine.
113 n-mediated amyloidosis is a rare, inherited, progressive disease caused by mutations in the transthyr
114 Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary
116 lmonary fibrosis (IPF) is a lethal, chronic, progressive disease characterized by formation of scar t
117 Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by interstitial remode
118 Pulmonary arterial hypertension (PAH) is a progressive disease characterized by lung endothelial ce
120 early postnatal development, but resulted in progressive disease characterized by reduced activity an
121 flammatory bowel diseases (IBD) are chronic, progressive diseases characterized by aberrant immune re
122 e elevated MIF and D-DT levels in males with progressive disease compared with relapsing-remitting ma
123 nts who discontinued chemotherapy because of progressive disease could cross over to the ceritinib gr
127 ith multiple sclerosis who display a rapidly progressive disease course and in whom potent pharmacoth
128 745G>A mutation generally had a less rapidly progressive disease course than the 17 cases with other
129 ever, men with MS tend to demonstrate a more progressive disease course than women, suggesting a disc
134 f patients with plasma cell neoplasms die of progressive disease despite high response rates to novel
137 ned positive for HER1/2 and who did not have progressive disease during chemotherapy (four to eight c
139 atic or recurrent endometrial cancer who had progressive disease following one or two lines of chemot
141 nor response, 18.2% stable disease, and 9.1% progressive disease for pancreatic NET; and 22.0% partia
142 by +/-2 SDs were identified with significant progressive disease for RV, with a decrease in RV-FAC gr
143 or response, 35.1% stable disease, and 10.8% progressive disease for the entire cohort; 54.5% partial
145 roven, opportunities to intervene to prevent progressive disease, founded in a thorough cellular and
146 65) for docetaxel; for stable disease versus progressive disease, hazard ratios were 0.52 (0.37-0.71)
147 : A new pattern of response, so-called hyper-progressive disease (HPD), is emerging during treatment
148 PC2 in the kidney exhibited severe, rapidly progressive disease, illustrating the importance of comp
149 as stable disease in 90% (9/10 patients) and progressive disease in 10% (1/10 patients) at 3 mo, and
152 n reasons for treatment discontinuation were progressive disease in 34 (24%) patients and adverse eve
157 actory diffuse large B-cell lymphoma (due to progressive disease in four patients, infections in thre
159 which point 86 (67%) of 128 patients without progressive disease in the placebo group chose to cross
160 osis was found for those patients who showed progressive disease, in comparison with patients with cu
161 were enucleated: one at diagnosis, nine with progressive disease including three eyes treated with EB
162 oblastoma patients had no response and 7 had progressive disease, including 6 of 8 entering the study
163 h-salt diet (5-9 weeks after I/R) manifested progressive disease indicated by enhanced inflammation,
164 PGSs stratified patients with high risk for progressive disease indicated by worse prognostic outcom
165 ate that RLBP1 mutations are associated with progressive disease involving RPE atrophy and photorecep
169 was an excellent inter-observer agreement in progressive disease (k=0.94, percent agreement=97.1%), s
174 pants with disease control versus those with progressive disease (median, 121 Gy [IQR: 86-190 Gy] vs
175 vival than nonresponding patients (stable or progressive disease) (median, 19 mo vs. 7.5 mo; log-rank
176 trophy and WM abnormalities in patients with progressive disease might indicate a more independent ne
177 Importantly, these experiments establish a progressive disease model that can contribute toward ide
179 igible for intermittent sunitinib because of progressive disease (n = 13), toxicity (n = 1), or conse
182 onders vs stable disease/minimal response vs progressive disease/NE, median PFS was 15.0 months (95%
183 iscontinued nivolumab for reasons other than progressive disease; nine (50%) of those had responses l
185 Idiopathic pulmonary fibrosis (IPF) is a progressive disease of the middle aged and elderly with
186 Age-related macular degeneration (AMD) is a progressive disease of the retinal pigment epithelium (R
187 or stable disease in patients with formerly progressive disease) of up to 95%, with a low incidence
188 re carcinoembryonic antigen (CEA) >80 mug/L, progressive disease on chemotherapy, size of largest les
189 ere used to screen patients with and without progressive disease on ibrutinib, and ibrutinib-naive di
193 s had discontinued study drug as a result of progressive disease or clinical signs of progressive dis
194 ry endpoint was time to progression (time of progressive disease or death from any cause), with inten
195 l, defined as the time from randomisation to progressive disease or death, whichever occurred first.
196 mg orally on days 1-21 every 28 days) until progressive disease or intolerability, or single-agent i
198 ients with advanced grades 1 and 2 NETs with progressive disease or other poor prognostic features.
199 DLBCL which, for this study, was defined as progressive disease or stable disease as best response a
203 t-baseline scans, or discontinued because of progressive disease or treatment-related adverse events
205 was administered (100 mg) twice a day until progressive disease or unacceptable toxic effects occurr
207 ory NHL received venetoclax once daily until progressive disease or unacceptable toxicity at target d
211 ed on empirical data derived from studies of progressive disease or whether treatment decisions are b
212 0.017-0.518), but increased the frequency of progressive disease (OR, 2.717; 95% CI, 1.391-5.304).
214 lasses (complete response, partial response, progressive disease, or stable disease) and in the diffe
215 ated with greater brain atrophy in secondary progressive disease over a period of short term follow-u
216 n particularly in patients who had secondary progressive disease (P (CSF) < 4 x 10(-5), P (plasma) <
218 lth states (progression-free survival (PFS), progressive disease (PD) and death) were analyzed in the
219 ently, we identified significant RD3 loss in progressive disease (PD) and defined its association wit
220 ging findings during treatment suggestive of progressive disease (PD) despite evidence of clinical be
221 her whole-body MRI enables identification of progressive disease (PD) earlier than CT and bone scinti
223 nsition, whereas those present at on-therapy progressive disease (PD) upregulated kynurenine, plasmin
226 ations at baseline, co-acquired mutations at progressive disease (PD), and the clonal evolution remai
227 Results: Of the 4 patients with clinically progressive disease (PD), mean K(i) significantly increa
229 artial response [PR] v stable disease [SD] v progressive disease [PD]), disease control rate (DCR; CR
231 h criteria (n = 331), 37.5% in patients with progressive disease per RECIST v1.1 but nonprogressive d
232 survived >/= 12 weeks, 84 (14%) experienced progressive disease per RECIST v1.1 but nonprogressive d
233 stages, it tends to have limited effect on a progressive disease, possibly due to adverse effects on
234 mitting and the central canal CSF surface in progressive disease, possibly implying CSF-mediated path
237 Patients with MSKCC poor-risk disease or progressive disease prior to surgery had a poor outcome
238 ssible that this gray matter loss reflects a progressive disease process irrespective of medication u
239 cted lesion due to ECD for >/=3 months), and progressive disease (progression or worsening of proven
240 ier intervention with ocrelizumab in primary progressive disease, progression remains an important un
241 hree with relapsed or refractory CLL (due to progressive disease, pulmonary infection, and pneumonia;
242 isease progression (clinical or radiological progressive disease, relapse, or death from any cause).
243 st effective at discriminating patients with progressive disease requiring surgery, with an AUC of 0.
249 ponders (n = 6) (stable metabolic disease or progressive disease) showed a median OS of 4.4 mo (1-y a
250 asyn is likely occurring in both initial and progressive disease stages, and preventing truncation ma
252 lysosomal storage was undetectable in iPSCs, progressive disease subtype-specific storage material wa
253 ) were significantly higher in patients with progressive disease than in patients with stable disease
254 malities was weaker in primary and secondary progressive disease than in relapsing-remitting disease.
256 Chronic wasting disease (CWD) is a fatal, progressive disease that affects cervid species, includi
258 otrophic lateral sclerosis (ALS) is a severe progressive disease that cannot be prevented or cured.
259 ive pulmonary disease (COPD) is a common and progressive disease that is influenced by both genetic a
263 spectrum from infancy (early onset, rapidly progressive disease) to childhood/adolescence and adulth
264 to-head trials of therapies for this complex progressive disease, to answer issues such as how best t
265 has led to several small clinical trials of progressive disease treatment as adjuvant for disease-mo
266 al response (treatment success) or stable or progressive disease (treatment failure)-according to pre
267 least one high-risk feature (aged >40 years, progressive disease, tumour size >5 cm, tumour crossing
268 least one high-risk feature (aged >40 years, progressive disease, tumour size >5 cm, tumour crossing
269 ays after discontinuing treatment because of progressive disease (two [5%]) and respiratory failure (
270 ive siltuximab locally (eight) or because of progressive disease (two), adverse events (two), or othe
272 nib orally once daily (45 mg or 30 mg) until progressive disease, unacceptable toxicity, or patient w
273 e chief producers of IL-17A in patients with progressive disease undergoing liver transplantation.
274 onse + partial response, 54.3% v 49.5%), and progressive disease was 3.2% versus 5.4%, respectively.
277 te and partial response, stable disease, and progressive disease were defined according to the 2014 N
278 sion profiles of MSCs from IPF subjects with progressive disease were enriched for genes regulating l
280 th recurrent disease, partial remission, and progressive disease were retreated, with either surgery
281 increased MIF and D-DT levels in males with progressive disease were significantly correlated with t
284 therapy protocol (8 Complete Response and 11 Progressive Disease) were evaluated for serum SEVs size,
287 recurrent disease after local treatment, and progressive disease while undergoing systemic treatment.
288 Cholangiopathies are a diverse group of progressive diseases whose primary cell targets are chol
292 Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a prevalence of 1 million perso
293 Severe alcoholic hepatitis (SAH) is often a progressive disease with high mortality and limited ster
294 ic pulmonary fibrosis (IPF) is a devastating progressive disease with limited therapeutic options.
296 tocellular adenomas were more likely to show progressive disease, with hepatic nuclear factor 1alpha-
297 al centres in 12 countries who had confirmed progressive disease within 24 weeks after two or more ip
298 e imaging findings meeting RANO criteria for progressive disease within 6 months of initiating immuno
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