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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)
55 the primary reasons for discontinuation were progressive disease (21%) and AEs (11%).
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
59 te or partial response than in patients with progressive disease (95% CI, 20%-180%).
60 ase after treatment (hazard ratio, 0.017 vs. progressive disease; 95% confidence interval, 0.001-0.35
61             Twenty-three (32%) patients with progressive disease according to PERCIST5 had controlled
62 lear distinction between tumor shrinkage and progressive disease according to RECIST.
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
67              Friedreich's ataxia (FRDA) is a progressive disease affecting multiple organs that is ca
68 ents with metastatic solid malignancies with progressive disease after >/= one line of palliative che
69                       Two patients developed progressive disease after a complete response for 38 mon
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
73             One additional patient developed progressive disease after the 6-mo follow-up period but
74                                Patients with progressive disease after two or more HER2-directed regi
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
77                                  In cases of progressive disease, an additional evaluation was perfor
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
85 onse, 17 cases as stable disease, 5 cases as progressive disease, and 14 cases as HPD.
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
88 omplete or partial response, stable disease, progressive disease, and HPD (P = 0.001).
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
91      However, many HLA-B*57 patients develop progressive disease, and some studies have suggested tha
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
97                              One patient had progressive disease at 0.4 months.
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
100 s on bevacizumab and 11% on temsirolimus had progressive disease at 6 weeks.
101                   Two deaths occurred due to progressive disease at 7 mo.
102 ients in this trial, 184 had symptomatic and progressive disease at baseline.
103                                              Progressive disease at bone scintigraphy was evident in
104 as associated with worse PFS ( P < .001) and progressive disease at first restaging ( P < .001).
105 us, with both patients having no evidence of progressive disease at last follow-up.
106  week 12 (delayed) that was not confirmed as progressive disease at next assessment.
107  of progressive disease or clinical signs of progressive disease at the data cutoff.
108  3 (18%) had stable disease, and 2 (12%) had progressive disease at the final follow-up.
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
111                               In the case of progressive disease, bevacizumab was combined with erlot
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
115                      Pulmonary fibrosis is a progressive disease characterized by fibroblast prolifer
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
119             Advanced heart failure (HF) is a progressive disease characterized by recurrent hospitali
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
124 gressive, and 12% of patients with secondary progressive disease course (2% of eyes).
125                                              Progressive disease course (P=0.017), thoracic aorta inv
126                                              Progressive disease course (P=0.018) and carotidynia (P=
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
130 m HIV-1-infected patients who have the usual progressive disease course.
131  progression and conversion into a secondary progressive disease course.
132 ss, which is more prominent in patients with progressive disease course.
133                Nine patients with documented progressive disease despite all established therapy unde
134 f patients with plasma cell neoplasms die of progressive disease despite high response rates to novel
135  with median survival of 1 year or less, and progressive disease despite second-line therapy.
136 he second biopsy, abdominal imaging revealed progressive disease despite sorafenib treatment.
137 ned positive for HER1/2 and who did not have progressive disease during chemotherapy (four to eight c
138                        Only two patients had progressive disease during the first two vaccine courses
139 atic or recurrent endometrial cancer who had progressive disease following one or two lines of chemot
140 or response, 48.8% stable disease, and 12.2% progressive disease for nonpancreatic GEP NET.
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
144 ded independent central review (BICR) showed progressive disease for the patient.
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
150 , and stable disease in 8 of 10 patients and progressive disease in 2 of 10 patients at 6 mo.
151            Ibrutinib was discontinued due to progressive disease in 27% of patients.
152 n reasons for treatment discontinuation were progressive disease in 34 (24%) patients and adverse eve
153 al remission in 5, stable disease in 13, and progressive disease in 7 patients.
154 al remission in 14, stable disease in 2, and progressive disease in 9 patients.
155  adaptive immunity in driving persistent and progressive disease in acute MPTP-intoxicated mice.
156                 Diabetic cardiomyopathy is a progressive disease in diabetic patients, and myocardial
157 actory diffuse large B-cell lymphoma (due to progressive disease in four patients, infections in thre
158  in 2 patients, a mixed response in one, and progressive disease in one.
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
166               Gauging the risk of developing progressive disease is a major challenge in prostate can
167                                              Progressive disease is characterized by hepatic leukocyt
168 , traditionally considered relapsing but non-progressive diseases, is poorly defined.
169 was an excellent inter-observer agreement in progressive disease (k=0.94, percent agreement=97.1%), s
170                                Patients with progressive disease lack these immune niches, suggesting
171                              IBM is a slowly progressive disease, leading to wheelchair use, on avera
172                                              Progressive disease leads to pathologic tissue remodelin
173 ractory patients with distant metastases and progressive disease (mean age, 71.4 y).
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
178                                  For chronic progressive diseases, mortality may not be a feasible en
179 igible for intermittent sunitinib because of progressive disease (n = 13), toxicity (n = 1), or conse
180 s were nonresponders (stable disease, n = 9; progressive disease, n = 2).
181 esponse, n = 11; stable disease, n = 17; and progressive disease, n = 8.
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
184                   Biochemical progression or progressive disease occurred in 391 patients (221 [57%]
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
190 nostic significant in patients classified as progressive disease on the basis of irRC.
191 ignificance in patients classified as having progressive disease on the basis of irRC.
192      This method identifies 41% of the later progressive diseases on CT, with no false-positives.
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
197 cytosis (HLH) with refractory, recurrent, or progressive disease or intolerance to HLH therapy.
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
200              During BEP, 15 patients died of progressive disease or toxicity, including one patient f
201 ery 4 weeks thereafter (28-day cycles) until progressive disease or toxicity.
202 ived only a single course of HDCT because of progressive disease or toxicity.
203 t-baseline scans, or discontinued because of progressive disease or treatment-related adverse events
204            Study patients were treated until progressive disease or unacceptable adverse effects occu
205  was administered (100 mg) twice a day until progressive disease or unacceptable toxic effects occurr
206 ntinuous oral ibrutinib (560 mg) daily until progressive disease or unacceptable toxic effects.
207 ory NHL received venetoclax once daily until progressive disease or unacceptable toxicity at target d
208 ed >75 years) on days 1, 8, 15, and 22 until progressive disease or unacceptable toxicity.
209 eived oral ibrutinib 420 mg once daily until progressive disease or unacceptable toxicity.
210 6 cycles with daily ibrutinib (420 mg) until progressive disease or unacceptable toxicity.
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).
213 lth states: progression-free survival (PFS), progressive disease, or dead.
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) <
217              Patients with stable disease or progressive disease (PD) after no more than 6 months of
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
222     A limitation of this targeted therapy is progressive disease (PD) in some patients.
223 nsition, whereas those present at on-therapy progressive disease (PD) upregulated kynurenine, plasmin
224                                   In case of progressive disease (PD), an additional evaluation was p
225 es with stable disease (SD), 5 patients with progressive disease (PD), and 14 with HPD.
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
228 ntiating between pseudoprogression (PsP) and progressive disease (PD).
229 artial response [PR] v stable disease [SD] v progressive disease [PD]), disease control rate (DCR; CR
230 er irRC (n = 84), and 17.3% in patients with progressive disease per both criteria (n = 177).
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
235 d all patients in this group died of rapidly progressive disease postrelapse.
236 ts with multiple sclerosis (MS) have primary progressive disease (PPMS).
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.
244 rsus 18% +/- 32% in patients with stable and progressive disease, respectively.
245                                Glaucoma is a progressive disease responsible for the second commonest
246         Type 2 diabetes mellitus (T2DM) is a progressive disease resulting from increasing insulin re
247                                Patients with progressive disease show alterations in their serum prot
248                    Tumors from patients with progressive disease showed a higher variance of the intr
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
251                                  Focusing on progressive disease stages, we could then demonstrate th
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.
255               Rheumatoid arthritis (RA) is a progressive disease that affects both pediatric and adul
256    Chronic wasting disease (CWD) is a fatal, progressive disease that affects cervid species, includi
257                                    NASH is a progressive disease that can lead to cirrhosis, cancer,
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
260                 Seventeen patients (23%) had progressive disease: their PSA level rose by more than 2
261                                              Progressive disease thresholds for studies that did not
262 espond, and many patients eventually develop progressive disease to daratumumab monotherapy.
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
271                                        These progressive diseases typically have an insidious onset,
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.
275                                              Progressive disease was detected in 2 patients (7.2%) by
276                                              Progressive disease was detected on week 2 scans in 3 pa
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
279 relevant preoperative predictors of in-field progressive disease were identified.
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
282                         Patients with stable/progressive disease were to have radiation before TME, w
283          Eight of 12 patients with recurrent/progressive disease were upstaged, 1 was downstaged, and
284 therapy protocol (8 Complete Response and 11 Progressive Disease) were evaluated for serum SEVs size,
285                    There are 2 forms of this progressive disease: wet and dry.
286                   Type 2 diabetes (T2D) is a progressive disease whereby there is often deterioration
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
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  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.
295                           CG is considered a progressive disease with variable rates of progression.
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

 
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