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1 umors associated with acquired resistance to conventional therapy.
2 esistant and refractory tuberculosis failing conventional therapy.
3 ical heterogeneous brain tumor refractory to conventional therapy.
4 LL cells to LNs and increase the efficacy of conventional therapy.
5 all-cause mortality rate when compared with conventional therapy.
6 retinopathy by as much as 76% compared with conventional therapy.
7 geted therapies more successful than current conventional therapy.
8 ity and efficacy against tumors resistant to conventional therapy.
9 ells (CSCs) that are relatively resistant to conventional therapy.
10 versus 98.4% (97.3-99.1) (p < 0.001) during conventional therapy.
11 H. pylori infections that fail to respond to conventional therapy.
12 ra of symptoms that are poorly controlled by conventional therapy.
13 IIIC-IV OC patients in first remission after conventional therapy.
14 pies to ameliorate poor clinical response to conventional therapy.
15 ls (GSCs), which are relatively resistant to conventional therapy.
16 e an overall survival benefit as compared to conventional therapy.
17 ivation to treat CAPS that was refractory to conventional therapy.
18 l T-cell lymphomas (PTCLs) respond poorly to conventional therapy.
19 inical trial because they did not respond to conventional therapy.
20 was less frequent with alemtuzumab than with conventional therapy.
21 been evaluated in severe asthma as add-on to conventional therapy.
22 o severe uncontrolled asthma despite maximal conventional therapy.
23 the underlying insensitivity of the CSCs to conventional therapy.
24 biotherapy could be applied before or after conventional therapy.
25 ose that cannot be successfully treated with conventional therapy.
26 utoimmune rheumatic diseases who have failed conventional therapy.
27 leukemia (t-AML) have a poor prognosis with conventional therapy.
28 ent of aggressive prolactinomas resistant to conventional therapy.
29 isease, approximately half will relapse with conventional therapy.
30 of hemochromatosis, which responds poorly to conventional therapy.
31 D to treat severe infections unresponsive to conventional therapy.
32 ailure or hemodynamic lability refractory to conventional therapy.
33 nts with acute cardiac failure refractory to conventional therapy.
34 70 years of age who were not candidates for conventional therapy.
35 ents in clinical remission who are receiving conventional therapy.
36 cancer stem cells (CSC), that survive after conventional therapy.
37 tations in leukaemic cells not eliminated by conventional therapy.
38 ependent manner enhanced the efficacy of the conventional therapy.
39 treat imatinib-refractory patients who fail conventional therapy.
40 risk of diabetes complications compared with conventional therapy.
41 ts for ATLL and HHM, which are refractory to conventional therapy.
42 n and DHA in patients with ATL refractory to conventional therapy.
43 ogenic therapy of cancer in combination with conventional therapy.
44 is in MM cells, including those resistant to conventional therapy.
45 y in those treated intensively compared with conventional therapy.
46 ith burosumab compared with those continuing conventional therapy.
47 diac arrest in early childhood refractory to conventional therapy.
48 elated symptoms insufficiently controlled by conventional therapy.
49 est risk of experiencing a relapse following conventional therapy.
50 ould lead to improved outcomes compared with conventional therapy.
51 any chronic pain conditions are resistant to conventional therapy.
52 y large B-cell lymphoma after the failure of conventional therapy.
53 nucleic acids to overcome the limitations of conventional therapy.
54 lated symptoms, insufficiently controlled by conventional therapy.
55 ad failed or were intolerant to at least one conventional therapy.
56 s owing to diverse biology and resistance to conventional therapy.
57 for a 55-year-old) of survival compared with conventional therapy.
58 al efficacy in treating tumors refractory to conventional therapy.
59 clinical responses in patients resistant to conventional therapy.
60 rs that are highly invasive and resistant to conventional therapy.
61 who do not respond to, or are intolerant to, conventional therapy.
62 iating stem cells that are not eliminated by conventional therapies.
63 ment of a range of diseases not treatable by conventional therapies.
64 age follicular lymphoma (FL) is incurable by conventional therapies.
65 velopment of resistance to both targeted and conventional therapies.
66 use as anticancer agents in combination with conventional therapies.
67 d attenuating cancer stem cells, which evade conventional therapies.
68 nitis of the shoulder can be unresponsive to conventional therapies.
69 geted therapies at the time of relapse after conventional therapies.
70 ods in a dormant state that is refractory to conventional therapies.
71 s are required to clarify the future role of conventional therapies.
72 tic agents for cancers that are resistant to conventional therapies.
73 nts aged >/= 60 years and are incurable with conventional therapies.
74 on of adjacent stromal cells, and evasion of conventional therapies.
75 rapidly fatal disease, poorly responsive to conventional therapies.
76 can have off-target effects, a limitation to conventional therapies.
77 oneuroblastoma deemed unsuitable for further conventional therapies.
78 te-stage diagnosis and resistance to current conventional therapies.
79 rigor to provide a useful comparison to more conventional therapies.
80 of leukaemia, which are often refractory to conventional therapies.
81 h an unfavorable prognosis when treated with conventional therapies.
82 stem cell-like properties and resistance to conventional therapies.
83 essive and highly lethal cancer resistant to conventional therapies.
84 nt with disease that is poorly responsive to conventional therapies.
85 henotype, promoting tumor growth and evading conventional therapies.
86 and hemodynamic support for patients failing conventional therapies.
87 emonstrating a benefit for SCT compared with conventional therapies.
88 eemptive therapies and integrating novel and conventional therapies.
89 of WL-276 against HRPC that is resistant to conventional therapies.
90 ighly aggressive neoplasms resistant to most conventional therapies.
91 the Western world and remains incurable with conventional therapies.
92 ve ALCL patients who fail to respond well to conventional therapies.
93 ases, and resistance of pancreatic cancer to conventional therapies.
94 r to metastasis as it is highly resistant to conventional therapies.
95 t at present remains largely unresponsive to conventional therapies.
96 re ulcerative colitis despite treatment with conventional therapies.
97 ious for its poor survival and resistance to conventional therapies.
98 which are rich in CSCs and respond poorly to conventional therapies.
99 does not rely on the cytotoxic mechanism of conventional therapies.
100 e seizure types that are often refractory to conventional therapies.
101 ggressive malignancy with a poor response to conventional therapies.
102 pidly progressive, severe, and refractory to conventional therapies.
103 urrence of tumors and to their resistance to conventional therapies.
104 cancer stem-like cells that are resistant to conventional therapies.
105 , full remission is not always achieved with conventional therapies.
106 apy (hazard ratio with high-rate therapy vs. conventional therapy, 0.21; 95% confidence interval [CI]
107 0.001; hazard ratio with delayed therapy vs. conventional therapy, 0.24; 95% CI, 0.15 to 0.40; P<0.00
108 ity (hazard ratio with high-rate therapy vs. conventional therapy, 0.45; 95% CI, 0.24 to 0.85; P=0.01
109 =0.01; hazard ratio with delayed therapy vs. conventional therapy, 0.56; 95% CI, 0.30 to 1.02; P=0.06
110 to 1.18; difference in risk [apixaban minus conventional therapy], -0.4 percentage points; 95% CI, -
112 ute myeloid leukemia (AML)(5), resistance to conventional therapies(6-8) and dismal outcomes(9).
115 ta blocker, MRA, and SGLT2 inhibitor) versus conventional therapy (ACE inhibitor or ARB and beta bloc
116 re for FEF75, -0.97 with HFOV vs. -1.19 with conventional therapy; adjusted difference, 0.23 [95% con
117 receive either intensive diabetes therapy or conventional therapy aimed at preventing hyperglycemic s
118 ntional systemic therapy (strategy A) versus conventional therapy alone (strategy B) versus newer tar
119 ptomatically and may be easier to treat with conventional therapy, an understanding of the mechanisms
120 ncer cells that have increased resistance to conventional therapies and are capable of establishing m
121 cells (HSCs) that persist and expand through conventional therapies and are major contributors to dis
122 anti-CTLA-4 therapy may differ from those of conventional therapies and consist of inflammatory event
123 cate exciting opportunities for synergy with conventional therapies and for combining PARAs with othe
124 Follicular lymphoma (FL) is incurable with conventional therapies and has a clinical course typifie
125 , such therapies might be used to supplement conventional therapies and help ease patient symptoms.
127 geting CD19 may overcome many limitations of conventional therapies and induce remission in patients
129 a quickly actionable approach to supporting conventional therapies and overcoming GC resistance in p
130 ith breast tumour progression, resistance to conventional therapies and poor clinical prognosis.
131 ymal tumor phenotype, mediates resistance to conventional therapies and small-molecule targeted thera
132 re not consistent data about the response to conventional therapies and the immunological balance bet
133 were randomly assigned to continue receiving conventional therapy and 29 (16 girls, 13 boys) to recei
134 these monogenic conditions do not respond to conventional therapy and are associated with high morbid
135 ncer stem cells are exquisitely resistant to conventional therapy and are the "drivers" of local recu
136 tes, or both who had inadequate responses to conventional therapy and intravenous immune globulin.
138 high specificity, non-cross resistance with conventional therapies, and promise of long-term immunop
139 erlying disease recurrence and resistance to conventional therapies, and we detail our current unders
140 opoietic cancers are frequently resistant to conventional therapy, and novel highly active strategies
145 he addition of tyrosine kinase inhibitors to conventional therapy are required to evaluate the clinic
147 cause mortality in patients allocated to the conventional therapy arm of MADIT (Multicenter Automatic
148 Multivariate analysis showed that in the conventional therapy arm of the trial, 10-mm Hg incremen
149 ern since it can reduce the effectiveness of conventional therapies as well as cancer immunotherapy.
150 -3 study involving patients who had received conventional therapy before enrollment (previously treat
151 TRD) that otherwise fails to respond to more conventional therapies, but DBS is invasive, costly, and
153 eated with V/C salvage therapy after failing conventional therapy consisting of a triazole, amphoteri
154 ith reduced ejection fraction (HFrEF) beyond conventional therapy consisting of angiotensin-convertin
155 mpared the efficacy and safety of continuing conventional therapy, consisting of oral phosphate and a
157 other cancers is the intrinsic resistance to conventional therapies demonstrated by the stem/progenit
158 mpaired quality of life, HSCT, compared with conventional therapy, did not result in a statistically
159 209 were randomly assigned to receive either conventional therapy (dietary restriction) or intensive
160 9 [SE 0.1] with burosumab vs +0.8 [0.1] with conventional therapy; difference 1.1, 95% CI 0.8-1.5; p<
161 ssive drugs, biologic agents, and reason for conventional therapy discontinuation were gathered.
162 tion (CDI) have a >/=60% risk of relapse, as conventional therapies do not address the underlying gas
163 fects (metabolic memory) of intensive versus conventional therapy during the Diabetes Control and Com
164 rolonged beneficial effects of intensive vs. conventional therapy during the Diabetes Control and Com
165 ry to conventional treatment or for which no conventional therapy existed, and if they had a WHO perf
167 UNITI-2 trial included 628 patients in whom conventional therapy failed or unacceptable side effects
170 atment with vascular targeting therapies and conventional therapies (focal chemotherapy and radiation
172 inhibitors provide a survival advantage over conventional therapies for treatment of advanced or meta
174 -linked dominant inheritance, and receipt of conventional therapy for at least 6 consecutive months f
176 The adjusted hazard ratios (HRs) of ICD:conventional therapy for first and recurrent HF events w
178 acy and safety of brentuximab vedotin versus conventional therapy for previously treated patients wit
181 regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous t
182 ns [identified by endoscopy], and failure of conventional therapy) from March 2015 through December 2
183 Change global score than did patients in the conventional therapy group (least squares mean +1.9 [SE
184 d at EDIC Study baseline from 32 cases (DCCT conventional therapy group subjects showing retinopathy
188 group, as compared with 9.7% of those in the conventional-therapy group (relative risk, 0.44; 95% CI,
189 p, as compared with 71 of 2635 (2.7%) in the conventional-therapy group (relative risk, 0.84; 95% con
190 y lower in the alemtuzumab group than in the conventional-therapy group at both 6 months (3% vs. 15%,
192 f adults with moderate or severe OSA in whom conventional therapy had failed, combined palatal and to
193 ve patient care and outcomes of targeted and conventional therapies has been the center of many recen
196 ersible cardiac or respiratory failure, when conventional therapy has been inadequate, or as bridge t
197 icturing, ileocaecal Crohn's disease in whom conventional therapy has failed could be considered a re
198 cturing, ileocaecal Crohn's disease, in whom conventional therapy has failed were randomly allocated
206 heckpoint antagonists or in combination with conventional therapies in patients with early-stage dise
207 vacizumab may offer an adjunctive measure to conventional therapies in preventing graft rejection in
208 ypothermia applied for at least 24 hours and conventional therapy in critically ill patients were inc
209 endpoints traditional for clinical trials of conventional therapy in Crohn's disease, HSCT resulted i
210 l survival with comprehensive therapy versus conventional therapy in patients with chronic HFrEF.
211 t mobilisation and were randomly assigned to conventional therapy in the ASTIC trial were offered HSC
214 sistant primary leukemia in combination with conventional therapy in vitro and significantly prolongs
215 ll as its resistance to chemotherapy renders conventional therapies inadequate in its treatment.
216 ment for juvenile DM is often difficult, and conventional therapies include corticosteroids and other
217 tory biomarkers in ACS patients treated with conventional therapy including atorvastatin 80 mg daily.
218 ts) or placebo (439 infants), in addition to conventional therapy (including aspirin in 87.9% of infa
219 ents who have failed to achieve benefit from conventional therapies, including chemotherapy and exter
220 itates tumor dissemination and resistance to conventional therapies, including chemotherapy and radio
221 chemotherapy offers several advantages over conventional therapies, including high intratumoral drug
222 ts protein product (Reg IV) are resistant to conventional therapies, including irradiation (IR).
223 end stage renal disease that is resistant to conventional therapies, including liver transplantation.
225 s with acute cardiogenic shock refractory to conventional therapy irrespective of the given location.
227 in chronic periodontitis (CP) refractory to conventional therapy is associated with severe destructi
228 al Crohn's disease who have not responded to conventional therapy is commonly scaled up to biological
229 arious clinical studies or between laser and conventional therapy is difficult at best and likely imp
233 le hypoxia renders tumours resistant to many conventional therapies, little is known about its influe
236 As memory T cells are poorly controlled by 'conventional' therapies, memory T-cell mediated attack i
237 that combines specific inhibitors of ATR and conventional therapies might promote synthetic lethality
238 culties in early diagnosis and resistance to conventional therapies, MM remains a challenge for patho
240 the nondiabetic range as safely possible, or conventional therapy (n = 730) with the goal of avoiding
242 profound hypocalcemia which is refractory to conventional therapy of vitamin D deficiency rickets eve
243 of the beneficial effect of intensive versus conventional therapy on progression of retinopathy is ex
244 effect of intensive therapy as compared with conventional therapy on the incidence and cost of ocular
245 mprehensive disease-modifying therapy versus conventional therapy on the primary endpoint of cardiova
247 therapy, whereas 38 patients were treated by conventional therapy only, consisting of corticosteroids
249 ported outcomes (PROs), whether treated with conventional therapy or hematopoietic stem cell transpla
251 y active ulcerative colitis despite previous conventional therapy or therapy with a tumor necrosis fa
252 afe suggesting their use in combination with conventional therapy or with other targeted therapies in
254 populations of tumor cells frequently escape conventional therapy owing to their particularly acidic
256 mparing cinacalcet to placebo in addition to conventional therapy (phosphate binders/vitamin D) in pa
257 0.8 mg/kg every 2 weeks (burosumab group) or conventional therapy prescribed by investigators (conven
258 gated whether the addition of clopidogrel to conventional therapy reduces mortality from any cause an
259 d apixaban and in 1.8% of those who received conventional therapy (relative risk, 0.31; 95% CI, 0.17
260 conservative protocol for oxygen therapy vs conventional therapy resulted in lower ICU mortality.
261 ab in the front-line setting are inferior to conventional therapy, rituximab is a reasonable choice f
262 JS-K showed significant cytotoxicity in both conventional therapy-sensitive and -resistant MM cell li
264 lowed by 5 mg twice daily for 6 months) with conventional therapy (subcutaneous enoxaparin, followed
265 europathy (CAN) in former DCCT intensive and conventional therapy subjects 13 to 14 years after DCCT
266 staphylococcal liver abscesses refractory to conventional therapy successfully treated with corticost
267 of reported patients, typically treated with conventional therapies such as adrenocorticotropin hormo
269 rrent RCTs suggest that PDL is equivalent to conventional therapies such as cryotherapy and cantharid
270 rs and enhance astrocytoma susceptibility to conventional therapy, such as radiation and chemotherapy
271 esidual breast cancer cell populations after conventional therapies, suggesting that CD44 may be an i
272 r cells, offering a promising alternative to conventional therapies that have unwanted side effects s
274 notypes show remarkably diverse responses to conventional therapy that mirror clinical experience.
275 easing prevalence of microbial resistance to conventional therapies, the development of novel antimic
276 rly development is a formidable obstacle for conventional therapies to stimulate recovery from protra
277 o eyes with pars planitis to those receiving conventional therapy (topical, regionally injected, or o
278 for cytomegalovirus (CMV) infection failing conventional therapy (trial 202) and 119 received mariba
279 ceived intensive therapy and 61 who received conventional therapy underwent cataract extraction (adju
280 ceived intensive therapy and 50 who received conventional therapy underwent vitrectomy, retinal-detac
281 HSCT) compared with mobilisation followed by conventional therapy using a stringent primary endpoint
282 s induces apoptosis in MM cells resistant to conventional therapies via caspase activation and poly-(
283 The adjusted hazard ratio (HR) of ICD versus conventional therapy was 0.64 (p = 0.01) among patients
285 elevated among cancer survivors treated with conventional therapy, we sought to determine the risk am
286 ) with inadequate response or intolerance to conventional therapies were randomized to receive subcut
288 ulcerative colitis who had not responded to conventional therapy were recruited from 40 referral cen
289 th refractory IBS, defined as failure of >=3 conventional therapies, were randomly assigned to single
290 th cetirizine and montelukast in addition to conventional therapy, whereas 38 patients were treated b
291 to-severe active ulcerative colitis, despite conventional therapy, who responded to golimumab inducti
292 otential to suppress viral loads beyond more conventional therapies with the ultimate goal of HIV-1 e
293 actorial and includes hypogammaglobulinemia, conventional therapy with alkylating drugs, and recently
294 NL-constructed tri-Fab, bsMAb, compared with conventional therapy with directly radiolabeled antibody
295 nd had not responded to at least 3 months of conventional therapy with glucocorticosteroids, thiopuri
297 mmonly regresses upon virus eradication, but conventional therapy with pegylated interferon and ribav
298 tis who did not have an adequate response to conventional therapy with steroids or immunosuppressants
299 parin (175 IU/kg) once daily for 6 months vs conventional therapy with tinzaparin (175 IU/kg) once da