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1 elated symptoms insufficiently controlled by conventional therapy.
2 ould lead to improved outcomes compared with conventional therapy.
3 H. pylori infections that fail to respond to conventional therapy.
4 ra of symptoms that are poorly controlled by conventional therapy.
5 pies to ameliorate poor clinical response to conventional therapy.
6 any chronic pain conditions are resistant to conventional therapy.
7 ls (GSCs), which are relatively resistant to conventional therapy.
8 e an overall survival benefit as compared to conventional therapy.
9 ivation to treat CAPS that was refractory to conventional therapy.
10 l T-cell lymphomas (PTCLs) respond poorly to conventional therapy.
11 inical trial because they did not respond to conventional therapy.
12 was less frequent with alemtuzumab than with conventional therapy.
13 been evaluated in severe asthma as add-on to conventional therapy.
14 o severe uncontrolled asthma despite maximal conventional therapy.
15 y large B-cell lymphoma after the failure of conventional therapy.
16 the underlying insensitivity of the CSCs to conventional therapy.
17 biotherapy could be applied before or after conventional therapy.
18 ose that cannot be successfully treated with conventional therapy.
19 utoimmune rheumatic diseases who have failed conventional therapy.
20 leukemia (t-AML) have a poor prognosis with conventional therapy.
21 ent of aggressive prolactinomas resistant to conventional therapy.
22 of hemochromatosis, which responds poorly to conventional therapy.
23 D to treat severe infections unresponsive to conventional therapy.
24 ailure or hemodynamic lability refractory to conventional therapy.
25 nts with acute cardiac failure refractory to conventional therapy.
26 70 years of age who were not candidates for conventional therapy.
27 ents in clinical remission who are receiving conventional therapy.
28 cancer stem cells (CSC), that survive after conventional therapy.
29 tations in leukaemic cells not eliminated by conventional therapy.
30 ependent manner enhanced the efficacy of the conventional therapy.
31 treat imatinib-refractory patients who fail conventional therapy.
32 risk of diabetes complications compared with conventional therapy.
33 ts for ATLL and HHM, which are refractory to conventional therapy.
34 n and DHA in patients with ATL refractory to conventional therapy.
35 ogenic therapy of cancer in combination with conventional therapy.
36 is in MM cells, including those resistant to conventional therapy.
37 Advanced disease is often unresponsive to conventional therapy.
38 es appear to offer promising alternatives to conventional therapy.
39 nucleic acids to overcome the limitations of conventional therapy.
40 re and/or fistulizing) who are refractory to conventional therapy.
41 opoietin or who are unlikely to benefit from conventional therapy.
42 and may be a marker of failure to respond to conventional therapy.
43 osed in advanced stages and is refractory to conventional therapy.
44 ng primary brain tumors and are resistant to conventional therapy.
45 perience bleeding episodes not responsive to conventional therapy.
46 rom the addition of ACE inhibitors to modern conventional therapy.
47 lated symptoms, insufficiently controlled by conventional therapy.
48 an ejection fraction of < or =30% to ICD or conventional therapy.
49 matic, still surpasses that anticipated with conventional therapy.
50 diabetes results in greater weight gain than conventional therapy.
51 ll lines that are sensitive and resistant to conventional therapy.
52 VHD of 2 years duration that is resistant to conventional therapy.
53 survival of waiting-list patients receiving conventional therapy.
54 creased weight gain with either intensive or 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 al efficacy in treating tumors refractory to conventional therapy.
58 clinical responses in patients resistant to conventional therapy.
59 rs that are highly invasive and resistant to conventional therapy.
60 who do not respond to, or are intolerant to, conventional therapy.
61 esistant and refractory tuberculosis failing conventional therapy.
62 ical heterogeneous brain tumor refractory to conventional therapy.
63 LL cells to LNs and increase the efficacy of conventional therapy.
64 est risk of experiencing a relapse following conventional therapy.
65 all-cause mortality rate when compared with conventional therapy.
66 retinopathy by as much as 76% compared with conventional therapy.
67 geted therapies more successful than current conventional therapy.
68 ity and efficacy against tumors resistant to conventional therapy.
69 ells (CSCs) that are relatively resistant to conventional therapy.
70 versus 98.4% (97.3-99.1) (p < 0.001) during conventional therapy.
71 tic agents for cancers that are resistant to conventional therapies.
72 does not rely on the cytotoxic mechanism of 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 e seizure types that are often refractory to conventional therapies.
78 te-stage diagnosis and resistance to current conventional therapies.
79 rigor to provide a useful comparison to more conventional therapies.
80 ggressive malignancy with a poor response to conventional therapies.
81 of leukaemia, which are often refractory to conventional therapies.
82 h an unfavorable prognosis when treated with conventional therapies.
83 stem cell-like properties and resistance to conventional therapies.
84 essive and highly lethal cancer resistant to conventional therapies.
85 nt with disease that is poorly responsive to conventional therapies.
86 henotype, promoting tumor growth and evading conventional therapies.
87 and hemodynamic support for patients failing conventional therapies.
88 emonstrating a benefit for SCT compared with conventional therapies.
89 eemptive therapies and integrating novel and conventional therapies.
90 of WL-276 against HRPC that is resistant to conventional therapies.
91 ighly aggressive neoplasms resistant to most conventional therapies.
92 the Western world and remains incurable with conventional therapies.
93 ve ALCL patients who fail to respond well to conventional therapies.
94 ases, and resistance of pancreatic cancer to conventional therapies.
95 r to metastasis as it is highly resistant to conventional therapies.
96 t at present remains largely unresponsive to conventional therapies.
97 integrate novel therapeutic approaches with conventional therapies.
98 may offer additional, novel alternatives to conventional therapies.
99 , and variant syndromes may be refractory to conventional therapies.
100 tumorigenesis and recurrence of cancer after conventional therapies.
101 role in cancer treatment when combined with conventional therapies.
102 ultiple myeloma (MM) cell lines resistant 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 iating stem cells that are not eliminated by conventional therapies.
107 ment of a range of diseases not treatable by conventional therapies.
108 age follicular lymphoma (FL) is incurable by conventional therapies.
109 velopment of resistance to both targeted and conventional therapies.
110 use as anticancer agents in combination with conventional therapies.
111 d attenuating cancer stem cells, which evade conventional therapies.
112 nitis of the shoulder can be unresponsive to conventional therapies.
113 geted therapies at the time of relapse after conventional therapies.
114 ods in a dormant state that is refractory to conventional therapies.
115 apy (hazard ratio with high-rate therapy vs. conventional therapy, 0.21; 95% confidence interval [CI]
116 0.001; hazard ratio with delayed therapy vs. conventional therapy, 0.24; 95% CI, 0.15 to 0.40; P<0.00
117 ity (hazard ratio with high-rate therapy vs. conventional therapy, 0.45; 95% CI, 0.24 to 0.85; P=0.01
118 =0.01; hazard ratio with delayed therapy vs. conventional therapy, 0.56; 95% CI, 0.30 to 1.02; P=0.06
119 to 1.18; difference in risk [apixaban minus conventional therapy], -0.4 percentage points; 95% CI, -
122 re for FEF75, -0.97 with HFOV vs. -1.19 with conventional therapy; adjusted difference, 0.23 [95% con
123 receive either intensive diabetes therapy or conventional therapy aimed at preventing hyperglycemic s
124 ntional systemic therapy (strategy A) versus conventional therapy alone (strategy B) versus newer tar
125 ntional systemic therapy (strategy A) versus conventional therapy alone (strategy B) versus newer tar
127 ptomatically and may be easier to treat with conventional therapy, an understanding of the mechanisms
128 ncer cells that have increased resistance to conventional therapies and are capable of establishing m
129 cells (HSCs) that persist and expand through conventional therapies and are major contributors to dis
130 anti-CTLA-4 therapy may differ from those of conventional therapies and consist of inflammatory event
131 cate exciting opportunities for synergy with conventional therapies and for combining PARAs with othe
132 Follicular lymphoma (FL) is incurable with conventional therapies and has a clinical course typifie
133 , such therapies might be used to supplement conventional therapies and help ease patient symptoms.
134 geting CD19 may overcome many limitations of conventional therapies and induce remission in patients
136 a quickly actionable approach to supporting conventional therapies and overcoming GC resistance in p
137 ith breast tumour progression, resistance to conventional therapies and poor clinical prognosis.
138 re not consistent data about the response to conventional therapies and the immunological balance bet
139 these monogenic conditions do not respond to conventional therapy and are associated with high morbid
140 ncer stem cells are exquisitely resistant to conventional therapy and are the "drivers" of local recu
141 challenge to the host immune system through conventional therapy and improvement of personal oral hy
142 tes, or both who had inadequate responses to conventional therapy and intravenous immune globulin.
143 high specificity, non-cross resistance with conventional therapies, and promise of long-term immunop
144 inst tumors that have acquired resistance to conventional therapy, and could augment the efficacy of
148 he addition of tyrosine kinase inhibitors to conventional therapy are required to evaluate the clinic
150 cause mortality in patients allocated to the conventional therapy arm of MADIT (Multicenter Automatic
151 Multivariate analysis showed that in the conventional therapy arm of the trial, 10-mm Hg incremen
152 ern since it can reduce the effectiveness of conventional therapies as well as cancer immunotherapy.
153 lls that are both sensitive and resistant to conventional therapy as well as primary MM cells from pa
154 TRD) that otherwise fails to respond to more conventional therapies, but DBS is invasive, costly, and
155 l examining the effects of prostacyclin plus conventional therapy compared with conventional therapy
157 eated with V/C salvage therapy after failing conventional therapy consisting of a triazole, amphoteri
159 other cancers is the intrinsic resistance to conventional therapies demonstrated by the stem/progenit
160 mpaired quality of life, HSCT, compared with conventional therapy, did not result in a statistically
161 209 were randomly assigned to receive either conventional therapy (dietary restriction) or intensive
162 ssive drugs, biologic agents, and reason for conventional therapy discontinuation were gathered.
163 tion (CDI) have a >/=60% risk of relapse, as conventional therapies do not address the underlying gas
164 rolonged beneficial effects of intensive vs. conventional therapy during the Diabetes Control and Com
165 fects (metabolic memory) of intensive versus conventional therapy during the Diabetes Control and Com
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
173 ion fraction (LVEF) of 35 percent or less to conventional therapy for CHF plus placebo (847 patients)
176 The adjusted hazard ratios (HRs) of ICD:conventional therapy for first and recurrent HF events w
180 acy and safety of brentuximab vedotin versus conventional therapy for previously treated patients wit
183 regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous t
185 d at EDIC Study baseline from 32 cases (DCCT conventional therapy group subjects showing retinopathy
186 sk of SCD in the ICD group compared with the conventional therapy group was 0.33 (95% confidence inte
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 ears at baseline randomized to intensive and conventional therapy groups in the Diabetes Control and
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
200 highly aggressive behavior and resistance to conventional therapy, has evolved into a health crisis b
206 leviate hypoxia and increase the efficacy of conventional therapies if both are carefully scheduled.
209 heckpoint antagonists or in combination with conventional therapies in patients with early-stage dise
210 vacizumab may offer an adjunctive measure to conventional therapies in preventing graft rejection in
211 f studies demonstrating its superiority over conventional therapy in challenging patient subsets with
212 on or deletion predicts for poor response to conventional therapy in chronic lymphocytic leukemia (CL
213 endpoints traditional for clinical trials of conventional therapy in Crohn's disease, HSCT resulted i
214 a mean of 7.3 days after AMI) in addition to conventional therapy in patients with an LVEF < or =40%
215 t mobilisation and were randomly assigned to conventional therapy in the ASTIC trial were offered HSC
218 sistant primary leukemia in combination with conventional therapy in vitro and significantly prolongs
219 ll as its resistance to chemotherapy renders conventional therapies inadequate in its treatment.
220 ment for juvenile DM is often difficult, and conventional therapies include corticosteroids and other
222 in multiple myeloma (MM) cells resistant to conventional therapies including melphalan (LR-5), doxor
223 tory biomarkers in ACS patients treated with conventional therapy including atorvastatin 80 mg daily.
224 ts) or placebo (439 infants), in addition to conventional therapy (including aspirin in 87.9% of infa
225 ents who have failed to achieve benefit from conventional therapies, including chemotherapy and exter
226 itates tumor dissemination and resistance to conventional therapies, including chemotherapy and radio
227 chemotherapy offers several advantages over conventional therapies, including high intratumoral drug
228 ts protein product (Reg IV) are resistant to conventional therapies, including irradiation (IR).
229 end stage renal disease that is resistant to conventional therapies, including liver transplantation.
231 s with acute cardiogenic shock refractory to conventional therapy irrespective of the given location.
233 in chronic periodontitis (CP) refractory to conventional therapy is associated with severe destructi
234 al Crohn's disease who have not responded to conventional therapy is commonly scaled up to biological
235 arious clinical studies or between laser and conventional therapy is difficult at best and likely imp
240 As memory T cells are poorly controlled by 'conventional' therapies, memory T-cell mediated attack i
241 that combines specific inhibitors of ATR and conventional therapies might promote synthetic lethality
242 culties in early diagnosis and resistance to conventional therapies, MM remains a challenge for patho
244 the nondiabetic range as safely possible, or conventional therapy (n = 730) with the goal of avoiding
246 profound hypocalcemia which is refractory to conventional therapy of vitamin D deficiency rickets eve
247 of the beneficial effect of intensive versus conventional therapy on progression of retinopathy is ex
248 effect of intensive therapy as compared with conventional therapy on the incidence and cost of ocular
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 new evidence is emerging that the effect of conventional therapies, particularly radiotherapy, may e
257 mparing cinacalcet to placebo in addition to conventional therapy (phosphate binders/vitamin D) in pa
258 l therapy plus amiodarone (845 patients), or conventional therapy plus a conservatively programmed, s
259 therapy for CHF plus placebo (847 patients), conventional therapy plus amiodarone (845 patients), or
260 the DCCT than in the group that had received conventional therapy (progression of the intima-media th
261 gated whether the addition of clopidogrel to conventional therapy reduces mortality from any cause an
262 d apixaban and in 1.8% of those who received conventional therapy (relative risk, 0.31; 95% CI, 0.17
263 conservative protocol for oxygen therapy vs conventional therapy resulted in lower ICU mortality.
264 ab in the front-line setting are inferior to conventional therapy, rituximab is a reasonable choice f
265 JS-K showed significant cytotoxicity in both conventional therapy-sensitive and -resistant MM cell li
267 lowed by 5 mg twice daily for 6 months) with conventional therapy (subcutaneous enoxaparin, followed
268 europathy (CAN) in former DCCT intensive and conventional therapy subjects 13 to 14 years after DCCT
269 staphylococcal liver abscesses refractory to conventional therapy successfully treated with corticost
270 of reported patients, typically treated with conventional therapies such as adrenocorticotropin hormo
272 rrent RCTs suggest that PDL is equivalent to conventional therapies such as cryotherapy and cantharid
273 o induces apoptosis in MM cells resistant to conventional therapies such as dexamethasone (Dex), we c
274 rly useful for tumors that do not respond to conventional therapies, such as many metastatic cancers.
275 rs and enhance astrocytoma susceptibility to conventional therapy, such as radiation and chemotherapy
276 esidual breast cancer cell populations after conventional therapies, suggesting that CD44 may be an i
277 rituximab in patients with AAV refractory to conventional therapy suggests that B lymphocyte depletio
278 explore the legitimacy of providing CAM and conventional therapies that have been demonstrated to be
279 r cells, offering a promising alternative to conventional therapies that have unwanted side effects s
280 notypes show remarkably diverse responses to conventional therapy that mirror clinical experience.
281 easing prevalence of microbial resistance to conventional therapies, the development of novel antimic
282 rly development is a formidable obstacle for conventional therapies to stimulate recovery from protra
283 o eyes with pars planitis to those receiving conventional therapy (topical, regionally injected, or o
284 ceived intensive therapy and 61 who received conventional therapy underwent cataract extraction (adju
285 ceived intensive therapy and 50 who received conventional therapy underwent vitrectomy, retinal-detac
286 HSCT) compared with mobilisation followed by conventional therapy using a stringent primary endpoint
287 s induces apoptosis in MM cells resistant to conventional therapies via caspase activation and poly-(
288 The adjusted hazard ratio (HR) of ICD versus conventional therapy was 0.64 (p = 0.01) among patients
289 elevated among cancer survivors treated with conventional therapy, we sought to determine the risk am
292 ulcerative colitis who had not responded to conventional therapy were recruited from 40 referral cen
293 efractory to or intolerant of treatment with conventional therapy were treated with a single 1 mg/kg
294 to-severe active ulcerative colitis, despite conventional therapy, who responded to golimumab inducti
295 actorial and includes hypogammaglobulinemia, conventional therapy with alkylating drugs, and recently
296 NL-constructed tri-Fab, bsMAb, compared with conventional therapy with directly radiolabeled antibody
297 nd had not responded to at least 3 months of conventional therapy with glucocorticosteroids, thiopuri
299 mmonly regresses upon virus eradication, but conventional therapy with pegylated interferon and ribav
300 tis who did not have an adequate response to conventional therapy with steroids or immunosuppressants
301 parin (175 IU/kg) once daily for 6 months vs conventional therapy with tinzaparin (175 IU/kg) once da
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