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1 han did outpatients (10 vs 18 weeks to a 25% relapse risk).
2  is significantly associated with heightened relapse risk.
3 roups of patients with leukemia at differing relapse risk.
4 ceptably high and abrogated the reduction in relapse risk.
5 only be life threatening but may also affect relapse risk.
6 of treatment is associated with an increased relapse risk.
7 ears, type of induction also correlated with relapse risk.
8  to radiation therapy cost and breast cancer relapse risk.
9 mber of strategies can attempt to reduce the relapse risk.
10 uld be approached cautiously because of high relapse risk.
11 erious posttransplant toxicities, may reduce relapse risk.
12 igh transplant-related mortality but a lower relapse risk.
13 rly abstinence are associated with increased relapse risk.
14 imited CAR-T cell persistence, and increased relapse risk.
15  of melphalan were associated with a lowered relapse risk.
16 treatment identifies patients at the highest relapse risk.
17 y in chronic hepatitis C mediated by reduced relapse risk.
18 a hazards ratio greater than 8 for increased relapse risk.
19 g states significantly influence craving and relapse risk.
20 was reported to be associated with increased relapse risk.
21 amide (P = 0.005) were associated with lower relapse risk.
22 th lower, but not statistically significant, relapse risk.
23 on the basis of primarily differences in the relapse risk.
24 e who relapse point to a neural correlate of relapse risk.
25 d the postpartum period to reduce peripartum relapse risk.
26         Lower adherence to oral MP increases relapse risk.
27 and alcohol cues contribute significantly to relapse risk.
28 p) retained their significance for effect on relapse risk.
29       Chronic GVHD was associated with lower relapse risk.
30 in a better CR (94% v 76%, P =.001), reduced relapse risk (13% v 35%, P =.04), and improved survival
31  was moderately associated with an increased relapse risk (18.4 vs. 10.3%; relative risk, 1.79, 95% c
32                        Extended ATRA reduced relapse risk (20% v 36% at 4 years, P =.04) and resulted
33      Six patients relapsed (estimated 2-year relapse risk, 20%).
34  better CR (85% v 62%, P =.0001) and reduced relapse risk (22% v 42%, P =.002) and superior survival
35 T genotype, exposure to GO did not influence relapse risk (39% v 40%; P = .85).
36 ssociation between 6-MP ingestion habits and relapse risk (6-MP with food: hazard ratio [HR], 0.7; 95
37 ical changes and the effect of the latter on relapse risk (a critical variable in addiction treatment
38                   Knowledge of the threshold relapse risks above which adjuvant treatment is worth pr
39                           Here, we estimated relapse risks according to disease characteristics.
40                                          The relapse risk after a subsequent pregnancy for women with
41                                 Local cancer relapse risk after breast conservation surgery followed
42 oup analysis, we found a significantly lower relapse risk after double-unit transplantation in patien
43 ort demonstrates a modest reduction in early relapse risk after HCT associated with CMV reactivation
44 tional exploration confirmed that the higher relapse risks after transplantation of BM were limited t
45 iscontinuation or continuation on depressive relapse risk among bipolar subjects successfully treated
46 ions could serve as useful neural markers of relapse risk and alcoholism treatment outcome.
47       Nonadherence to oral MP could increase relapse risk and also contribute to inferior outcome in
48                        For example, reducing relapse risk and glucocorticoid toxicity.
49 3 mg/m(2)) to induction chemotherapy reduces relapse risk and improves survival with little increase
50 ve ALCL identifies patients with a very high relapse risk and inferior survival.
51  tolerable toxicity, and acceptable rates of relapse risk and overall survival.
52 s associated with a significantly higher CNS relapse risk and poorer outcome.
53 herapy with donor lymphocytes both to reduce relapse risk and to induce durable antitumor responses i
54 s) were significantly associated with higher relapse risk and worse event-free survival.
55 IT, and particularly mutKIT17, confer higher relapse risk, and both mutKIT17 and mutKIT8 appear to ad
56 ) subgroups showed similar overall survival, relapse risk, and leukemia-free survival, whereas high r
57 ycles of chemotherapy can accurately predict relapse risk, and most studied patients with abnormal po
58 he basis of response to induction treatment, relapse risk, and overall survival, three prognostic gro
59 espectively (P <.001), while no gradation of relapse risk (approximately 18%) could be identified at
60   Readily identified markers of tuberculosis relapse risk are needed, particularly in resource-limite
61 e imatinib was significantly associated with relapse risk, as was slower achievement of UMRD after sw
62                        To further define the relapse risk associated with bcr-abl molecular detection
63 uli may be a critical factor in long-lasting relapse risk associated with cocaine addiction.
64  allografts was not associated with a higher relapse risk, but was associated with improved overall s
65 CT NGS positivity resulted in an increase in relapse risk by multivariate analysis (hazard ratio, 7.7
66 deactivating MTHFR allele would increase ALL relapse risk by potentially increasing 5,10-methylenetet
67                                    The final relapse risk did not significantly differ, but relapses
68                         Ethnic difference in relapse risk differs by level of adherence-an observatio
69 ned prognostic after adjusting for all known relapse risk factors, including minimal residual disease
70        We review the method of assessing CNS relapse risk, factors that increase the likelihood of re
71 ile maintaining excellent survival and a low relapse risk for both SR and HR patients with APL.
72                                              Relapse risk for patients in AAML0631 from end consolida
73 urvival (OS), event-free survival (EFS), and relapse risk from the end of induction 1 (hazard ratio [
74 ter associated with heavy smoking and higher relapse risk has led to the identification of the midbra
75 c differences in dexamethasone contribute to relapse risk has never been studied.
76 rly alcohol recovery, but their influence on relapse risk has not been well studied.
77 rate below 90% was associated with increased relapse risk (hazard ratio, 3.9; P = .01).
78 ility in TGN levels contributed to increased relapse risk (hazard ratio, 4.4; 95% CI, 1.2-15.7; P = .
79                          Similarly, standard relapse risk (HR, 1.67 [95% CI, 1.10-2.54]) and high rel
80  0.5), but this was offset by an increase in relapse risk (HR, 2.0), and the conditioning intensity d
81 risk (HR, 1.67 [95% CI, 1.10-2.54]) and high relapse risk (HR, 2.22 [95% CI, 1.43-3.43]) were associa
82 ached genome-wide significance in predicting relapse risk (HR=2.18, p=3.30x10(-8)).
83 ionships between ARID5B SNP genotype and ALL relapse risk in 1,605 children treated on the Children's
84 levant level of adherence needed to minimize relapse risk in a multiracial cohort of children with AL
85 ntation in CR1 was associated with a reduced relapse risk in all molecular subgroups with the excepti
86       Multivariate analysis showed increased relapse risk in children with >/=0.1% minimal residual d
87 the most sensitive and specific predictor of relapse risk in children with acute lymphoblastic leukae
88 d disease (MDD) at diagnosis correlates with relapse risk in children with anaplastic lymphoma kinase
89    Pregnancy has a well documented effect on relapse risk in multiple sclerosis (MS).
90 r impact of pretransplant VitD deficiency on relapse risk in myeloid diseases was also observed in an
91 also confirm the adverse impact of mutKIT on relapse risk in t(8;21) AML.
92 with the CC genotype had significantly lower relapse risk in the GO arm than in the No-GO arm (26% v
93          Assessment of expected locoregional relapse risk informs the magnitude and timeframe of expe
94 S) could distinguish 2 groups with differing relapse risks: low (4-year RFS, 81%, n = 109) versus hig
95  and intermediate-risk groups and have a CNS relapse risk &lt; 5%; they may be spared any diagnostic and
96       As a result of this 3-fold increase in relapse risk, newly diagnosed patients with iAMP21 recru
97  diagnosis was significantly associated with relapse risk (odds ratio, 2.4; p = 0.03).
98 years or older was a risk factor for greater relapse risk (odds ratio, 4.9; P =.006) and worse surviv
99 testicular primary identified a group with a relapse risk of 50%.
100 with and without RD at the EOI1 had a 3-year relapse risk of 60% and 29%, respectively (P < .001); th
101          It was previously reported that the relapse risk of bcr-abl detection 6 to 12 months after t
102 ar invasion positivity, or estimated distant relapse risk of greater than 15% at 10 years based on On
103  or Oncotype DX RS with an estimated distant relapse risk of less than 15% at 10 years.
104                                The effect on relapse risk of this variability is unknown.
105 ere the most useful prognostic variables for relapse risk on multivariate analysis.
106  favored over surveillance for patients with relapse risk on surveillance greater than 33% and 37% by
107 before or after HCT, may reduce the post-HCT relapse risk or delay relapse.
108      For patients with PEPI = 0 disease, the relapse risk over 5 years was only 3.6% without chemothe
109             This study aimed to quantify the relapse risk over time in patients with schizophrenia fo
110 ciated with worse survival compared with low relapse risk (P < .001 overall).
111 h NQ exceeding 10(-5) had 4.1-fold increased relapse risk (P =.008); however, 73% of patients who exp
112 between these states and alcohol craving and relapse risk remain unclear.
113 reshold RR10 for an absolute 1% reduction in relapse risk remained fairly low (5% to 6% for tamoxifen
114                                              Relapse risk remains higher than for B-lineage ALL and o
115  10(-6) had 17.5-fold and 7.6-fold increased relapse risk, respectively (P <.001), while no gradation
116  to the RR10 for an absolute 1% reduction in relapse risk, rose sharply.
117  a highly significant trend for worsening in relapse risk (RR) and overall survival (OS) with increas
118 ion randomizations except for a reduction in relapse risk (RR) on the mitoxantrone arm, which was off
119 88% v. 85%; P = .15), posthoc analyses found relapse risk (RR) was significantly reduced among GO rec
120  (P =.04), and was associated with increased relapse risk (RR), adverse disease-free survival (DFS),
121 addition of GO to conventional chemotherapy (relapse risk [RR]: GO 36% v No-GO 34%, P = .731; event-f
122 justed for the white blood cell count or the relapse risk score, none of these outcomes were signific
123                   All patients were assigned relapse risk scores based on their respective clinicopat
124 atterns of deregulation that correspond with relapse risk scores to refine prognosis with the clinico
125 increased impulsivity that may contribute to relapse risk.SIGNIFICANCE STATEMENT Persons with alcohol
126        The FLT3ITD mRNA level contributes to relapse risk stratification and might help to guide post
127 tive of an earlier return to alcohol use and relapse risk, suggesting a significant role for gray mat
128 h risk of relapse and was more predictive of relapse risk than c-KIT mutations.
129 autografts had a two-fold (P =.0009) greater relapse risk than patients who received purged autograft
130 ted to identify genetic factors that predict relapse risk (the primary endpoint of many pivotal clini
131 solidation therapies are to be determined by relapse risk, then NPM1(MUT) cases with low-level FLT3(I
132 ation in CR1 and CR2 is associated with less relapse risk, this analysis reveals an enhanced graft-ve
133 red with TAU, produced significantly reduced relapse risk to drug use and heavy drinking.
134 ality therapy did not mitigate the continued relapse risk, underscoring the value of prolonged clinic
135 to identify genetic variants that predict MS relapse risk, using a three-stage approach.
136 t disease, transplant-related mortality, and relapse risk vary by donor source.
137                    Without risk factors, the relapse risk was 12%.
138                                     Although relapse risk was 26%, this was significantly reduced whe
139  estimated nonrelapse mortality was 32%, and relapse risk was 33%.
140                       The overall postpartum relapse risk was 35% (95% CI=29, 41).
141                                          The relapse risk was 57% if the RT-PCR was positive versus 2
142 rate higher relapse, whereas at rates < 90%, relapse risk was comparable to that of non-Hispanic whit
143 tterns of pathway deregulation in predicting relapse risk was established using related but not ident
144 on of SET index and ESR1 levels with distant relapse risk was evaluated from microarrays of ER-positi
145                                              Relapse risk was high among persons who were underweight
146                                          The relapse risk was high within 6 months of discontinuing o
147                                              Relapse risk was reduced by both C-CT and fluoxetine in
148 ut antithymocyte globulin (ATG), whereas the relapse risk was similar in the group treated with busul
149 NGS)-MRD better identifies pre- and post-HCT relapse risk, we performed immunoglobulin heavy chain (I
150              Ancestry-related differences in relapse risk were abrogated by the addition of a single
151 apse mortality risks (HR, 0.92; P = .74) but relapse risks were higher after transplantation of BM (H
152 ts with AML, and integration of toxicity and relapse risks will determine the best approach for allog
153 showed lower nonrelapse mortality but higher relapse risk with RIC; however, overall survivals were s

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