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1 ed by N-MYC, is itself a strong predictor of poor clinical outcome.
2 th MSI1(high)/TNS3(low) pattern tend to have poor clinical outcome.
3 This culminates in an extremely poor clinical outcome.
4 y aggressive acute leukaemia associated with poor clinical outcome.
5 yeloid leukemia (AML) and is associated with poor clinical outcome.
6 ypes, loss of RB function is associated with poor clinical outcome.
7 xpression were associated significantly with poor clinical outcome.
8 is a mature B-cell lymphoma characterized by poor clinical outcome.
9 rexpression is significantly associated with poor clinical outcome.
10 identified mutations in Gbeta correlate with poor clinical outcome.
11 linked to tumor initiation, progression, and poor clinical outcome.
12 ric cancer (GC) and has been correlated with poor clinical outcome.
13 ature in renal cancer and is associated with poor clinical outcome.
14 stem cell gene signatures is associated with poor clinical outcome.
15 f primary breast cancers and correlates with poor clinical outcome.
16 tastasize even when small, leading to a very poor clinical outcome.
17 of breast cancer, advanced tumor stages and poor clinical outcome.
18 rachnoid hemorrhage often leads to death and poor clinical outcome.
19 B and when expressed at high levels predicts poor clinical outcome.
20 ent to invasive disease is associated with a poor clinical outcome.
21 lloprotease disintegrin, are correlated with poor clinical outcome.
22 -like and HER2 breast tumors associated with poor clinical outcome.
23 rcinoma, a relatively uncommon cancer with a poor clinical outcome.
24 pe characterized by mesenchymal elements and poor clinical outcome.
25 tive (ER+/HER2-) breast cancer patients with poor clinical outcome.
26 of the most important prognostic factors of poor clinical outcome.
27 tance and aggressive clinical behaviour with poor clinical outcome.
28 n of this gene signature was associated with poor clinical outcome.
29 from children with FSGS and correlated with poor clinical outcome.
30 erapy resistance, ultimately contributing to poor clinical outcome.
31 high incidence of mutations associated with poor clinical outcome.
32 erogeneous group of neoplasms with generally poor clinical outcome.
33 LC), and high levels of EPHA2 correlate with poor clinical outcome.
34 man CRCs and correlates with tumor stage and poor clinical outcome.
35 , 2.1 to 20.5) were strongly associated with poor clinical outcome.
36 5-HT levels were an independent predictor of poor clinical outcome.
37 characterised by an aggressive phenotype and poor clinical outcome.
38 asis and drug resistance and contribute to a poor clinical outcome.
39 -carbon metabolism with high tumor stage and poor clinical outcome.
40 it is associated with basal-like subtype and poor clinical outcome.
41 hilia and immunopathology were linked to the poor clinical outcome.
42 eterogeneous group of tumors associated with poor clinical outcome.
43 aling modulation) may be responsible for the poor clinical outcome.
44 represent a strong independent predictor of poor clinical outcome.
45 need for aggressive therapy in patients with poor clinical outcome.
46 rength of this activation is associated with poor clinical outcome.
47 malignancies and pediatric brain tumors with poor clinical outcome.
48 d with CD44 expression, chemoresistance, and poor clinical outcome.
49 (NHL) that, in general, is associated with a poor clinical outcome.
50 primary colorectal tumors that manifested a poor clinical outcome.
51 ncide with low levels of E2F-1 and reflect a poor clinical outcome.
52 filtrating Tregs are often associated with a poor clinical outcome.
53 d high LDHB expression in their tumors had a poor clinical outcome.
54 , contributing to tumor immune tolerance and poor clinical outcome.
55 t are more likely to be severe and result in poor clinical outcome.
56 e most common subtype of renal cancer, has a poor clinical outcome.
57 in breast cancer tissue is associated with a poor clinical outcome.
58 and is associated with tumor aggression and poor clinical outcome.
59 al infection, which strongly correlates with poor clinical outcome.
60 or receptor (EGFR), which is associated with poor clinical outcome.
61 nts and associated with disease severity and poor clinical outcome.
62 of the most important prognostic factors of poor clinical outcome.
63 d with decreased PTEN expression, portends a poor clinical outcome.
64 L) is a heterogeneous clonal disorder with a poor clinical outcome.
65 and that this reactivity is associated with poor clinical outcome.
66 orrelated with aggressive tumor behavior and poor clinical outcome.
67 that loss of RB function was associated with poor clinical outcome.
68 ent correlates with ENG gene methylation and poor clinical outcome.
69 ts level of (over)expression correlates with poor clinical outcome.
70 egia in the immediate post-CPB period and of poor clinical outcome.
71 ith mesenchymal differentiation and predicts poor clinical outcome.
72 n of ROCK is related to tumor metastases and poor clinical outcome.
73 .82, p = 0.031) as independent predictors of poor clinical outcome.
74 t in misdiagnosis, failure of treatment, and poor clinical outcome.
75 elated with nonresponsiveness to therapy and poor clinical outcome.
76 s, correlating with treatment resistance and poor clinical outcome.
77 n and epithelial markers and correlated with poor clinical outcome.
78 increased Fzd expression is associated with poor clinical outcome.
79 ssociated with early biochemical relapse and poor clinical outcome.
80 ture was predictive of metastatic burden and poor clinical outcome.
81 y mutated genes in human cancers and predict poor clinical outcome.
82 in pancreatic cancer and is associated with poor clinical outcome.
83 tatic gene sets and pathways associated with poor clinical outcome.
84 equency, leading to treatment resistance and poor clinical outcome.
85 ve glioblastoma-like molecular features with poor clinical outcome.
86 varian cancers and its levels correlate with poor clinical outcome.
87 -10 anti-inflammatory response that portends poor clinical outcome.
88 ly overexpressed in TNBC and associated with poor clinical outcome.
89 s expression correlates with KRAS levels and poor clinical outcome.
90 (PNI) is an ominous event strongly linked to poor clinical outcome.
91 at diagnosis and recurrence associated with poor clinical outcome.
92 ma (BL) are highly aggressive lymphomas with poor clinical outcome.
93 ion with suppression of immune effectors and poor clinical outcome.
94 ents, but relapse rates are high and lead to poor clinical outcomes.
95 Left ventricular myocardial scar portends poor clinical outcomes.
96 Slug expression, enhanced invasiveness, and poor clinical outcomes.
97 nflammatory cytokines and is correlated with poor clinical outcomes.
98 (non-DS-AMKL) is frequently associated with poor clinical outcomes.
99 cer progression and serves as a biomarker of poor clinical outcomes.
100 ly promoting tumor progression that leads to poor clinical outcomes.
101 tributes to invasive phenotypes and leads to poor clinical outcomes.
102 levels of PRL associate with metastasis and poor clinical outcomes.
103 tems are 2 virulence factors associated with poor clinical outcomes.
104 rst episode psychosis and is associated with poor clinical outcomes.
105 of acute intracerebral haemorrhage (ICH) and poor clinical outcomes.
106 ll patients are associated with persistently poor clinical outcomes.
107 the identified networks are associated with poor clinical outcomes.
108 h resistance to neoadjuvant chemotherapy and poor clinical outcomes.
109 se entity given the uniform association with poor clinical outcomes.
110 nthamoeba sclerokeratitis is associated with poor clinical outcomes.
111 CD73 levels in tumor tissues correlate with poor clinical outcomes.
112 ion, many of which were associated also with poor clinical outcomes.
113 eloid leukemia (AML) and are associated with poor clinical outcomes.
114 ed with invasion, lymph node metastasis, and poor clinical outcomes.
115 ctors that contribute to disease biology and poor clinical outcomes.
116 ver transplantation is often associated with poor clinical outcomes.
117 and severity of lung diseases, resulting in poor clinical outcomes.
118 l tissue, respectively, were associated with poor clinical outcomes.
119 itically ill patients and is associated with poor clinical outcomes.
120 tegies and may provide a route to addressing poor clinical outcomes.
121 sociated with aggressive cancer subtypes and poor clinical outcomes.
122 ilar to primary tissue from patients who had poor clinical outcomes.
123 ssociated with nephron injury and results in poor clinical outcomes.
124 e density, which was in turn associated with poor clinical outcomes.
125 and is associated with tumor progression and poor clinical outcomes.
126 cation and are independently associated with poor clinical outcomes.
127 ociated with smoking-induced lung cancer and poor clinical outcomes.
128 covery efforts, may be responsible for these poor clinical outcomes.
129 ssociated with aggressive disease course and poor clinical outcomes.
130 MRCs were associated with Akt activation and poor clinical outcomes.
131 mon in the United States and associates with poor clinical outcomes.
132 emotherapy and significantly associated with poor clinical outcomes.
133 cell carcinomas (HNSCC) and associated with poor clinical outcomes.
134 ic attention because of its association with poor clinical outcomes.
135 isease severity and identifies patients with poor clinical outcomes.
136 injured, functionally coagulopathic and have poor clinical outcomes.
137 es related to cachexia, atherosclerosis, and poor clinical outcomes.
138 yopathy is increasing and is associated with poor clinical outcomes.
139 rogression and, as such, are associated with poor clinical outcomes.
140 le solid tumour types and is associated with poor clinical outcomes.
141 association with advanced disease-stage and poor clinical outcomes.
142 of cancer therapies and are associated with poor clinical outcomes.
143 n critically ill patients is associated with poor clinical outcomes.
144 atidylinositol 3-kinase (PI3K) signaling and poor clinical outcomes.
145 untreated psychosis (DUP) is associated with poor clinical outcomes.
146 ad in a number of cancer types, resulting in poor clinical outcomes.
147 is a chronic disease of preterm babies with poor clinical outcomes.
148 anoma, and its expression is correlated with poor clinical outcomes.
149 primary human tumors and was associated with poor clinical outcomes.
150 oid leukemia (AML), where it associates with poor clinical outcomes.
151 perative depressive symptoms are at risk for poor clinical outcomes after HIPEC + CS, including great
152 sociated with greater hematoma expansion and poor clinical outcomes after intracerebral hemorrhage.
154 ssion was also significantly associated with poor clinical outcomes, although this effect was reduced
155 tion correlates with increased morbidity and poor clinical outcomes among patients living with human
157 iven tumors are aggressive malignancies with poor clinical outcome and lack of sensitivity to therapi
159 ssociated tip-cell signature correlated with poor clinical outcome and the loss of LSEC marker gene e
160 e presence of TAMs in LMS is associated with poor clinical outcome and the overall effect of TAMs in
161 rget genes are significantly correlated with poor clinical outcomes and are often associated with gen
162 ulation of TET2 protein also correlated with poor clinical outcomes and miR-22 overexpression in MDS
163 eriatric depression (GD) is common, predicts poor clinical outcomes and often persists despite remiss
164 ral carcinoma, significantly associated with poor clinical outcomes and representing an independent p
166 vel overseas for kidney transplantation have poor clinical outcomes and should be counseled according
167 w that miR-22 overexpression correlates with poor clinical outcomes and silencing of the TET-miR-200
168 irium as a dangerous syndrome which portends poor clinical outcomes and which is potentially modifiab
169 tors involved in ovarian cancer progression, poor clinical outcome, and chemotherapy resistance.
170 ons, deep GM, and NAWM, is closely linked to poor clinical outcome, and is at least partly linked to
171 is associated with aggressive tumor growth, poor clinical outcome, and resistance to chemotherapy, b
172 ioblastomas versus NSCs, are associated with poor clinical outcomes, and are required for glioblastom
173 , the emergence of less-susceptible strains, poor clinical outcomes, and increased nephrotoxicity wit
174 Heart failure (HF) is common, results in poor clinical outcomes, and is associated with large hea
177 profile associated with severe COVID-19 and poor clinical outcome, as well as early immune signature
179 sistance to antipsychotic treatment mediated poor clinical outcomes associated with cannabis use.
180 Tumor genetic heterogeneity may underlie poor clinical outcomes because diverse subclones could b
181 The AKI subphenotypes discriminated risk for poor clinical outcomes better than the Kidney Disease: I
182 -amplified neuroblastomas and correlate with poor clinical outcome, but how these oncogenes cooperate
183 cer (BLBC) subtype have been associated with poor clinical outcomes, but a molecular basis for this d
184 associated with cancer subtype, grades, and poor clinical outcomes, but also facilitated primary tum
185 roteinase MMP16 (MT3-MMP) is associated with poor clinical outcome, collagen bundle assembly around t
190 tection in primary tumors is correlated with poor clinical outcome (disease-free survival: P = 0.03;
191 with cystic fibrosis (CF) is associated with poor clinical outcome due to broad drug resistance and t
192 (UBC) patients at muscle invasive stage have poor clinical outcome, due to high propensity for metast
193 r Alzheimer's disease and is associated with poor clinical outcome following traumatic brain injury a
196 viously unrecognized molecular subgroup with poor clinical outcome for which more effective therapeut
198 BST2 expression correlated with a trend for poor clinical outcome, further supporting its role in co
199 , which is responsible for tumor relapse and poor clinical outcomes, has been linked to the acquisiti
200 ects of AURKA overexpression associated with poor clinical outcomes have been attributed to increased
201 Both complications were associated with poor clinical outcome in a similar percentage of partici
202 expressed in human aRMS and that portends a poor clinical outcome in an expression level-dependent m
203 ving early tumor recurrence, metastasis, and poor clinical outcome in breast and prostate cancers.
204 v-1(-/-) MSF gene signature is predictive of poor clinical outcome in breast cancer patients treated
205 l expression of CtBP-targeted genes predicts poor clinical outcome in breast cancer patients, and ele
212 changes in both NOX2 and TRPM8 mRNA predict poor clinical outcome in estrogen receptor (ER)-negative
213 ls, increasing genomic instability linked to poor clinical outcome in estrogen receptor-positive dise
216 on of glandular architecture associates with poor clinical outcome in high-grade colorectal cancer (C
217 f both PINCH-1 and myoferlin correlates with poor clinical outcome in human breast cancer patients.
218 asthma that leads to airway dysfunction and poor clinical outcome in humans, was investigated in a m
219 ctivation of TBC1D16-47KD is associated with poor clinical outcome in melanoma, while conferring grea
222 , high LIN28B expression was associated with poor clinical outcome in our JMML patient series but was
226 weight cyclin E (LMW-E), is associated with poor clinical outcome in patients with breast cancer and
227 -181 regulatory axis and may contribute to a poor clinical outcome in patients with ER+ breast tumors
229 with normal tissues and were associated with poor clinical outcome in patients with non-small cell lu
230 s are prevalent and significantly related to poor clinical outcome in patients with ovarian cancer.
236 ty (ADCC) and their presence correlated with poor clinical outcome in two prospective clinical trial
238 ted in gliomas and its levels correlate with poor clinical outcomes in a dose-dependent manner, it ma
240 Allergic sensitization is associated with poor clinical outcomes in asthma, chronic obstructive pu
242 like cells contribute to chemoresistance and poor clinical outcomes in many cancers, including ovaria
244 se FXR1 is overexpressed and associated with poor clinical outcomes in multiple cancers, these result
245 he association of epithelial plasticity with poor clinical outcomes in multiple human carcinoma types
247 xpression were associated significantly with poor clinical outcomes in ovarian cancer patients (n = 3
248 t predictor of reduced exercise capacity and poor clinical outcomes in patients with heart failure (H
250 her elucidate the inflammatory correlates of poor clinical outcomes in patients with S. aureus bacter
251 with focal segmental glomerulosclerosis and poor clinical outcomes in patients with various conditio
255 in macrophage activation syndrome (MAS) and poor clinical outcomes in severe inflammatory and septic
256 ts tumor microenvironment (TME) is linked to poor clinical outcomes in treatment of resistant breast
259 bacteremic isolates of P. aeruginosa confers poor clinical outcomes independent of antibiotic suscept
261 s with colorectal cancer was associated with poor clinical outcome, irrespective of HIF-1 In addition
262 al-like, or high grade, its association with poor clinical outcome is independent of these clinicopat
264 ed therapy are significantly correlated with poor clinical outcomes, making TNBC the only type of bre
266 mab regardless of ADA status correlated with poor clinical outcome (median sample PASI 10.1, 6.5 [95%
267 in tumor tissue was strongly associated with poor clinical outcomes (n = 10, hazard ratio (HR) (mean)
268 quired ER regulatory regions associated with poor clinical outcome observed in primary tumours reveal
269 BSI, relative to Ecc BSI, was predictive of poor clinical outcome (odds ratio 3.3; 95% confidence in
274 a key factor for driving the progression and poor clinical outcome of human ER-negative breast cancer
279 .704; 95% CI 2.054 to 21.883; p = 0.002) and poor clinical outcome (OR 2.281; 95% CI 1.022 to 5.093;
281 s (CF) patients and has been associated with poor clinical outcomes, particularly following lung tran
282 k factor for breast cancer and also predicts poor clinical outcomes regardless of menopausal status.
284 3 patients with continually elevated BDG had poor clinical outcomes (stroke, meningitis relapse, or d
285 entify patients who are at increased risk of poor clinical outcomes, such as exercise intolerance and
287 ell-like features, disseminated disease, and poor clinical outcomes, suggesting pivotal significance
288 e of stromal Cav-1 was a strong predictor of poor clinical outcome, suggestive of tamoxifen resistanc
289 mune activation, a well-defined surrogate of poor clinical outcome that is elevated in PWID, can regr
290 EPHA2 overexpression is associated with poor clinical outcomes; therefore, EPHA2 may represent a
292 of myocardial infarction-is associated with poor clinical outcome, we hypothesized that morphine low
293 re considered, significant associations with poor clinical outcome were detected exclusively in tumor
294 strategies were reviewed, and predictors of poor clinical outcomes were determined through multivari
296 ted exhaustion of T cells as a mechanism for poor clinical outcome when IL-12 is administered to FL p
297 T-cell exhaustion in cancer is linked to poor clinical outcomes, where evidence suggests T-cell m
298 ery low trough levels of less than 4 g/L had poor clinical outcomes, whereas higher trough levels wer
299 of hypoxia within a tumor is associated with poor clinical outcome, which is often exacerbated by los