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1 from children with FSGS and correlated with poor clinical outcome.
2 erapy resistance, ultimately contributing to poor clinical outcome.
3 erogeneous group of neoplasms with generally poor clinical outcome.
4 LC), and high levels of EPHA2 correlate with poor clinical outcome.
5 man CRCs and correlates with tumor stage and poor clinical outcome.
6 , 2.1 to 20.5) were strongly associated with poor clinical outcome.
7 5-HT levels were an independent predictor of poor clinical outcome.
8 characterised by an aggressive phenotype and poor clinical outcome.
9 asis and drug resistance and contribute to a poor clinical outcome.
10 varian cancers and its levels correlate with poor clinical outcome.
11 -carbon metabolism with high tumor stage and poor clinical outcome.
12 it is associated with basal-like subtype and poor clinical outcome.
13 hilia and immunopathology were linked to the poor clinical outcome.
14 eterogeneous group of tumors associated with poor clinical outcome.
15 aling modulation) may be responsible for the poor clinical outcome.
16 represent a strong independent predictor of poor clinical outcome.
17 -10 anti-inflammatory response that portends poor clinical outcome.
18 need for aggressive therapy in patients with poor clinical outcome.
19 rength of this activation is associated with poor clinical outcome.
20 malignancies and pediatric brain tumors with poor clinical outcome.
21 d with CD44 expression, chemoresistance, and poor clinical outcome.
22 (NHL) that, in general, is associated with a poor clinical outcome.
23 primary colorectal tumors that manifested a poor clinical outcome.
24 ncide with low levels of E2F-1 and reflect a poor clinical outcome.
25 filtrating Tregs are often associated with a poor clinical outcome.
26 d high LDHB expression in their tumors had a poor clinical outcome.
27 ly overexpressed in TNBC and associated with poor clinical outcome.
28 , contributing to tumor immune tolerance and poor clinical outcome.
29 t are more likely to be severe and result in poor clinical outcome.
30 in breast cancer tissue is associated with a poor clinical outcome.
31 s expression correlates with KRAS levels and poor clinical outcome.
32 and is associated with tumor aggression and poor clinical outcome.
33 al infection, which strongly correlates with poor clinical outcome.
34 or receptor (EGFR), which is associated with poor clinical outcome.
35 nts and associated with disease severity and poor clinical outcome.
36 (PNI) is an ominous event strongly linked to poor clinical outcome.
37 of the most important prognostic factors of poor clinical outcome.
38 d with decreased PTEN expression, portends a poor clinical outcome.
39 and that this reactivity is associated with poor clinical outcome.
40 orrelated with aggressive tumor behavior and poor clinical outcome.
41 at diagnosis and recurrence associated with poor clinical outcome.
42 that loss of RB function was associated with poor clinical outcome.
43 ent correlates with ENG gene methylation and poor clinical outcome.
44 ma (BL) are highly aggressive lymphomas with poor clinical outcome.
45 ts level of (over)expression correlates with poor clinical outcome.
46 egia in the immediate post-CPB period and of poor clinical outcome.
47 ith mesenchymal differentiation and predicts poor clinical outcome.
48 n of ROCK is related to tumor metastases and poor clinical outcome.
49 rs, and elevation of Prx1 is associated with poor clinical outcome.
50 lood pressure curve serves as a predictor of poor clinical outcome.
51 ion with suppression of immune effectors and poor clinical outcome.
52 ociated with aggressive tumor behavior and a poor clinical outcome.
53 NHL) that, in general, are associated with a poor clinical outcome.
54 s, often of the basal-like subtype, and with poor clinical outcome.
55 en correlated with malignant progression and poor clinical outcome.
56 8(+) cells within clones are associated with poor clinical outcome.
57 plete inactivation of GPx3 correlates with a poor clinical outcome.
58 oxic anticancer therapies and predicts for a poor clinical outcome.
59 3 months after HPE was also associated with poor clinical outcome.
60 h human prostate cancer (PCa) metastasis and poor clinical outcome.
61 arian and other cancers and is predictive of poor clinical outcome.
62 after surgery or trauma is associated with a poor clinical outcome.
63 to chemo/hormone therapy and predicts for a poor clinical outcome.
64 ntly identified as prognostic biomarkers for poor clinical outcome.
65 the extent of tumor hypoxia correlates with poor clinical outcome.
66 es with metastases, N-myc amplification, and poor clinical outcome.
67 es with metastases, N-myc amplification, and poor clinical outcome.
68 ical or microbiologic factor predictive of a poor clinical outcome.
69 h low expression in invasive carcinomas with poor clinical outcome.
70 th MSI1(high)/TNS3(low) pattern tend to have poor clinical outcome.
71 s statistically significantly correlate with poor clinical outcome.
72 tin 5/6 in tumor cells was associated with a poor clinical outcome.
73 This culminates in an extremely poor clinical outcome.
74 y aggressive acute leukaemia associated with poor clinical outcome.
75 yeloid leukemia (AML) and is associated with poor clinical outcome.
76 ypes, loss of RB function is associated with poor clinical outcome.
77 xpression were associated significantly with poor clinical outcome.
78 is a mature B-cell lymphoma characterized by poor clinical outcome.
79 rexpression is significantly associated with poor clinical outcome.
80 identified mutations in Gbeta correlate with poor clinical outcome.
81 linked to tumor initiation, progression, and poor clinical outcome.
82 ric cancer (GC) and has been correlated with poor clinical outcome.
83 ature in renal cancer and is associated with poor clinical outcome.
84 stem cell gene signatures is associated with poor clinical outcome.
85 equency, leading to treatment resistance and poor clinical outcome.
86 f primary breast cancers and correlates with poor clinical outcome.
87 tastasize even when small, leading to a very poor clinical outcome.
88 of breast cancer, advanced tumor stages and poor clinical outcome.
89 rachnoid hemorrhage often leads to death and poor clinical outcome.
90 B and when expressed at high levels predicts poor clinical outcome.
91 ent to invasive disease is associated with a poor clinical outcome.
92 lloprotease disintegrin, are correlated with poor clinical outcome.
93 -like and HER2 breast tumors associated with poor clinical outcome.
94 pe characterized by mesenchymal elements and poor clinical outcome.
95 tive (ER+/HER2-) breast cancer patients with poor clinical outcome.
96 ve glioblastoma-like molecular features with poor clinical outcome.
97 of the most important prognostic factors of poor clinical outcome.
98 tance and aggressive clinical behaviour with poor clinical outcome.
99 n of this gene signature was associated with poor clinical outcome.
100 n critically ill patients is associated with poor clinical outcomes.
101 untreated psychosis (DUP) is associated with poor clinical outcomes.
102 ll patients are associated with persistently poor clinical outcomes.
103 the identified networks are associated with poor clinical outcomes.
104 h resistance to neoadjuvant chemotherapy and poor clinical outcomes.
105 ad in a number of cancer types, resulting in poor clinical outcomes.
106 nthamoeba sclerokeratitis is associated with poor clinical outcomes.
107 eloid leukemia (AML) and are associated with poor clinical outcomes.
108 ed with invasion, lymph node metastasis, and poor clinical outcomes.
109 ctors that contribute to disease biology and poor clinical outcomes.
110 ver transplantation is often associated with poor clinical outcomes.
111 and severity of lung diseases, resulting in poor clinical outcomes.
112 l tissue, respectively, were associated with poor clinical outcomes.
113 itically ill patients and is associated with poor clinical outcomes.
114 tegies and may provide a route to addressing poor clinical outcomes.
115 sociated with aggressive cancer subtypes and poor clinical outcomes.
116 anoma, and its expression is correlated with poor clinical outcomes.
117 ssociated with nephron injury and results in poor clinical outcomes.
118 and is associated with tumor progression and poor clinical outcomes.
119 cation and are independently associated with poor clinical outcomes.
120 ociated with smoking-induced lung cancer and poor clinical outcomes.
121 covery efforts, may be responsible for these poor clinical outcomes.
122 ssociated with aggressive disease course and poor clinical outcomes.
123 MRCs were associated with Akt activation and poor clinical outcomes.
124 mon in the United States and associates with poor clinical outcomes.
125 emotherapy and significantly associated with poor clinical outcomes.
126 cell carcinomas (HNSCC) and associated with poor clinical outcomes.
127 ependence of prostate cancer cells accompany poor clinical outcomes.
128 primary human tumors and was associated with poor clinical outcomes.
129 serum creatinine levels are associated with poor clinical outcomes.
130 mphocytic leukemia (CLL) are associated with poor clinical outcomes.
131 coccus aureus infections and correlates with poor clinical outcomes.
132 cell transfusions, which are associated with poor clinical outcomes.
133 fection is common and may be associated with poor clinical outcomes.
134 oid leukemia (AML), where it associates with poor clinical outcomes.
135 asal epithelial cells and is associated with poor clinical outcomes.
136 Left ventricular myocardial scar portends poor clinical outcomes.
137 e presence of these cells is associated with poor clinical outcomes.
138 cclusion, impaired myocardial perfusion, and poor clinical outcomes.
139 Slug expression, enhanced invasiveness, and poor clinical outcomes.
140 nflammatory cytokines and is correlated with poor clinical outcomes.
141 (non-DS-AMKL) is frequently associated with poor clinical outcomes.
142 cer progression and serves as a biomarker of poor clinical outcomes.
143 ly promoting tumor progression that leads to poor clinical outcomes.
144 tributes to invasive phenotypes and leads to poor clinical outcomes.
145 levels of PRL associate with metastasis and poor clinical outcomes.
146 tems are 2 virulence factors associated with poor clinical outcomes.
147 atidylinositol 3-kinase (PI3K) signaling and poor clinical outcomes.
148 rst episode psychosis and is associated with poor clinical outcomes.
149 of acute intracerebral haemorrhage (ICH) and poor clinical outcomes.
150 ee groups in the proportion of patients with poor clinical outcome (24% in the placebo group, 26% in
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
157 iven tumors are aggressive malignancies with poor clinical outcome and lack of sensitivity to therapi
160 a specimens, we noted an association between poor clinical outcome and the expression of cytokeratin
161 e presence of TAMs in LMS is associated with poor clinical outcome and the overall effect of TAMs in
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 marker of severity of MR consequences and of poor clinical outcome, and its assessment should be cons
172 is associated with aggressive tumor growth, poor clinical outcome, and resistance to chemotherapy, b
174 , the emergence of less-susceptible strains, poor clinical outcomes, and increased nephrotoxicity wit
175 Heart failure (HF) is common, results in poor clinical outcomes, and is associated with large hea
179 sistance to antipsychotic treatment mediated poor clinical outcomes associated with cannabis use.
180 -amplified neuroblastomas and correlate with poor clinical outcome, but how these oncogenes cooperate
181 cer (BLBC) subtype have been associated with poor clinical outcomes, but a molecular basis for this d
182 roteinase MMP16 (MT3-MMP) is associated with poor clinical outcome, collagen bundle assembly around t
184 nalysis was used to identify predictors of a poor clinical outcome; complexity of collection, history
187 tection in primary tumors is correlated with poor clinical outcome (disease-free survival: P = 0.03;
188 with cystic fibrosis (CF) is associated with poor clinical outcome due to broad drug resistance and t
189 (UBC) patients at muscle invasive stage have poor clinical outcome, due to high propensity for metast
191 (RV) dysfunction is a strong risk factor for poor clinical outcome following pulmonary embolism (PE),
192 r Alzheimer's disease and is associated with poor clinical outcome following traumatic brain injury a
195 viously unrecognized molecular subgroup with poor clinical outcome for which more effective therapeut
196 BST2 expression correlated with a trend for poor clinical outcome, further supporting its role in co
197 , which is responsible for tumor relapse and poor clinical outcomes, has been linked to the acquisiti
198 ects of AURKA overexpression associated with poor clinical outcomes have been attributed to increased
199 pression of this signature was predictive of poor clinical outcome in 12 cancer data sets representin
200 expressed in human aRMS and that portends a poor clinical outcome in an expression level-dependent m
202 ving early tumor recurrence, metastasis, and poor clinical outcome in breast and prostate cancers.
203 v-1(-/-) MSF gene signature is predictive of poor clinical outcome in breast cancer patients treated
204 l expression of CtBP-targeted genes predicts poor clinical outcome in breast cancer patients, and ele
211 ls, increasing genomic instability linked to poor clinical outcome in estrogen receptor-positive dise
213 on of glandular architecture associates with poor clinical outcome in high-grade colorectal cancer (C
215 asthma that leads to airway dysfunction and poor clinical outcome in humans, was investigated in a m
217 ctivation of TBC1D16-47KD is associated with poor clinical outcome in melanoma, while conferring grea
218 which this gene signature is repressed show poor clinical outcome in multiple microarray data sets o
219 ociated with enhanced tumor angiogenesis and poor clinical outcome in neuroblastoma, we serially char
222 , high LIN28B expression was associated with poor clinical outcome in our JMML patient series but was
225 weight cyclin E (LMW-E), is associated with poor clinical outcome in patients with breast cancer and
226 -181 regulatory axis and may contribute to a poor clinical outcome in patients with ER+ breast tumors
228 s are prevalent and significantly related to poor clinical outcome in patients with ovarian cancer.
234 ty (ADCC) and their presence correlated with poor clinical outcome in two prospective clinical trial
236 ted in gliomas and its levels correlate with poor clinical outcomes in a dose-dependent manner, it ma
238 ate inhibition of COX-1, are responsible for poor clinical outcomes in aspirin-treated patients, and
241 be associated with cisplatin resistance and poor clinical outcomes in head and neck cancer patients
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 xpression were associated significantly with poor clinical outcomes in ovarian cancer patients (n = 3
246 sus early nephrologist referral (LR, ER) and poor clinical outcomes in patients with end-stage renal
247 t predictor of reduced exercise capacity and poor clinical outcomes in patients with heart failure (H
249 ed by Alk5(T204D) expression correlated with poor clinical outcomes in patients with invasive breast
250 sis of survival data revealed a trend toward poor clinical outcomes in patients with medulloblastomas
251 with focal segmental glomerulosclerosis and poor clinical outcomes in patients with various conditio
256 resistance to anti-HER2 therapies; and (iii) poor clinical outcomes in women with breast cancer.
257 els of erythropoietin hyporesponsiveness and poor clinical outcome, including a 4-fold increase in mo
258 bacteremic isolates of P. aeruginosa confers poor clinical outcomes independent of antibiotic suscept
260 s with colorectal cancer was associated with poor clinical outcome, irrespective of HIF-1 In addition
261 al-like, or high grade, its association with poor clinical outcome is independent of these clinicopat
263 in tumor tissue was strongly associated with poor clinical outcomes (n = 10, hazard ratio (HR) (mean)
264 clin E provide a molecular mechanism for the poor clinical outcome observed in breast cancer patients
265 quired ER regulatory regions associated with poor clinical outcome observed in primary tumours reveal
273 fortunately, lung transplant recipients have poor clinical outcomes, often due to the development of
275 .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;
278 5'-UTR 28 bp 3R polymorphism correlated with poor clinical outcome (P=0.029), however, this was not t
279 s (CF) patients and has been associated with poor clinical outcomes, particularly following lung tran
280 3 patients with continually elevated BDG had poor clinical outcomes (stroke, meningitis relapse, or d
281 entify patients who are at increased risk of poor clinical outcomes, such as exercise intolerance and
282 gic effects of aspirin on platelets but also poor clinical outcomes, such as recurrent vascular event
284 r alterations, and this is associated with a poor clinical outcome, suggesting a biologic role of the
285 ell-like features, disseminated disease, and poor clinical outcomes, suggesting pivotal significance
286 e of stromal Cav-1 was a strong predictor of poor clinical outcome, suggestive of tamoxifen resistanc
287 mune activation, a well-defined surrogate of poor clinical outcome that is elevated in PWID, can regr
288 betics, and also suggest a mechanism for the poor clinical outcomes that occur after ischemic injury
289 EPHA2 overexpression is associated with poor clinical outcomes; therefore, EPHA2 may represent a
290 ssociated with cancer cell proliferation and poor clinical outcomes to the 50-kDa cyclin E form that
293 of myocardial infarction-is associated with poor clinical outcome, we hypothesized that morphine low
294 re considered, significant associations with poor clinical outcome were detected exclusively in tumor
296 ted exhaustion of T cells as a mechanism for poor clinical outcome when IL-12 is administered to FL p
297 er is a common malignancy characterized by a poor clinical outcome when tumors progress into invasive
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
300 (kip1) protein expression is correlated with poor clinical outcome, yet p27(kip1) rarely undergoes mu
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