1 ated patients (85.2%) ultimately achieved
an NED state, and 38 (46.9%) remain continuously NED with m
2 /serotonin products, in CR2-TAg NE cells
and NED.
3 e different fluorescent dyes (6FAM, VIC,
and NED), demonstrating that it is possible to analyze up to
4 zo-dye formation, abbreviated as "4-ATP-
AuNP+
NED" colorimetric method.
5 A drug that targets GRP78
blocked NED in castrated mice.
6 The two-pore channel
blocker NED-19 (1 mum) and the nicotinic acid adenine dinucleoti
7 Within
complexes,
NED proteins have larger interaction interfaces and asse
8 Seven of these 10 are
continuously NED and three are currently NED with salvage therapy.
9 15 of these patients (48%) are
continuously NED despite no further therapy and five additional patie
10 However, 22 of 41 (53.7%) are
continuously NED despite no further therapy.
11 R with initial chemotherapy are
continuously NED with VeIP.
12 Overall, 16 of 47 patients have
continuously NED, an additional four patients have NED with further t
13 sease at presentation, two have
continuously NED.
14 STMs at time of resection have
continuously NED.
15 nt chemotherapy, and seven have
continuously NED.
16 isease at presentation, 14 have
continuously NED.
17 Five of these patients remain
continuously NED after chemotherapy alone, including three who were c
18 ED state, and 38 (46.9%) remain
continuously NED with median follow-up from LR therapy of 24.5 months
19 otherapy surgery, and 12 remain
continuously NED.
20 ee (NED), and 20 (46.5%) remain
continuously NED.
21 ), whereas nine other patients are
currently NED after therapy for subsequent relapses.
22 five additional patients (16%) are
currently NED with salvage therapy.
23 ht additional patients (19.5%) are
currently NED with salvage therapy.
24 are continuously NED and three are
currently NED with salvage therapy.
25 One additional CR is
currently NED more than 63 months after paclitaxel plus gemcitabin
26 nts have NED with further therapy (
currently NED), two patients are alive with disease, 23 patients d
27 n from the NASA/IPAC Extragalactic
Database (
NED)(1)) is unique among compact groups of galaxies(2-12
28 Many non-exponentially
degraded (
NED) proteins are subunits of complexes that are produce
29 ticles (AuNPs) and naphthylethylene
diamine (
NED) as coupling agent for azo-dye formation, abbreviate
30 lphaVbeta3 that promotes NE
differentiation (
NED).
31 Neuroendocrine
differentiation (
NED) in adenocarcinoma of the human prostate (CaP) is as
32 (CRPC) with neuroendocrine
differentiation (
NED) is a lethal disease for which effective therapies a
33 Fatal neuroendocrine
differentiation (
NED) of castration-resistant prostate cancer is a recurr
34 mice display neuroendocrine
differentiation (
NED), but NE cancer does not develop.
35 ferred to as neuroendocrine
differentiation (
NED).
36 inducing the neuroendocrine
differentiation (
NED).
37 Patients with no evidence of
disease (
NED) after metastasectomy for renal cell carcinoma are a
38 etween patients with no evidence of
disease (
NED) after radiation and those who had persistent or rec
39 ts continuously show no evidence of
disease (
NED) and eight additional patients (19.5%) are currently
40 (20%) patients have no evidence of
disease (
NED) at a median follow-up of 39 months (32-65 months).
41 who continuously had no evidence of
disease (
NED) were as follows: group A, 92%; group B, 40%; group
42 ease-free survivors (no evidence of
disease (
NED)).
43 ients currently have no evidence of
disease (
NED), and four patients died of disease.
44 ts continuously have no evidence of
disease (
NED).
45 omains: the amino terminal extension
domain (
NED), amino terminal domain (NTD), catalytic core domain
46 Amplifying genes
encoding NED proteins increases their initial degradation.
47 s of four domains: amino terminal
extension (
NED), amino terminus (NTD), catalytic core (CCD), and ca
48 t population) are continuously disease
free (
NED) with paclitaxel plus gemcitabine alone (no postchem
49 nderwent surgery were rendered disease
free (
NED), and 20 (46.5%) remain continuously NED.
50 dditional patient was rendered disease-
free (
NED) with the resection of residual carcinoma.
51 tinguished those with future metastasis
from NED.
52 wledge of the molecular mechanisms
governing NED.
53 All five patients currently
have NED.
54 uously NED, an additional four patients
have NED with further therapy (currently NED), two patients a
55 and (naphthyl)ethylenediamine
hydrochloride (
NED) with nitrite in acidic medium, yielding a coloured
56 biting apoptosis and activating autophagy
in NED PCa cells.
57 mor-stroma cross-talk that is able to
induce NED under the pressure of androgen deprivation.
58 t EZH2 inhibitor could block the Enz-
induced NED.
59 y miRNAs alterations driving therapy-
induced NED, we performed small RNA-NGS in a retrospective cohor
60 cer specimens from patients developing
local NED after ADT showed GRP78 upregulation in tumor cells a
61 Further, we identify novel
miRNA NED drivers that can be exploited for NEPC therapeutic t
62 a (ED donors, n=589) and those that did
not (
NED donors, n=703).
63 The molecular basis
of NED is not completely understood leading to a lack of ef
64 hway inhibition prevented the development
of NED and castration resistance in vivo.
65 ) in normal and CR2-TAg NE cells and foci
of NED in human CaP, (b) glutamic acid decarboxylase and it
66 P78) positively correlates with hallmarks
of NED.
67 mal cells to release IL6, a known inducer
of NED.
68 a possible strategy to prevent the onset
of NED by targeting the NTS signaling pathway.
69 Liver profiles
of NED closely resembled those of controls.
70 Moreover, the removal
of NED genes from an MMN significantly reduces its global e
71 it associates; we also show that it
promotes NED and anchorage-independent growth, as well as a motil
72 We find that the outer
protomer NED and NTD domains have no significant effects on integ
73 MAOA inhibitors significantly
reduced NED and autophagy activation of PCa cells.
74 er ADT/ARPI induces stromal cells to
release NED-promoting molecules and the underlying molecular net
75 urvival (DFS) in patients with mRCC
rendered NED after metastasectomy.
76 these 32 patients were successfully
rendered NED by postchemotherapy surgery, and 12 remain continuou
77 ith an N-2-amino-3-phenylpropyl
substituent (
NED-3238), example 43, inhibits arginase I and II with I
78 Following recent reports showing
that NED of PCa requires down-regulation of repressor element
79 The NED, NTD, and CTD of the outer monomers are disordered i
80 direct costs were significantly lower in
the NED donors ($29,879.4+/-11590.1 vs. $19,019.6+/-7599.60,
81 ransplanted were significantly higher in
the NED donors ($8,414.5+/-138.29 vs. $9,272.04+/-344.56, P<
82 transplanted was significantly longer in
the NED donors (23.1+/-0.8 hr vs. 36.9+/-3.2 hr, P<0.001).
83 d per donor was significantly shorter in
the NED donors (91.2+/-44.9 hr vs. 86.8+/-78.6 hr, P=0.01).
84 could increase the lncRNA-p21 to induce
the NED.
85 Bioinformatic analyses of
the NED genes have revealed that not only do these genes hav
86 These features confirm the importance of
the NED genes to the metabolic network, including why they a
87 quently methylating the STAT3 to promote
the NED.
88 nd activated downstream signaling leading
to NED through activation of neurotensin receptor 1 (NTSR1)
89 tential early biomarker of tumors
undergoing NED.
90 plexing using the fluorescent dyes FAM,
VIC,
NED, and ROX.
91 +/-0.8, P<0.0001) in ED donors compared
with NED donors.
92 role of NTS in the development of CRPC
with NED, and a possible strategy to prevent the onset of NED
93 echanism underlying development of CRPC
with NED, however, remains largely uncharacterized.
94 in cell line and animal models of CRPC
with NED.
95 h blinded placebo in patients with mRCC
with NED after metastasectomy.
96 Patients
with NED after metastasectomy were randomly assigned 1:1 to r
97 atify mCRPC patients into those with/
without NED and guide treatment decisions.
98 In
yeast,
NED genes are predominantly single-copy and are highly c