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1 gainst HPV-stimulated aerobic glycolysis and tumor progression.
2 showed protumor gene expression and promoted tumor progression.
3 capture host macrophage functions that drive tumor progression.
4 esting an important role for RAD6 in ovarian tumor progression.
5 tumor microenvironment, a step critical for tumor progression.
6 ients who initially respond often experience tumor progression.
7 that loss of stromal 5-LO expression favors tumor progression.
8 les for PEITC and PcG proteins in control of tumor progression.
9 ther dietary fatty acids are correlated with tumor progression.
10 Cs) provide angiocrine factors orchestrating tumor progression.
11 associated with EMT in breast cancer during tumor progression.
12 expression correlates with poor survival and tumor progression.
13 sm improves the CD8(+) TILs' ability to slow tumor progression.
14 o how the Warburg effect is regulated during tumor progression.
15 can be observed in malignant exudates during tumor progression.
16 line its potential role in tumorigenesis and tumor progression.
17 deficiency resulted in markedly delayed lung tumor progression.
18 increased concentrations of CCR5 ligands and tumor progression.
19 , as opposed to representing natural primary tumor progression.
20 ypoxia-inducible factor-1 (HIF-1) to promote tumor progression.
21 of epithelial cancers and is associated with tumor progression.
22 o significantly promote GSC self-renewal and tumor progression.
23 ange of cellular processes, including during tumor progression.
24 xpanded through in situ proliferation during tumor progression.
25 d stimulates high-fat diet-mediated prostate tumor progression.
26 crophages (TAM) contribute to all aspects of tumor progression.
27 CL20, which promote cancer cell invasion and tumor progression.
28 th a role in sustaining EGFR activity during tumor progression.
29 cer-associated fibroblasts (CAF) and promote tumor progression.
30 n-induced squamous tumors, without affecting tumor progression.
31 transition (EMT) in cancer cells to promote tumor progression.
32 widely exploited as an active participant in tumor progression.
33 rease in contrast enhancement on MRI despite tumor progression.
34 ate tumor cell gene expression, and modulate tumor progression.
35 ling in SCLC cells, and markedly accelerates tumor progression.
36 possible tissue marker for regions of active tumor progression.
37 onal contributor versus only a biomarker for tumor progression.
38 ndent on RhoA and RhoB as a potent driver of tumor progression.
39 of EGF receptor to NF-kappaB activation and tumor progression.
40 trategy for the control of Rac1 activity and tumor progression.
41 ing of tumor growth, as shown in modeling of tumor progression.
42 ion synergistically reduced angiogenesis and tumor progression.
43 tion of cancer cell behavior associated with tumor progression.
44 lar milieu accelerating ErbB2-driven mammary tumor progression.
45 by O-GlcNAc, thereby significantly affecting tumor progression.
46 ical mechanism for mutant p53 GOF to promote tumor progression.
47 nt, maintains tissue homeostasis, and limits tumor progression.
48 al ECM to promote non-cell autonomous breast tumor progression.
49 ctivation is also peculiarly associated with tumor progression.
50 ne suppressive stroma that is obligatory for tumor progression.
51 f complex signaling networks that facilitate tumor progression.
52 cantly reduced in number with increasing HCC tumor progression.
53 o target GSC and to inhibit angiogenesis and tumor progression.
54 Likewise, CXCL5-deficient mice had reduced tumor progression.
55 ential to serve as noninvasive biomarkers of tumor progression.
56 s exerting immune suppressive effects during tumor progression.
57 vation is important in EGFR-associated solid-tumor progression.
58 cal and distant stroma modulate MDSCs during tumor progression.
59 ng a large vessel were associated with local tumor progression.
60 signature that implicates MAC as a driver of tumor progression.
61 has a close connection with inflammation and tumor progression.
62 and play critical roles in the regulation of tumor progression.
63 irmed a functional role for basophils during tumor progression.
64 ators on development, tissue engineering, or tumor progression.
65 within an ablation zone was related to local tumor progression.
66 nduced EMT is coupled to either apoptosis or tumor progression.
67 distinct populations play specific roles in tumor progression.
68 implicated in cancer cell proliferation and tumor progression.
69 tors in the microenvironmental regulation of tumor progression.
70 atients, no (18)F-FET uptake was detected at tumor progression.
71 iltrating hematopoietic cells and subsequent tumor progression.
72 ation of immature myeloid cells that promote tumor progression.
73 ensitive to NK killing, resulting in reduced tumor progression.
74 rbB2 mouse model resulted in delayed mammary tumor progression.
75 mechanism for development, regeneration, and tumor progression.
76 ding neutrophils and NK cells and suppressed tumor progression.
77 ht alter regulation of these pathways during tumor progression.
78 what extent the elevated TSH contributes to tumor progression.
79 signaling and cellular heterogeneity during tumor progression.
80 have different effects on cell behavior with tumor progression.
81 ing to tumor cell survival and thus favoring tumor progression.
82 the carcinoma microenvironment that promote tumor progression.
83 a crucial role in PrP(C) accumulation during tumor progression.
84 lucidate developing ELNs and their impact on tumor progression.
85 te Src-induced and high-fat diet-accelerated tumor progression.
86 inorganic phosphate as a new TME marker for tumor progression.
87 (90)Y TARE, and 41 patients (53%) died from tumor progression.
88 cer stem cell (CSC) maintenance resulting in tumor progression.
89 thus leading to the upregulation of Slug and tumor progression.
90 etween tumor cells and the stroma to promote tumor progression.
91 oncogenic TGF-beta signaling and subsequent tumor progression.
92 for the dichotomy of TGFbeta function during tumor progression.
93 Rorc(fm-) ILC1s or NK cells fail to inhibit tumor progression.
94 mary transforming proteins in HPV that drive tumor progression.
95 ing growth factor (TGF)-beta and facilitates tumor progression.
96 L2 as a potential therapeutic target against tumor progression.
97 d to decipher their roles in oncogenesis and tumor progression.
98 es identify YAP1 as a downstream effector in tumor progression.
99 18 mRNA in transplanted hepatoblasts delayed tumor progression.
100 ing their behavior is crucial for monitoring tumor progression.
101 oblastoma and the influential role of RD3 in tumor progression.
102 echanism.Angiogenesis is essential for solid tumor progression.
103 may control cellular processes important for tumor progression.
104 hich mediates the degradation of PKM2 during tumor progression.
105 previous associations to various cancers and tumor progression.
106 idences indicate that it is also involved in tumor progression.
107 ogresses and acquires chemoresistance during tumor progression.
108 ellular function in the Wnt-signaling-driven tumor progression.
109 o the regulatory roles of miRNAs and PMPs in tumor progression.
110 of both CCL9 and IL-23 abrogates Myc-induced tumor progression.
112 oposed biosimilar vs trastuzumab for time to tumor progression (41.3% vs 43.0%; -1.7%; 95% CI, -11.1%
113 activity in tumors has been associated with tumor progression after chemotherapy failure, and patien
116 e complex 2-mediated epigenetic silencing in tumor progression and antitumor immunity in primary cuta
119 e genetic and epigenetic events characterize tumor progression and define the identity of the tumors.
120 for target genes associated with pancreatic tumor progression and demonstrated that PLAC8 is strongl
121 EMT) is believed to be important for primary tumor progression and dissemination, whereas a mesenchym
124 indings suggest vascular cells contribute to tumor progression and establish this culture system as a
125 the ability of antiangiogenic drugs to delay tumor progression and extend survival is limited, due to
127 and aberrant vascular network that promotes tumor progression and hinders effective treatment; the m
130 les were effective in significantly delaying tumor progression and improving survival rates in mice m
133 re, we demonstrate that ST18 is critical for tumor progression and maintenance in a mouse model of li
134 t FAM83H-AS1 plays an important role in lung tumor progression and may be potentially used as diagnos
139 hi3l1 is a multifaceted immune stimulator of tumor progression and metastasis whose elaboration and t
140 in LOXL2 has been suggested to contribute to tumor progression and metastasis, but in vivo evidence h
147 s GLUT1), and VEGFA has been associated with tumor progression and poor prognosis of patients with co
150 EAP1-NRF2 cytoprotective pathway to regulate tumor progression and radiochemoresistance, implying tha
151 tein (PrP(C)) is associated with metastasis, tumor progression and recurrence; however, the precise m
152 the colorectal tumor stroma associates with tumor progression and reduced survival time of patients
154 ysis revealed pathways broadly implicated in tumor progression and resistance, such as epithelial-to-
158 hts into the role of exosomal miRNA-mediated tumor progression and suggest a new therapeutic approach
159 ms by which epigenetic regulators can affect tumor progression and suggest that prosenescence therapi
160 tors, and have a pivotal role in the bladder tumor progression and the regulation of stem-like charac
161 UMMARY BACKGROUND DATA: Pre-LT LRT mitigates tumor progression and waitlist dropout in HCC patients w
162 ining whether PERK positively contributes to tumor progression and whether it represents a significan
163 effectors ETV4 and MMP24, is a biomarker of tumor progression and worse outcomes in people with lung
164 ctor (EGF)/neuregulin family are involved in tumor progression and, accordingly, antibodies that inte
167 sion is a potential prognostic biomarker for tumor progression, and that interfering with GNA13-induc
168 lls expanded from PD-1(+) CD8 TILs contained tumor progression, and their efficacy was enhanced by PD
169 , tumor tissue tends to stiffen during solid tumor progression, and tissue stiffness is known to alte
171 ment via c-Kit/stem cell factor and increase tumor progression, angiogenesis, EMT switch, and ECM deg
175 this study provides novel insights into the tumor progression associated with MFN2 deficiency and su
178 ent integrin-mediated pathways that suppress tumor progression, but how integrins can signal to restr
179 erformed a distinctive role as suppressor of tumor progression by cooperating with TAp63 to modulate
180 FD circulation models were designed to mimic tumor progression by escalating flow complexity and chao
181 ve barrier against further TGFbeta-dependent tumor progression by preventing genomic instability.
182 ntrast, epithelial STAT3 ablation attenuated tumor progression by reducing the stromal stiffening and
185 sive sub-clones can contribute to accelerate tumor progression by spreading malignant properties that
188 fibroblasts and prostate cancer cells during tumor progression, clarifying how the tumor microenviron
189 emergence of specific subpopulations during tumor progression corresponded with the onset of seizure
190 roRNA (miRNA) biomarkers in liver injury and tumor progression could improve cancer diagnosis, progno
191 NCoR loss can be propagated, contributing to tumor progression even in the absence of NCoR gene mutat
193 f follow-up, 3- and 5-year local and overall tumor progression-free survival were 96%, 94%, 52%, and
195 ch issues as pseudoresponse and nonenhancing tumor progression from antiangiogenic therapies, and pse
196 irment) and holds promise in differentiating tumor progression from benign causes of enhancement.
198 K3CA and PDK1 protein levels correlated with tumor progression, highlighting the significance of this
199 ber variation (CNV) alters genes involved in tumor progression; however, identification of specific d
200 flammatory mediator IL-32 is associated with tumor progression; however, the mechanisms remain unknow
201 erved in solid tumors and is correlated with tumor progression; however, the underlying mechanism is
203 ngly, engineered deletion of Fes accelerated tumor progression in a BRAFV600E-driven mouse model of m
204 well established that hypoxia contributes to tumor progression in a hypoxia inducible factor-2alpha (
205 comparison, MALT1 deficiency does not affect tumor progression in a mouse model (LSL-K-ras(G12D); CCS
206 gs indicate that R-ketorolac treatment slows tumor progression in an aggressive model of breast cance
208 against cell-surface GRP78 drive TF-mediated tumor progression in an experimental model of prostate c
210 ever, the role of RGC32 in tumorigenesis and tumor progression in colorectal cancer (CRC) has not bee
212 components relate to the different stages of tumor progression in each esophageal cancer subtype will
215 Rictor/mTORC2 signaling drives Akt-dependent tumor progression in HER2-amplified breast cancers, rati
220 ced HSPC infiltration into tumors as well as tumor progression in murine models of melanoma and mamma
222 ish during early tumorigenesis and long-term tumor progression in our previously established inducibl
223 ting protein), a U-box E3 ligase, suppresses tumor progression in ovarian carcinomas by inhibiting ae
225 ronmental changes and, consequently, natural tumor progression in real time without the use of artifi
227 nanoparticle-formulated miRNAs, we inhibited tumor progression in seven mouse xenograft models, inclu
229 ta-catenin activity has a profound impact on tumor progression in this basal model of ErbB2-positive
231 omerization of ILEI is essential for EMT and tumor progression in vivo The structures and the activit
232 To investigate the role of Hic-5 in breast tumor progression in vivo, Hic-5(-/-) mice were generate
238 anoma and demonstrated significantly delayed tumor progression induced by IL-15:IL-15Ralpha-coated na
243 ce in the diagnosis and prognosis of PCa, as tumor progression is associated with changes in fPSA gly
244 inoblastoma (RB) protein inactivation during tumor progression is often associated with acquisition o
245 e major mechanisms by which Muc4 potentiates tumor progression is via its engagement of the ErbB2/HER
246 which contributes to cell transformation and tumor progression, is a prominent feature of malignant c
247 tional capillaries with no flow, a result of tumor progression, limited access to all particles, whil
251 We compared overall survival (OS), local tumor progression (LTP), postoperative complications, an
252 dysregulation either facilitates or impedes tumor progression, making it important to clarify the re
255 t the top of the hierarchy, where they drive tumor progression, metastasis, and chemoresistance.
256 the role of these integrins in angiogenesis, tumor progression, metastasis, and myocardial infarct he
259 s for cancer exosomes in specific aspects of tumor progression: modulation of immune response, tumor
261 amplification were synergistic in promoting tumor progression, PIK3CA mutation was found to have all
262 Secondary outcome measures included time to tumor progression, progression-free and overall survival
264 ugh co-inhibitor expression increases during tumor progression regardless of CD8(+) TILs' antigen spe
268 promoter-associated epiallele shifts during tumor progression showed increased single-cell transcrip
269 sociated fibroblasts (CAFs) as regulators of tumor progression, specifically vascular growth, has onl
270 c cell development and has opposing roles in tumor progression that are dependent on cellular context
271 it (IL-11Ralpha) as a cell surface marker of tumor progression that correlates with poor prognosis in
272 wed that these cells play a critical role in tumor progression that is independent of clinical subtyp
273 tumor microenvironment by directly promoting tumor progression that leads to poor clinical outcomes.
276 l-intrinsic effects of EMT are important for tumor progression, the reciprocal dynamic crosstalk betw
277 ad BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF" by Heidorn and colleague
279 emonstrated essential metabolic processes in tumor progression through the development of a methodolo
280 ecently, both proteins were found to promote tumor progression through the establishment of premetast
281 nd demonstrate that they efficiently inhibit tumor progression, thus identifying this class of compou
282 s of CCND2 markedly correlated with prostate tumor progression to high Gleason score and elevated PSA
286 a promising therapeutic approach to prevent tumor progression.Tumor associated macrophages (TAMs) pr
288 t endogenous ligand for TLR4, which promotes tumor progression via TLR4/NF-kappaB/STAT3 signaling, pr
289 is that plays important roles in metabolism, tumor progression, viral replication, and skin barrier f
295 r distribution changes in vasculature during tumor progression, we combined intra-vital imaging of me
296 w elevated stromal tRNAi(Met) contributes to tumor progression, we generated a mouse expressing addit
297 the stroma may mediate the effects of iAs in tumor progression, which may have future therapeutic imp
299 gene-regulatory regions was observed during tumor progression, with the lowest degree of methylation
300 ficient to blunt tumor initiation and impair tumor progression without compromising IL-6 classic sign
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