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1 iological processes including metastasis and cancer progression.
2 nistic insights into its significant role in cancer progression.
3 de is unlikely to prevent carcinogen-induced cancer progression.
4 potential therapeutic target to alter breast cancer progression.
5 coproteins in pathogen-host interactions and cancer progression.
6 ajor regulators of neuronal excitability and cancer progression.
7 associated with cellular transformation and cancer progression.
8 ical for maintaining stem cell phenotype and cancer progression.
9 as receptors that mediate immune evasion in cancer progression.
10 ulin and insulin receptor signalling promote cancer progression.
11 y, LAT1 significantly contributed to bladder cancer progression.
12 the nervous system plays a critical role in cancer progression.
13 also contribute to chronic inflammation and cancer progression.
14 regulate many biological processes, notably cancer progression.
15 xhibiting oncogenic properties and promoting cancer progression.
16 l tumor microenvironment facilitates ovarian cancer progression.
17 ed interest for its potential role in breast cancer progression.
18 ulated in cancer cells and how it influences cancer progression.
19 growth and metastasis at multiple stages of cancer progression.
20 n transcriptional programs to promote breast cancer progression.
21 ght into the role of gap junctions in breast cancer progression.
22 pproach to discover DNA elements influencing cancer progression.
23 logy, metabolism and immune responses during cancer progression.
24 ation of c-Myc is frequently associated with cancer progression.
25 se, regulates cellular activities, including cancer progression.
26 ies and preferences of a tumor change during cancer progression.
27 signaling and RTK trafficking that controls cancer progression.
28 n, for example, and their products can favor cancer progression.
29 own how mutations in BRG1 contribute to lung cancer progression.
30 e variety of cancers and plays a key role in cancer progression.
31 correlated with HAI-2 levels during prostate cancer progression.
32 s-accelerating kinase with emerging roles in cancer progression.
33 , the latter of which catalogs genes driving cancer progression.
34 s oscillatory expression of DeltaNp63 during cancer progression.
35 ls the tumour microenvironment and restrains cancer progression.
36 , infiltrating sympathetic nerves facilitate cancer progression.
37 ve therapeutic targets for controlling liver cancer progression.
38 highlighting a critical role of cortactin in cancer progression.
39 the axis of gene expression during prostate cancer progression.
40 wing them to play a cancer-promoting role in cancer progression.
41 and that these microbiota can contribute to cancer progression.
42 Tissue stiffening plays a critical role in cancer progression.
43 dedifferentiation is a key mechanism driving cancer progression.
44 bition of aggressive mesenchymal-like breast cancer progression.
45 lay a crucial role in normal development and cancer progression.
46 f functional relevance of biomarker genes to cancer progression.
47 including innate immune responses are key in cancer progression.
48 ncer cells, both in early and late stages of cancer progression.
49 epithelial-mesenchymal transition (EMT), and cancer progression.
50 tions may inhibit certain stages of prostate cancer progression.
51 play important roles in preventing prostate cancer progression.
52 ication that is increasingly associated with cancer progression.
53 on and metastasis is a universal hallmark of cancer progression.
54 IL23-mediated Th17 expansion associated with cancer progression.
55 , cellular and biophysical features of human cancer progression.
56 MT processes and discuss their properties in cancer progression.
57 phosphatase activity to promote endometrial cancer progression.
58 display heterogeneous features that support cancer progression.
59 OR2B6 to be potentially correlated to breast cancer progression.
60 ng a non-cell autonomous mechanism for colon cancer progression.
61 se distribution, suggesting a driver role in cancer progression.
62 upporting the expansion of Th17 cells during cancer progression.
63 64-3p and their target genes are involved in cancer progression.
64 onmental conditions to metabolically benefit cancer progression.
65 us posttranslational effectors that can tune cancer progression.
66 umor cells (CTCs) play a fundamental role in cancer progression.
67 tent and severely repressed in vivo prostate cancer progression.
68 ages play important and diverse roles during cancer progression.
69 at genomic instability is a prerequisite for cancer progression.
70 apillomavirus (HPV) infection and associated cancer progression.
71 molecule consistently associated with colon cancer progression.
72 ic aids and treatment strategies to mitigate cancer progression.
73 skeleton can lead to birth defects or enable cancer progression.
74 eased tissue stiffness is a driver of breast cancer progression.
75 ce a positive feedback regulation in gastric cancer progression.
76 ancer cells has a driving role in pancreatic cancer progression.
77 table example of such signaling diversity in cancer progression.
78 cross-talk surfaced as a key contributor to cancer progression.
79 d in inflammation, autoimmune disorders, and cancer progression.
80 unctions of gammadelta T cell subsets during cancer progression.
81 oop that expands the glycocalyx and furthers cancer progression.
82 ned proliferation is a significant driver of cancer progression.
83 ll processes required for transformation and cancer progression.
84 ession activates serine synthesis to promote cancer progression.
85 n oscillatory expression of DeltaNp63 during cancer progression.
86 a transmembrane protein that is critical for cancer progression.
87 ausible mechanism linking diabetes and liver cancer progression.
88 CH-1-deficiency induced inhibition on breast cancer progression.
89 platelets and a tumor may promote or prevent cancer progression.
90 unanticipated role of Norrin in human brain cancer progression.
91 pression of EMT regulators to promote breast cancer progression.
92 d GPCR-targeted drugs may promote or inhibit cancer progression.
93 ization of Cyclin D1 to drive cell-cycle and cancer progression.
94 ves expression of genes for survival but not cancer progression.
95 growth and metastasis and therefore promotes cancer progression.
96 may in part explain how obesity drives colon cancer progression.
97 ot significantly reduce the risk of prostate cancer progression.
98 hey mediate cellular activities important in cancer progression.
99 the PI3K/AKT pathway, two events crucial for cancer progression.
100 ion and may contribute to ER-positive breast cancer progression.
101 ting in activation of AR-driven pathways and cancer progression.
102 dation of tryptophan in mRNA translation and cancer progression.
103 ng carcinogenesis and cellular events during cancer progression.
104 e underlying mechanisms by which they affect cancer progression.
105 cell growth and development, metabolism, and cancer progression.
106 abnormalities in the vasculature that foster cancer progression(5,6); however, neutralization of proa
108 f a potential role of ferritin in colorectal cancer progression, an analysis of The Cancer Genome Atl
109 For a fundamental understanding of lung cancer progression and an exploration of therapeutic opt
110 mitochondria play a multifunctional role in cancer progression and Ca(2+) signaling is remodeled in
111 currence positively correlates with prostate cancer progression and castration-resistant prostate can
112 Metastasis is the most devastating stage of cancer progression and causes the majority of cancer-rel
113 mesenchymal transition, enhancing colorectal cancer progression and chemoresistance both in vitro and
114 sion repair (BER) is increased with prostate cancer progression and correlates with poor prognosis.
116 ghts into the opposing roles of Daple during cancer progression and define the G-protein regulatory G
117 epithelial-mesenchymal transition (EMT) for cancer progression and drug resistance remains to be ful
119 etabolism reprogramming is critical for both cancer progression and effective immune responses in the
120 ne and miRNA expression profiling focused on cancer progression and EMT, and metabolomics by mass spe
122 have uncovered an important role for EZH2 in cancer progression and have suggested that it may be a u
123 on on why metabolic properties evolve during cancer progression and how this information might be use
124 xcessive and abnormal vascularity that fuels cancer progression and immunosuppression, and also induc
126 mortality that tracks five stages of breast cancer progression and incorporates the effects of age o
127 ng of many immune escape contexts, including cancer progression and intracellular pathogenic infectio
129 ryonic program frequently reactivated during cancer progression and is implicated in cancer invasion
130 eract with different protein partners during cancer progression and may exhibit significant function-
131 thetic nerves may have a dichotomous role in cancer progression and may induce Wnt-beta-catenin signa
132 nomodulatory role of the neuroglial cells in cancer progression and metastasis and the response to th
133 axis), however, their role as a regulator of cancer progression and metastasis is poorly understood.
135 ere the target genes showed association with cancer progression and metastasis with statistical signi
136 vin, G3BP2, and TWIST1 that regulates breast cancer progression and metastasis, and suggest that the
137 secretion of cancer exosomes, which promote cancer progression and metastasis, may not only accelera
149 n a tissue specific manner, as a key step of cancer progression and pre-metastatic niche formation.
150 riptional regulation in suppressing prostate cancer progression and provide a mechanistic framework f
152 echanism for cancer cell survival leading to cancer progression and resistance, and provide a potenti
154 MUC1) tumor antigen, a biomarker for ovarian cancer progression and response to therapy, using contra
155 dentify Norrin as a modulator of human brain cancer progression and reveal an unanticipated Notch-med
156 prove identification of patients at risk for cancer progression and selection of additional therapy.
157 n signaling axis that is critical for breast cancer progression and suggest a new strategy for therap
158 proteins become upregulated with pancreatic cancer progression and that this system of proteins can
159 ered BCAA metabolism have been implicated in cancer progression and the key proteins in the BCAA meta
163 nce of the stromal tumor microenvironment in cancer progression and therapeutic responses, effects on
164 Vs) are emerging as strategies for informing cancer progression and therapies, since the lipid conten
165 rview of the impact of lineage plasticity on cancer progression and therapy resistance, with a focus
167 nvironment (TME) plays a significant role in cancer progression and thus modeling it will advance our
168 the impact of these chemoresistant cells in cancer progression and to improve patient outcomes with
174 ifies CDCP1 as a powerful driver of prostate cancer progression and uncovers different potential ther
175 amily of zinc-dependent enzymes that promote cancer progression and undesired inflammation under path
176 ion of miRNA expression may influence breast cancer progression, and experimental evidence suggests t
177 I editing as an important pathway in thyroid cancer progression, and highlight RNA editing as a poten
178 entiation, was upregulated during pancreatic cancer progression, and its genetic or pharmacologic inh
179 sm through which UPEC contributes to bladder cancer progression, and may provide potential therapeuti
180 lpha/2alpha functions associated with breast cancer progression, and may provide potential therapeuti
181 the role of plasticity in initiating cancer, cancer progression, and metastasis and in developing the
182 n about CAF subtypes, the roles they play in cancer progression, and molecular mediators of the CAF "
183 prognostic outcomes, increased frequency of cancer progression, and poor responses to chemotherapy.
184 r considering the various mechanisms driving cancer progression, and the same might be useful for wou
185 ation are a critical component of colorectal cancer progression, and they are used as reliable progno
188 ociated with purinergic signaling, including cancer progression, apoptotic cell clearance, inflammati
190 D4(+) T cells, but not CD8(+) T cells, halts cancer progression as a result of tissue healing and rem
191 s manuscript defines a novel role of E2F2 in cancer progression beyond cell cycle and could impact pa
193 ing it in the active state to enhance breast cancer progression, but also rendering the cells highly
194 he adjacent normal epithelium contributes to cancer progression, but its regulators have remained elu
196 ts (CAF) play a critical biophysical role in cancer progression, but the precise pro-metastatic mecha
197 l adhesion complex, has been associated with cancer progression, but the underlying mechanisms are po
198 e chemoattractant protein-1 (MCP-1) promotes cancer progression by directly stimulating tumor cell pr
199 l stem cells (MSCs) drive accelerated breast cancer progression by inducing differentiation of monocy
201 RNAs induce the activation of AKT to promote cancer progression by regulating the nuclear to cytoplas
202 the tumour microenvironment further promotes cancer progression by shaping the architecture of the tu
203 mechanisms whereby myeloid cells drive human cancer progression by thwarting protective immunity and
204 g the sequence of mutation occurrence during cancer progression can assist early and accurate diagnos
205 single gene (Slit2) can promote or suppress cancer progression depending on its cellular source.
206 iome-derived agonists, may reduce or enhance cancer progression depending on the composition of dieta
208 level of NO in breast cells plummets during cancer progression due to reduction of the NO synthase c
209 As EDN1 and its receptor (EDNR) is linked to cancer progression, EDNR-antagonists have been evaluated
210 ironment plays a critical regulatory role in cancer progression, especially in central nervous system
212 its role in immunity, cancer initiation, and cancer progression has evolved significantly over the pa
213 extensively, and the role of L1 elements in cancer progression has garnered interest in recent years
214 nisms underlying the role of mitochondria in cancer progression has potential implications in the dev
218 NAT1 has also been implicated in breast cancer progression however the exact role of NAT1 remain
219 everal proteases that play critical roles in cancer progression; however, the expression or function
220 idence of citrullination being in control of cancer progression; however, there is no comprehensive o
222 a(2+) entry, and eventually promoted gastric cancer progression in a Ca(2+) signaling-dependent manne
223 acrophages have been shown to promote breast cancer progression in advanced disease and more recently
224 ding proteins relevant for tumorigenesis and cancer progression in archival patient-derived tumor tis
225 M5B in epigenetic dysregulation and prostate cancer progression in cultured cells and in mouse models
226 The depletion of PHF8 significantly reduced cancer progression in GC cells and in mouse xenografts.
227 wnregulation of genes associated with breast cancer progression in secretome-cultured TNBC cells.
228 se of this intervention to decrease prostate cancer progression in this population, although the stud
229 l human leukocyte antigen-G (HLA-G) promotes cancer progression in various malignancies including epi
233 es the multiple roles of mutant ER in breast cancer progression, including constant ER activity and s
234 has many reported substrates with a role in cancer progression, including FOXO4, MDM2, N-Myc, and PT
235 uses on interrogating biomarkers of prostate cancer progression, including gene signatures that corre
240 tion of molecular alterations driving breast cancer progression is critical for the development of ef
241 e, the putative role of GCNT2/I-branching in cancer progression is discussed, including exciting insi
245 nderstanding of the role of this organism in cancer progression is limited, in part due to challenges
252 y of the N-MYC transcription factor to drive cancer progression is well demonstrated in neuroblastoma
253 is associated with reduced risk of prostate cancer progression, largely attributed to the biological
255 -catenin activation plays a critical role in cancer progression, metastasis, and drug resistance.
256 osine kinases (RTK) has been associated with cancer progression, metastasis, and drug resistance.
261 A alterations are passengers acquired during cancer progression or can act as tumorigenic drivers is
262 domisation to the initial date of documented cancer progression or death, whichever occurred first.
264 e the migration of CTCs is an early event in cancer progression, patients who still have tumor-free l
265 -kappaB are all among top crucial factors in cancer progression, pharmacological disruption of this p
266 ane rafts but can go into the nucleus during cancer progression, probably acquiring different signali
273 suppressor Nischarin in exosome biology and cancer progression.See related article by Maziveyi et al
274 components of multigenic loci in regulating cancer progression.See related commentary by Calin, p.
275 Using this approach, we show that during cancer progression specific APA profiles are established
276 proteoglycans take part in crucial events of cancer progression, such as epithelial-mesenchymal trans
277 usion-enriched RNAs encode factors linked to cancer progression, such as the RAB13 GTPase and the NET
278 of MMA represents a link between ageing and cancer progression, suggesting that MMA is a promising t
279 , human cells adopted phenotypes relevant to cancer progression, suggesting that we can define the re
280 promoters of lncRNAs play a pivotal role in cancer progression, suggesting the importance of epigene
281 ations can facilitate genome instability and cancer progression that are beyond the preexisting proli
282 We applied per-day hazard ratios (HRs) for cancer progression that we generated from observational
283 evidence has implicated GPCRs as drivers of cancer progression, therapeutic resistance, and metastas
285 factor (TF) STAT3 contributes to pancreatic cancer progression through its regulatory roles in both
289 at DZIP3 is a novel driver of cell-cycle and cancer progression via its control of Cyclin D1 mRNA and
290 1 as a key player in genome stability during cancer progression via its repression of POLQ.See relate
291 ial p38alpha promotes Kras(G12V)-driven lung cancer progression via maintenance of cellular self-grow
292 mine the relationship between aneuploidy and cancer progression, we analyzed a series of congenic cel
293 inoma mouse model and models of human breast cancer progression, we identified two TAp63-regulated on
294 d glioblastoma, genes highly associated with cancer progression were identified and designated as pro
295 novel YTHDF1-EIF3C axis critical for ovarian cancer progression which can serve as a target to develo
297 Further refinement of a roadmap of breast cancer progression will facilitate the development of im
298 for targeting the CSCs hypothesized to drive cancer progression - with some success in certain malign
299 appaB is a key regulator of inflammation and cancer progression, with an important role in leukemogen
300 tabolic dysregulation is a known hallmark of cancer progression, yet the oncogenic signals that promo