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1 ust tumour fitness maintained throughout the tumour progression.
2 ction during consecutive stages of multistep tumour progression.
3 oid-derived suppressor cell expansion during tumour progression.
4 nderlying epithelial development, growth and tumour progression.
5 nthesis of toxic deoxysphingolipids and slow tumour progression.
6 regulation of miRNA biogenesis and increased tumour progression.
7 er advantageous characteristics that promote tumour progression.
8 essed in prostate cancer and associated with tumour progression.
9 n receptors and Toll-like receptors, blocked tumour progression.
10 epigenetic alterations that drive or reflect tumour progression.
11 apoptosis result, forming a barrier against tumour progression.
12 Chemotherapy resistance frequently drives tumour progression.
13 ubsequent development of drug resistance and tumour progression.
14 ory factors, both in the neural crest and in tumour progression.
15 nce evasion of immune surveillance to permit tumour progression.
16 epithelial growth but are also implicated in tumour progression.
17 -mediated senescence or apoptosis to prevent tumour progression.
18 ageing microenvironment in the promotion of tumour progression.
19 furthermore, essential to wound healing and tumour progression.
20 genomes for genetic changes associated with tumour progression.
21 ion of cell proliferation, angiogenesis, and tumour progression.
22 iveness, suggesting that MPP8 contributes to tumour progression.
23 gesting that it has an important function in tumour progression.
24 glycoprotein, which has an important role in tumour progression.
25 at these changes act to retard, not promote, tumour progression.
26 olorectal cancer (CRC) and may contribute to tumour progression.
27 h and metastasis; this is a new mechanism of tumour progression.
28 alterations suggested possible mechanisms of tumour progression.
29 older people and functions as a mediator of tumour progression.
30 The primary endpoint was time to tumour progression.
31 on to activate EphB4 signalling will inhibit tumour progression.
32 umour-induced anorexia and leads to enhanced tumour progression.
33 aptation may mirror those of oncogenesis and tumour progression.
34 both tissue-specific cancer development and tumour progression.
35 rable tissue environment for carcinogens and tumour progression.
36 relationship between HPV, gap junctions and tumour progression.
37 This is thought to be the driving force for tumour progression.
38 that inflammation is a critical component of tumour progression.
39 nological regression in melanoma, stimulates tumour progression.
40 pair deficient tumours and are implicated in tumour progression.
41 cess due to low tumour penetrance or limited tumour progression.
42 ivation domain also appear to play a role in tumour progression.
43 involvement of the encoded protein in breast tumour progression.
44 pts liver metabolic homeostasis and promotes tumour progression.
45 from pre-existing vessels, is essential for tumour progression.
46 y is correlated with cellular senescence and tumour progression.
47 l in normal tissues and in various stages of tumour progression.
48 has been linked to cellular immortality and tumour progression.
49 of glioma TrkB expression robustly inhibits tumour progression.
50 rs that shape both immune cell behaviour and tumour progression.
51 croenvironment, serving diverse functions in tumour progression.
52 rocytic cholesterol efflux, via ABCA1, halts tumour progression.
53 rly characterised cells that variably impact tumour progression.
54 suggesting a link between polyclonality and tumour progression.
55 the mitochondrial stress response (MSR) with tumour progression.
56 cer cells can colonize lymph nodes and drive tumour progression.
57 hat enable timely and accurate prediction of tumour progression.
58 ANXA1-FPR1 as a driver of immune evasion and tumour progression.
59 cancers many deregulations liable to promote tumour progression.
60 play roles in both anti-cancer immunity and tumour progression.
61 how they influence therapeutic outcomes and tumour progression.
62 ivity of PMN-MDSCs and substantially delayed tumour progression.
63 dent or ER-independent mechanisms that drive tumour progression.
64 to assess the collagen fibre changes during tumour progression.
65 ellular matrix (ECM) plays a pivotal role in tumour progression.
66 , fibroblasts and immune cells, can modulate tumour progression.
67 sly replenished by thymic progenitors during tumour progression.
68 can be pharmacologically modulated to limit tumour progression.
69 xtracellular matrix (ECM) stiffening promote tumour progression.
70 s malignant synaptic plasticity and augments tumour progression.
71 are refractory to targeted agents and drive tumour progression.
72 , can result in malignant transformation and tumour progression.
73 ation rates are compatible with survival and tumour progression.
74 cells to bypass two distinct barriers during tumour progression.
75 and cell motility/contractility help mediate tumour progression.
76 ry factors are important factors that affect tumour progression.
77 melanoma diagnosis and in the monitoring of tumour progression.
78 with dasatinib/quercetin or ABT-263 inhibits tumour progression.
79 response, duration of response, and time to tumour progression.
80 donor cells instead of exosomes, inhibiting tumour progression.
81 ermal growth factor receptor (EGFR) to drive tumour progression.
82 their upregulation may contribute to breast tumour progression.
83 that has been implicated in angiogenesis and tumour progression.
84 o a proliferation of phylogenetic studies of tumour progression.
85 (alpha and beta) have been shown to support tumour progression.
86 mour suppressor miRNA into exosomes promotes tumour progression.
87 n of Wnt production or signalling suppressed tumour progression.
88 filtration may have clinical implications in tumour progression.
89 a type II collagen-rich matrix that promotes tumour progression.
90 at maintain cancer stem cells are crucial to tumour progression.
91 malignant tumour architectures and influence tumour progression.
92 ue movement during embryonic development and tumour progression.
93 tivation of genes driving EMT and ultimately tumour progression.
94 l instability are cardinal events that drive tumour progression.
95 ogenesis, fibrosis, cholestatic pruritus and tumour progression.
96 enescence-associated secretory phenotype and tumour progression.
97 r efficacy than monotherapies in controlling tumour progression.
98 aling the dual function of EZH2 in promoting tumour progression.
100 nger RNA storage(3), synaptic plasticity(4), tumour progression(5,6) and neurodegeneration(7-9).
101 dogenous FOXM1 (isoform B) expression during tumour progression across a panel of normal primary NOK
102 BRAF(V600E)-mutant NSCLC who had documented tumour progression after at least one previous platinum-
103 dicting cancer occurrence earlier, assessing tumour progression, aiding patient stratification and pr
104 nt studies suggest it can also contribute to tumour progression, although the underlying mechanisms a
105 pe features that underlie the differences in tumour progression and aggression between the zones.
108 kade and genetic Lifr deletion markedly slow tumour progression and augment the efficacy of chemother
109 s is crucial to determine the events driving tumour progression and better understand tumour adaptati
110 MMTV-PyMT transgenic mouse model of mammary tumour progression and clinical breast cancer samples.
111 gy metabolism has been hijacked to encourage tumour progression and eventually metastasis in breast c
112 evaluated clinically and by neuroimaging for tumour progression and evidence of necrosis, vasculopath
113 r quantitative LOH/CNV analysis for tracking tumour progression and evolution with a higher efficienc
117 tumour-associated inflammation that supports tumour progression and immune resistance to therapy.
120 ystem enhances antitumour immunity, inhibits tumour progression and improves the efficacy of anti-PD-
121 ole-body glycaemic control may contribute to tumour progression and incidence of type 2 diabetes in s
122 tion of ATF4 significantly delays MYC-driven tumour progression and increases survival in mouse model
123 ion 2) enhances cell proliferation, promotes tumour progression and inhibits the activity of neurogen
124 w blood vessels, is an essential process for tumour progression and is an area of significant therape
125 high levels during embryonic development and tumour progression and is important for cell growth.
126 cell death is a hallmark of cancer, driving tumour progression and limiting therapeutic efficacy.
128 anical forces and EV dynamics contributes to tumour progression and links EVs to key disease hallmark
131 reatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains thei
132 3306, on neuroblastoma cell differentiation, tumour progression and metastasis by utilising a 3R comp
134 ith metastatic lung cancer the mechanisms of tumour progression and metastasis remain largely unchara
135 esized to represent the driving force behind tumour progression and metastasis, making them attractiv
136 The E3 ubiquitin-ligase Hakai is involved in tumour progression and metastasis, through the regulatio
143 h as infections due to viruses and bacteria, tumour progression and migration, and inflammation proce
144 e-specific suppressive roles of p53 in early tumour progression and offer insights into clonal growth
145 tive is to further understand differences in tumour progression and physiology between animal models
146 ma induce transcriptional changes related to tumour progression and pro-metastatic phenotypes in targ
148 he contribution of epigenomic alterations to tumour progression and relapse is not well characterized
149 id cell subsets and how they are involved in tumour progression and resistance to cancer therapies, i
151 ma (cancer-associated fibroblasts) influence tumour progression and response to therapeutics; little
154 hibiting USP13 remarkably suppresses ovarian tumour progression and sensitizes tumour cells to the tr
155 s suppressive activity of PMN-MDSCs, reduces tumour progression and synergizes with immune checkpoint
158 indicate that miRNAs act together to promote tumour progression and that future therapeutic strategie
159 to evolutionary pressures is fundamental to tumour progression and the development of therapeutic re
162 e distinct metabolic processes that regulate tumour progression and therapy resistance by transducing
164 e tumour initiation events, those that drive tumour progression and those that confer lethality.
165 h glioblastoma is how to distinguish between tumour progression and treatment effects, especially whe
166 he critical role of telomerase activation in tumour progression and tumour maintenance has been well
167 ETV5, and its overexpression suppresses EPN tumour progression and tumour-associated network hyperac
168 t are independent yet synergistic drivers of tumour progression and underlie therapeutic resistance.
169 hat there was an important role for PI3Ks in tumour progression and, particularly, in the control of
171 onsistently lost the wild-type allele during tumour progression, and are therefore deficient in BRCA1
172 mutations that are thought to contribute to tumour progression, and eight were new mutations present
173 ector T-cell tumour infiltration, slows down tumour progression, and improves the therapeutic efficac
174 s an adrenergic phenotype that can stimulate tumour progression, and is a potential target for antica
175 associated with both tumour suppression and tumour progression, and its role in tumorigenesis seems
176 g networks and cell interactions critical in tumour progression, and provides a powerful new strategy
177 te telomerase is activated in late stages of tumour progression, and show for the first time that the
178 r microenvironment (TME) plays a key role in tumour progression, and soluble and cellular TME compone
179 er nonessential amino acids are critical for tumour progression, and strategies to limit their availa
180 of KRASG12D-driven CRC significantly alters tumour progression, and suppresses metastasis through mo
181 pment of a vascular network are required for tumour progression, and they involve the release of angi
182 strategy to reduce OPG incidence or mitigate tumour progression, and underscore the role of Nf1mutati
183 gulates EGFR cell surface retention to drive tumour progression, and we validate the therapeutic pote
187 DMX protein are strongly selected for during tumour progression as a mechanism to suppress the p53 re
188 st that restoration of pathways important in tumour progression, as opposed to initiation, may lead t
189 to enhance antitumour immunity that prevents tumour progression, as well as improving the efficacy of
190 e with metformin inhibits obesity-associated tumour progression associated with a marked decrease in
191 king p53, loss of autophagy no longer blocks tumour progression, but actually accelerates tumour onse
192 the acquisition of alterations that lead to tumour progression, but also, in the context of p53 rest
193 play critical roles in mortality as well as tumour progression, but much remains unknown about the u
194 ost from the development of cancer and alter tumour progression by driving the outgrowth of tumour ce
195 togenic diet (KD) are often thought to limit tumour progression by lowering blood glucose and insulin
196 prostate cancer, dietary SFI contributes to tumour progression by mimicking MYC over expression, set
197 mouse mammary tumour model inhibits mammary tumour progression by reducing the proliferative potenti
198 tionally, PIEZO1 was shown to be involved in tumour progression by serving as the central checkpoint
199 of specific apoA-I mimetic peptide (D-4F) on tumour progression by using mammary tumour virus-polyoma
201 proaches to identify molecular mechanisms of tumour progression, causal relationships between genes a
203 lating disease-risk in humans by suppressing tumour progression, decreasing inflammation and influenc
204 cytosis, which drives invasive migration and tumour progression, demonstrating that our high-content
205 ecificity of routine imaging for identifying tumour progression early or in a timely manner is poor d
206 ultiple tumours and are equipped to regulate tumour progression either directly by interacting with t
207 though increasing evidence demonstrates that tumour progression entails chromatin-mediated changes su
208 nimal-morbidity chemotherapy (in the case of tumour progression)-for paediatric patients with desmoid
209 4;14) translocation, somatic mutation during tumour progression frequently generates in FGFR3 protein
210 s of the UPR have key roles in every step of tumour progression: from cancer initiation to tumour gro
211 of the intrinsic cellular mechanisms driving tumour progression has considerably expanded, little is
214 Attempts to intervene at an early stage of tumour progression have not proven cost effective, altho
216 mework for evaluating treatment efficacy and tumour progression in clinical studies of paediatric bra
217 uch minority populations are associated with tumour progression in human patients, specific targeting
219 ic expression of neuronal receptors promotes tumour progression in many cancer types(1,2); neuroendoc
224 tibody-mediated blockade of BTNL2 attenuates tumour progression in multiple in vivo murine tumour mod
225 eloid-cell VEGF-A resulted in an accelerated tumour progression in multiple subcutaneous isograft mod
227 Here we demonstrate that an HFD promotes tumour progression in the small intestine of genetically
230 igand interaction plays an essential role in tumour progression, in embryonic tissue morphogenesis an
231 ant CpG methylation changes occurring during tumour progression include the loss (hypomethylation) an
232 ndicates that tumour neo-innervation propels tumour progression, inhibits tumour-related pro-inflamma
235 etic state of metastatic cells, we find that tumour progression is coupled with the activation of onc
240 bute gain-of-function activities that impact tumour progression, it remains unclear whether the delet
241 er the optimal Wnt level might change during tumour progression, leading to selection for more than t
242 Here, we report that SFTSV-NSs targets the tumour progression locus 2 (TPL2)-A20-binding inhibitor
243 cells and their appreciable contribution to tumour progression make them attractive immunotherapeuti
246 e surrounding microenvironment contribute to tumour progression, metastasis and recurrence(1-3).
247 ion that enables tumour evolution, including tumour progression, metastasis and resistance to treatme
248 orectal cancer, EMT has an important role in tumour progression, metastasis, and drug resistance.
249 for research including real-time studies of tumour progression, metastasis, and drug-response evalua
250 tabolic rewiring in malignant cells supports tumour progression not only by providing cancer cells wi
251 to as 'non-oncogene addiction'), to support tumour progression not only by providing malignant cells
252 s (range 0.4-10.4), 23 patients had died and tumour progression noted in 36, including local (n=14),
254 s in the aged microenvironment contribute to tumour progression, offering new possibilities for the d
255 ying expansion of the host vasculature, with tumour progression often correlated with vascular densit
256 ubsequent development of drug resistance and tumour progression.Oncogene advance online publication,
259 s not achieved, adjuvant therapy might delay tumour progression or recurrence, especially in high-ris
261 ollowed by 2 weeks without treatment), until tumour progression or unacceptable toxic effects arose.
263 a based on guidance for the determination of tumour progression outlined by the immune-related respon
265 telomere maintenance, immune regulation and tumour progression, providing deeper insight into the pa
266 opulations genetically diversify, leading to tumour progression, relapse and resistance to therapy.
271 act as a functional stromal barrier against tumour progression, representing a unique example of tis
272 iency, is known to be associated with breast tumour progression, resistance to conventional therapies
273 from the time of tumour initiation or after tumour progression, resulted in significantly reduced tu
274 h antibiotics completely blocked HFD-induced tumour progression, suggesting that distinct shifts in t
275 e-regulated pathways are known to also drive tumour progression, suggesting that metabolic reprogramm
276 mice is not sufficient to trigger malignant tumour progression, suggesting that other alterations ar
277 lic reprogramming is tightly associated with tumour progression, the effect of metabolic regulatory c
280 idence supports key contributions of MDSC to tumour progression through both immune-mediated mechanis
281 ia (ADM) during tumour initiation as well as tumour progression through intrinsic effects on prolifer
283 osphorylation and fuel lipogenesis, enabling tumour progression through metabolic reprogramming.
285 ntly, BAG-1 is thought to enhance colorectal tumour progression through promoting tumour cell surviva
287 lation of Bim expression was associated with tumour progression towards an anchorage-independent phen
288 t of additional mutations in key genes drive tumour progression towards more aggressive and less diff
289 s of the p53 checkpoint may be essential for tumour progression triggered by mutations in BRCA2.
291 nvasion view the normal tissue as inhibiting tumour progression via immune modulation or spatial cons
294 lthough c-Src has been implicated in colonic tumour progression, we demonstrate here that in the aden
295 f human cancers and multiple mouse models of tumour progression, we revealed that these two lncRNAs i
297 kinase activity, and effectively accelerates tumour progression when activated in advanced lung adeno
298 ypes raising the possibility of exacerbating tumour progression when targeting Rac1 in a clinical set
299 immune cell steroidogenesis restricted TNBC tumour progression with a significant reduction in immun