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1 and cell motility/contractility help mediate tumour progression.
2 ermal growth factor receptor (EGFR) to drive tumour progression.
3 genomes for genetic changes associated with tumour progression.
4 ion of cell proliferation, angiogenesis, and tumour progression.
5 iveness, suggesting that MPP8 contributes to tumour progression.
6 gesting that it has an important function in tumour progression.
7 glycoprotein, which has an important role in tumour progression.
8 at these changes act to retard, not promote, tumour progression.
9 their upregulation may contribute to breast tumour progression.
10 olorectal cancer (CRC) and may contribute to tumour progression.
11 h and metastasis; this is a new mechanism of tumour progression.
12 alterations suggested possible mechanisms of tumour progression.
13 The primary endpoint was time to tumour progression.
14 on to activate EphB4 signalling will inhibit tumour progression.
15 umour-induced anorexia and leads to enhanced tumour progression.
16 aptation may mirror those of oncogenesis and tumour progression.
17 both tissue-specific cancer development and tumour progression.
18 rable tissue environment for carcinogens and tumour progression.
19 relationship between HPV, gap junctions and tumour progression.
20 This is thought to be the driving force for tumour progression.
21 that inflammation is a critical component of tumour progression.
22 nological regression in melanoma, stimulates tumour progression.
23 pair deficient tumours and are implicated in tumour progression.
24 cess due to low tumour penetrance or limited tumour progression.
25 ivation domain also appear to play a role in tumour progression.
26 involvement of the encoded protein in breast tumour progression.
27 from pre-existing vessels, is essential for tumour progression.
28 y is correlated with cellular senescence and tumour progression.
29 l in normal tissues and in various stages of tumour progression.
30 that has been implicated in angiogenesis and tumour progression.
31 has been linked to cellular immortality and tumour progression.
32 o a proliferation of phylogenetic studies of tumour progression.
33 (alpha and beta) have been shown to support tumour progression.
34 mour suppressor miRNA into exosomes promotes tumour progression.
35 n of Wnt production or signalling suppressed tumour progression.
36 filtration may have clinical implications in tumour progression.
37 ry factors are important factors that affect tumour progression.
38 a type II collagen-rich matrix that promotes tumour progression.
39 at maintain cancer stem cells are crucial to tumour progression.
40 ue movement during embryonic development and tumour progression.
41 tivation of genes driving EMT and ultimately tumour progression.
42 l instability are cardinal events that drive tumour progression.
43 ogenesis, fibrosis, cholestatic pruritus and tumour progression.
44 r efficacy than monotherapies in controlling tumour progression.
45 aling the dual function of EZH2 in promoting tumour progression.
46 ction during consecutive stages of multistep tumour progression.
47 melanoma diagnosis and in the monitoring of tumour progression.
48 oid-derived suppressor cell expansion during tumour progression.
49 nderlying epithelial development, growth and tumour progression.
50 response, duration of response, and time to tumour progression.
51 regulation of miRNA biogenesis and increased tumour progression.
52 er advantageous characteristics that promote tumour progression.
53 n receptors and Toll-like receptors, blocked tumour progression.
54 epigenetic alterations that drive or reflect tumour progression.
55 donor cells instead of exosomes, inhibiting tumour progression.
56 apoptosis result, forming a barrier against tumour progression.
57 Chemotherapy resistance frequently drives tumour progression.
58 ubsequent development of drug resistance and tumour progression.
59 ory factors, both in the neural crest and in tumour progression.
60 nce evasion of immune surveillance to permit tumour progression.
61 epithelial growth but are also implicated in tumour progression.
62 -mediated senescence or apoptosis to prevent tumour progression.
63 furthermore, essential to wound healing and tumour progression.
64 dogenous FOXM1 (isoform B) expression during tumour progression across a panel of normal primary NOK
65 BRAF(V600E)-mutant NSCLC who had documented tumour progression after at least one previous platinum-
66 nt studies suggest it can also contribute to tumour progression, although the underlying mechanisms a
68 MMTV-PyMT transgenic mouse model of mammary tumour progression and clinical breast cancer samples.
69 r quantitative LOH/CNV analysis for tracking tumour progression and evolution with a higher efficienc
71 tumour-associated inflammation that supports tumour progression and immune resistance to therapy.
72 ion 2) enhances cell proliferation, promotes tumour progression and inhibits the activity of neurogen
73 w blood vessels, is an essential process for tumour progression and is an area of significant therape
74 high levels during embryonic development and tumour progression and is important for cell growth.
76 ith metastatic lung cancer the mechanisms of tumour progression and metastasis remain largely unchara
77 esized to represent the driving force behind tumour progression and metastasis, making them attractiv
81 h as infections due to viruses and bacteria, tumour progression and migration, and inflammation proce
82 e-specific suppressive roles of p53 in early tumour progression and offer insights into clonal growth
83 tive is to further understand differences in tumour progression and physiology between animal models
84 he contribution of epigenomic alterations to tumour progression and relapse is not well characterized
85 ma (cancer-associated fibroblasts) influence tumour progression and response to therapeutics; little
88 hibiting USP13 remarkably suppresses ovarian tumour progression and sensitizes tumour cells to the tr
91 indicate that miRNAs act together to promote tumour progression and that future therapeutic strategie
92 to evolutionary pressures is fundamental to tumour progression and the development of therapeutic re
94 he critical role of telomerase activation in tumour progression and tumour maintenance has been well
95 hat there was an important role for PI3Ks in tumour progression and, particularly, in the control of
96 onsistently lost the wild-type allele during tumour progression, and are therefore deficient in BRCA1
97 mutations that are thought to contribute to tumour progression, and eight were new mutations present
98 ector T-cell tumour infiltration, slows down tumour progression, and improves the therapeutic efficac
99 associated with both tumour suppression and tumour progression, and its role in tumorigenesis seems
100 te telomerase is activated in late stages of tumour progression, and show for the first time that the
101 pment of a vascular network are required for tumour progression, and they involve the release of angi
102 gulates EGFR cell surface retention to drive tumour progression, and we validate the therapeutic pote
105 DMX protein are strongly selected for during tumour progression as a mechanism to suppress the p53 re
106 st that restoration of pathways important in tumour progression, as opposed to initiation, may lead t
107 to enhance antitumour immunity that prevents tumour progression, as well as improving the efficacy of
108 e with metformin inhibits obesity-associated tumour progression associated with a marked decrease in
109 king p53, loss of autophagy no longer blocks tumour progression, but actually accelerates tumour onse
110 the acquisition of alterations that lead to tumour progression, but also, in the context of p53 rest
111 ost from the development of cancer and alter tumour progression by driving the outgrowth of tumour ce
112 mouse mammary tumour model inhibits mammary tumour progression by reducing the proliferative potenti
113 of specific apoA-I mimetic peptide (D-4F) on tumour progression by using mammary tumour virus-polyoma
115 lating disease-risk in humans by suppressing tumour progression, decreasing inflammation and influenc
116 though increasing evidence demonstrates that tumour progression entails chromatin-mediated changes su
117 nimal-morbidity chemotherapy (in the case of tumour progression)-for paediatric patients with desmoid
118 4;14) translocation, somatic mutation during tumour progression frequently generates in FGFR3 protein
120 Attempts to intervene at an early stage of tumour progression have not proven cost effective, altho
121 uch minority populations are associated with tumour progression in human patients, specific targeting
123 eloid-cell VEGF-A resulted in an accelerated tumour progression in multiple subcutaneous isograft mod
124 Here we demonstrate that an HFD promotes tumour progression in the small intestine of genetically
126 igand interaction plays an essential role in tumour progression, in embryonic tissue morphogenesis an
127 ant CpG methylation changes occurring during tumour progression include the loss (hypomethylation) an
129 bute gain-of-function activities that impact tumour progression, it remains unclear whether the delet
130 er the optimal Wnt level might change during tumour progression, leading to selection for more than t
133 for research including real-time studies of tumour progression, metastasis, and drug-response evalua
134 s (range 0.4-10.4), 23 patients had died and tumour progression noted in 36, including local (n=14),
136 s in the aged microenvironment contribute to tumour progression, offering new possibilities for the d
137 ying expansion of the host vasculature, with tumour progression often correlated with vascular densit
138 ubsequent development of drug resistance and tumour progression.Oncogene advance online publication,
141 s not achieved, adjuvant therapy might delay tumour progression or recurrence, especially in high-ris
142 ollowed by 2 weeks without treatment), until tumour progression or unacceptable toxic effects arose.
144 a based on guidance for the determination of tumour progression outlined by the immune-related respon
146 telomere maintenance, immune regulation and tumour progression, providing deeper insight into the pa
148 iency, is known to be associated with breast tumour progression, resistance to conventional therapies
149 from the time of tumour initiation or after tumour progression, resulted in significantly reduced tu
150 h antibiotics completely blocked HFD-induced tumour progression, suggesting that distinct shifts in t
151 mice is not sufficient to trigger malignant tumour progression, suggesting that other alterations ar
152 lic reprogramming is tightly associated with tumour progression, the effect of metabolic regulatory c
154 idence supports key contributions of MDSC to tumour progression through both immune-mediated mechanis
156 ntly, BAG-1 is thought to enhance colorectal tumour progression through promoting tumour cell surviva
158 lation of Bim expression was associated with tumour progression towards an anchorage-independent phen
159 s of the p53 checkpoint may be essential for tumour progression triggered by mutations in BRCA2.
160 nvasion view the normal tissue as inhibiting tumour progression via immune modulation or spatial cons
163 lthough c-Src has been implicated in colonic tumour progression, we demonstrate here that in the aden
164 kinase activity, and effectively accelerates tumour progression when activated in advanced lung adeno
165 ypes raising the possibility of exacerbating tumour progression when targeting Rac1 in a clinical set
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