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1 ular communications in CCA and their role in tumor progression.
2 ellular stress but, paradoxically, it favors tumor progression.
3 the presence of oncostreams correlates with tumor progression.
4 equence of MAGEA6 degradation contributes to tumor progression.
5 elopment in fallopian tubes through stepwise tumor progression.
6 ribute detrimental and beneficial effects on tumor progression.
7 al blood facilitates on-demand monitoring of tumor progression.
8 ifferent aneuploidies can uniquely influence tumor progression.
9 iminating between pseudoprogression and true tumor progression.
10 ology of the postpartum mammary gland drives tumor progression.
11 ck their fate in multiclonal mixtures during tumor progression.
12 umorigenesis and an inverse association with tumor progression.
13 g a neomorphism model paradigm for targeting tumor progression.
14 s of the gene p107 significantly accelerates tumor progression.
15 on and divergent lineage dependencies during tumor progression.
16 inhibition of tumor-induced neurogenesis and tumor progression.
17 derived suppressor cells (MDSCs) can promote tumor progression.
18 tumor microenvironment (TME) and its role in tumor progression.
19 l, underscoring its potential importance for tumor progression.
20 ggesting a possible role of this receptor in tumor progression.
21 Intercellular communication is vital to tumor progression.
22 to initiate oncogenic signaling and promote tumor progression.
23 normal mammary gland development and breast tumor progression.
24 lished and may suggest strategies to prevent tumor progression.
25 ene networks are up regulated throughout the tumor progression.
26 rkers, when co-expressed with PD-L1, predict tumor progression.
27 response to increasing ECM stiffness during tumor progression.
28 astases in contrast to its impact on primary tumor progression.
29 ascularization and, consequently, augmenting tumor progression.
30 while ASPP2-mediated YAP activation enhances tumor progression.
31 ant to platinum-based chemotherapy and drive tumor progression.
32 e processes, especially during infection and tumor progression.
33 henotypic modulations of these subsets along tumor progression.
34 ne expression, many of which are involved in tumor progression.
35 stinct molecular attributes and hallmarks of tumor progression.
36 hibit critical, but often opposing, roles in tumor progression.
37 aling between astrocytes and glioblastoma in tumor progression.
38 exert their effector functions and influence tumor progression.
39 e MBNL-based alternative splicing to promote tumor progression.
40 thus likely conferring growth advantage for tumor progression.
41 rative effects in T-cell-mediated control of tumor progression.
42 tinocytes promotes MDSC influx into skin and tumor progression.
43 involved in mammary gland transformation and tumor progression.
44 ntributing to the promotion or inhibition of tumor progression.
45 pression in tumor cells in arbitrating brain tumor progression.
46 vels and whether ICMT overexpression affects tumor progression.
47 to uncover mechanisms and key biomarkers of tumor progression.
48 ld-type cells could be valuable in arresting tumor progression.
49 sed in cancer and have been shown to support tumor progression.
50 s may be associated with high rates of local tumor progression.
51 eath mechanisms that would otherwise inhibit tumor progression.
52 Chronic inflammation facilitates tumor progression.
53 thway for Tam resistance, carcinogenesis and tumor progression.
54 land that was sustained during HR(+) mammary tumor progression.
55 vironmental IL-1beta as a master cytokine in tumor progression.
56 nown mechanism of ILEI signaling that drives tumor progression.
57 te both contrasting and synergistic roles in tumor progression.
58 r insights into the immune mechanisms during tumor progression.
59 the implication of both Sema4D and CXCR4 in tumor progression.
60 ome maintenance program required for mammary tumor progression.
61 , or different 3,4-dihydroquinazolines) slow tumor progression.
62 pressive barriers is an essential feature of tumor progression.
63 that constrains AR binding/function to limit tumor progression.
64 can suppress antitumor immunity and promote tumor progression.
65 nt (TME) can dampen their ability to control tumor progression.
66 signaling, independently of WNT, to promote tumor progression.
67 tic instability, altered gene expression and tumor progression.
68 invasion, and metastasis, thereby affecting tumor progression.
69 criminate between pseudoprogression and true tumor progression.
70 creating feedback loops in cells to enhance tumor progression.
71 AC and the consequences of its disruption on tumor progression.
72 /NF-kappaB-driven primary-to-metastatic lung tumor progression.
73 egulated splicing events are associated with tumor progression.
74 cells in Rag1 mutants does not alter SHH-MB tumor progression.
75 require high DPAGT1 expression in order for tumor progression.
76 lated integrin beta(3)-KRAS signaling drives tumor progression.
77 uggesting a critical role for these pDGVs in tumor progression.
78 issue microenvironment may enhance malignant tumor progression.
79 nome structure upon cell differentiation and tumor progression.
80 ntinuous clonal evolution is often linked to tumor progression.
81 or microenvironment that can limit or worsen tumor progression.
82 lations for locally and remotely suppressing tumor progression.
83 le single deficiency of each protein limited tumor progression.
84 er from normal vessels and play key roles in tumor progression.
85 we identified that TME-derived IGF1 promotes tumor progression.
86 mulates microglia to produce IGF1 to promote tumor progression.
87 tially restricting tumorigenesis, can induce tumor progression.
88 al hip arthroplasty surgery because of local tumor progression.
89 olic stress that has the potential to impact tumor progression.
90 condensation patterns to different stages of tumor progression.
91 associated with genetic instability favoring tumor progression.
92 for understanding the mechanisms underlying tumor progression.
93 sed to identify patients at highest risk for tumor progression.
94 tumor microenvironment (TME) is critical for tumor progression.
95 ular alterations that support oncogenesis or tumor progression.
96 ith ISFI + C-TUS showed a 62.6% reduction in tumor progression, a 50.0% increase in median survival t
97 mics of the mutational time series governing tumor progression, allowing accurate prediction of the m
98 and that elevated SRSF3 was associated with tumor progression and a poor prognosis for patients with
99 /Globo-H and the FAK/CAV1/AKT/RIP complex in tumor progression and apoptosis and suggests a direction
101 major mechanism by which stroma can promote tumor progression and confer resistance to immune-based
102 ARID1A inactivation accelerates endometrial tumor progression and dissemination, the major causes of
106 f action of anti-MARCO antibody treatment on tumor progression and further show that this is potentia
107 ent stages of HCC revealed the mechanisms of tumor progression and helped to identify biomarkers of r
108 germline variants as a major determinant of tumor progression and highlight the importance of integr
109 we show that IL-1alpha inactivation impairs tumor progression and immune cell infiltration without a
110 in KRAS and NRAS are common in CRC, driving tumor progression and influencing efficacy of both cytot
111 t targeting epigenetic elements that promote tumor progression and inhibit immune cell activity can e
112 in (mTOR) plays a pivotal role in growth and tumor progression and is an attractive target for cancer
113 trated actin polymerization is essential for tumor progression and maintenance of tumor tissue integr
116 the importance of nerve-cancer cross-talk to tumor progression and may provide the foundation for dev
117 s to respond to changing environments during tumor progression and metastases and facilitates treatme
119 f the biochemical alterations that accompany tumor progression and metastasis is necessary to inform
122 s to be driven by adenosine that accelerates tumor progression and metastasis via ECM remodeling.
124 normal melanocyte proliferation/motility, in tumor progression and metastasis, its genetic alteration
126 ical role for collagen cross-linking in OSCC tumor progression and metastasis, which may provide insi
139 These enzymes have also been implicated in tumor progression and metastatic disease and have thus b
140 discovered common early events that promote tumor progression and migration to different metastatic
142 t obesity results in increased immune aging, tumor progression and PD-1-mediated T cell dysfunction w
143 h a BMI1 inhibitor resulted in abrogation of tumor progression and reduced the frequency of CSCs in t
145 a-associated fibroblasts (CAF) contribute to tumor progression and resistance to androgen signaling d
147 e studies define a causative role for OGA in tumor progression and reveal PKM2 O-GlcNAcylation as a m
151 a crucial role of neutrophils in support of tumor progression and suggest yet unexplored treatment o
152 strongly regulate GBM invasive motility and tumor progression and support further exploration of LIM
153 function in CD8 + T cells may be involved in tumor progression and susceptibility to virus infection
155 changing nature of these interactions during tumor progression and the impact of the tissue environme
156 Tumor-associated macrophages contribute to tumor progression and therapeutic resistance in breast c
158 use models are highly favored for evaluating tumor progression and therapeutic response in a more rea
160 physical traits of tumors that contribute to tumor progression and treatment resistance: (i) elevated
162 han (18)F-FDG in the differentiation between tumor progression and treatment-related changes in high-
165 er, but the degree of their enactment during tumor progression and under the selective pressures of i
166 lish whether molecular targets change during tumor progression and, if so, whether this affects preci
167 s tumor cell dissemination is a key event in tumor progression, and clinical significance of DTCs and
168 models, repeated exertion reduces malignant tumor progression, and clinically, exercise can improve
169 g for secondary mutations that contribute to tumor progression, and that these mutations often act in
170 ing the antitumor response with an impact on tumor progression, and will have implications for the de
171 Nonetheless, reported effects of statins on tumor progression are ambiguous, making it unclear wheth
172 The etiology of the effects of exercise on tumor progression are unclear, as are the cellular actor
174 new alternative strategy to control ovarian tumor progression based on selectively disrupting a prev
175 herapies that are not only effective against tumor progression but also address comorbidities such as
176 sis, and MDSC recruitment at early stages of tumor progression, but failed to reverse established met
178 racellular matrix (ECM) critically influence tumor progression, but the molecular mechanisms underlyi
179 o the widely held view that this gene drives tumor progression, but this hypothesis has not been rigo
180 el role for CCL2/CCR2 chemokine signaling in tumor progression by altering the microenvironment.
182 he literature regarding the role of TIMP2 in tumor progression by analyzing co-expressed genes in tum
184 uppressed DeltaNp63-low EMT cells influenced tumor progression by leading the invasion of proliferati
185 egulation functionally contributes to breast tumor progression by recruiting macrophages to the tumor
186 at MALAT1 contributes to HCC development and tumor progression by reprogramming tumor glucose metabol
187 an-binding proteins, have broad influence in tumor progression by rewiring intracellular and extracel
189 suggest that the activation of TLR4 supports tumor progression by stimulating the release of more eff
191 gher tumor burden than WT mice and increased tumor progression, characterized by reduced intrahepatic
192 suppression with a significant reduction in tumor progression, compared to saline-treated tumors ass
193 edicted progression in 100% of patients with tumor progression, compared with 71% for only ctDNA dete
195 either advantageous or deleterious roles in tumor progression, depending on the initial lesion size,
196 However, TAM blockade failed to decrease tumor progression due to a compensatory emergence of gra
197 ssibility to closely screen our patients for tumor progression during therapy, in therapy-free phases
198 umor initiation and/or to the differences in tumor progression (e.g., non-linear, saltatory growth) a
199 ction in melanoma xenografts causes enhanced tumor progression, EMT-transdifferentiation, metastatic
200 ablative RT reduced complications from local tumor progression, fatal gastrointestinal bleeding was o
201 of the tumor microenvironment in regulating tumor progression, few in vitro models have been develop
202 e therapy resulted in complete inhibition of tumor progression for SK-MEL-147 when using nude mice wi
204 the different PET tracers in differentiating tumor progression from treatment-related changes in high
205 chemoradiotherapy is associated with risk of tumor progression (growth of local, regional, or distant
206 ted significant suppression of neuroblastoma tumor progression, growth, and viability in a dose-depen
208 Differentiating pseudoprogression from true tumor progression has become a significant challenge in
210 SHH canonical signaling, causally linked to tumor progression, have become rational targets for canc
211 after chemoradiotherapy was associated with tumor progression (hazard ratio, 18.7; P < .0001), forma
212 hin the tumor microenvironment can influence tumor progression; however, genetic alterations in strom
213 rtain tumor damage(s) occurring during early tumor progression (i.e. ischemia) recruits neutrophils t
215 onfirmed that the combined treatment limited tumor progression in a cytotoxic T-cell-dependent manner
219 now is whether IL-9 and IL-17 contribute to tumor progression in a sequential and stage-specific man
224 blished its functional importance in mammary tumor progression in mice and showed that mammary tumor
226 with poor patient survival and promotion of tumor progression in multiple cancers and is a known ris
230 fectors may be a useful therapy for blocking tumor progression in patients with primary or recurrent
234 ted macrophages/microglia (TAMs) can promote tumor progression in the sonic hedgehog subgroup of medu
237 oat1 impairs cell proliferation in vitro and tumor progression in vivo and reveals a mevalonate pathw
239 roduced a robust and sustained inhibition of tumor progression in vivo in a PDX mouse model, greater
240 itor disrupts vascular network formation and tumor progression in vivo without additional effects on
243 Pvt1b loss accelerates tumor growth, but not tumor progression, in an autochthonous mouse model of lu
244 )HK2(+) liver cancer cells reduced xenograft tumor progression, in contrast to HK1(+)HK2(+) cells.
245 to be directly involved in several stages of tumor progression, including primary tumor growth, angio
247 ating neutrophils and their modulation along tumor progression is an important advancement in underst
254 e required for cancer cell proliferation and tumor progression, is a key factor mediating Th17 cell d
255 of the endothelin type A receptor (ETAR) in tumor progression leading to the formation of metastasis
256 lex has also emerged as a critical player in tumor progression, leading to the identification of seve
257 he only driver of tumor initiation; and that tumor progression likely occurs via accumulation of CNVs
260 t and mechanical signals are observed during tumor progression, malignant transformation, and metasta
261 systems; and taking into account patterns of tumor progression may improve patient selection for ther
262 ese results demonstrate a novel mechanism of tumor progression mediated by OPN released in response t
263 ncer, detection of ctDNA was associated with tumor progression, metastasis, and disease-specific surv
264 e effect of periodontal inflammation (PI) on tumor progression, metastasis, and possible underlining
265 the gangliosides it generates are linked to tumor progression, migration, and suppression of tumor-s
267 Therefore, a mechanistic understanding of tumor progression must account for evolutionary and ecol
268 ts (7.7%) did not undergo surgery because of tumor progression (n = 1) or adverse events (n = 2).
270 nfer mutation order and clone origins during tumor progression, rendering the selection of the approp
271 escape this immune surveillance and promote tumor progression represents an outstanding challenge.
272 hed orthotopic tumors dramatically inhibited tumor progression, resulting in significantly prolonged
273 pite the importance of AKT overactivation in tumor progression, results from clinical trials of vario
274 that germline variants play a larger role in tumor progression than has been previously appreciated a
275 se OvCa cells is associated with accelerated tumor progression that can be blocked by an arginase inh
277 (EpCAM) has previously been shown to promote tumor progression, the underlying mechanisms remain larg
278 ormation are two paramount processes driving tumor progression, therapy resistance, and cancer metast
279 only at diagnosis, the mechanisms underlying tumor progression, therapy resistance, and metastasis re
280 Hippo signaling controls organ size and tumor progression through a conserved pathway leading to
282 dence indicates that MDSC also contribute to tumor progression through their pro-angiogenic activity
283 To test whether loss of TMPRSS13 impacts tumor progression, TMPRSS13 was genetically ablated in t
285 In glioma patients, differentiation between tumor progression (TP) and treatment-related changes (TR
286 anism by which NRF2 hyperactivation promotes tumor progression via primary cilia degeneration and abe
288 d how GNA13 contributes to tumorigenesis and tumor progression, we compared the entire transcriptome
289 sing a p53-null model of early stage mammary tumor progression, we found that Gas6 is highly expresse
290 sms by which clotting factors influence PDAC tumor progression, we generated and characterized C57Bl/
291 etal and cytoskeleton-regulatory proteins in tumor progression, we performed analyses of The Cancer G
292 c instability in prostate carcinogenesis and tumor progression, we performed ultrahigh depth exome se
293 of cancer-associated fibroblasts (CAF) with tumor progression, we tested the role of cancer-derived
294 ne cells (T cells and B cells) contribute to tumor progression when present in the tumor microenviron
295 plays an essential role in GBM stemness and tumor progression, where hypoxic responses within the tu
296 ory cancer-associated fibroblasts (iCAFs) in tumor progression, which is significantly related to poo
297 s population of mesenchymal cells supporting tumor progression, whose origin remains to be fully eluc
298 ockdown of GM-CSF in tumor cells also delays tumor progression with decreased accumulation of M-MDSC
299 tabolizing enzymes and dramatically suppress tumor progression without visible toxicity in vivo.
300 in limiting pre-invasive to invasive breast tumor progression, yet their differentiation and perturb