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1 ting mutations are initiating events in lung oncogenesis.
2 se transition and their deregulation induces oncogenesis.
3 7 to promote tumor growth during lung cancer oncogenesis.
4 se to DNA damage and an important barrier to oncogenesis.
5 cer can also exploit geometry to orchestrate oncogenesis.
6 ssion of regulatory genes, together, lead to oncogenesis.
7 y cellular processes, and play a key role in oncogenesis.
8 nd enhanced opportunities for virus-mediated oncogenesis.
9 ifferentiation, apoptosis, inflammation, and oncogenesis.
10 to aid in infection of endothelial cells and oncogenesis.
11 metimes associated with clonal expansion and oncogenesis.
12 help explain HTLV-1-related pathogenesis and oncogenesis.
13 elopment, its dysregulation can also promote oncogenesis.
14 PTMs to gene expression changes that promote oncogenesis.
15 ng, inflammation, allergy, autoimmunity, and oncogenesis.
16 -has the potential to limit aging-associated oncogenesis.
17 nes at the level of transcription to mediate oncogenesis.
18 leukemias and highlight a role for Tspan3 in oncogenesis.
19 help advance our knowledge of virus-induced oncogenesis.
20 lecular networks under selective pressure in oncogenesis.
21 to acquire genetic alterations that promote oncogenesis.
22 ts the role of inflammatory cytokines in CCA oncogenesis.
23 ions suggests that they have unique roles in oncogenesis.
24 expand our understanding of virus-associated oncogenesis.
25 progenitors and prevented NRAS(V12)-mediated oncogenesis.
26 he regulation of genes participating in KSHV oncogenesis.
27 ral immune infiltration, thereby diminishing oncogenesis.
28 ptional network in normal development and in oncogenesis.
29 ronic inflammation, autoimmune diseases, and oncogenesis.
30 ropic virus type 1 are major contributors to oncogenesis.
31 and ancient mechanism of retrovirus-induced oncogenesis.
32 loid cell division, genomic instability, and oncogenesis.
33 he association between ribosomal defects and oncogenesis.
34 targets in unraveling the mechanism of lung oncogenesis.
35 orward mechanism to potentiate MYC-dependent oncogenesis.
36 hanistic effects of other TLRs on pancreatic oncogenesis.
37 t provides new insight to H. pylori-mediated oncogenesis.
38 l transcription, development, phenotype, and oncogenesis.
39 opment, metabolism, tissue regeneration, and oncogenesis.
40 tor with PDZ-binding motif), as key steps in oncogenesis.
41 iously suspected and play important roles in oncogenesis.
42 s an important mechanism that contributes to oncogenesis.
43 te an environment conducive to infection and oncogenesis.
44 n essential component of matriptase-mediated oncogenesis.
45 These data implicate SMARCA4 in SCCOHT oncogenesis.
46 nd the aberrant expression may contribute to oncogenesis.
47 on events are an integral component of viral oncogenesis.
48 pothesize that BCL6 may act by 'hit-and-run' oncogenesis.
49 and melanoma, where it is thought to promote oncogenesis.
50 ivers, including known and new regulators of oncogenesis.
51 ic activity of ASPH is important for hepatic oncogenesis.
52 r a novel mechanism of polyomavirus-mediated oncogenesis.
53 uces chromosomal instability, thus promoting oncogenesis.
54 Reducing O-GlcNAcylation inhibits oncogenesis.
55 les may contribute to genome instability and oncogenesis.
56 ting a cooperative role of EZH2 mutations in oncogenesis.
57 uence stem cell maintenance, metabolism, and oncogenesis.
58 ated fibrosis progression rate and increased oncogenesis.
59 s linked ionizing radiation exposure (RE) to oncogenesis.
60 eases; and the role of commensal microbes in oncogenesis.
61 lored biological functions with relevance in oncogenesis.
62 euploidy, thus contributing to KSHV-mediated oncogenesis.
63 mined the mechanism of eIF3i action in colon oncogenesis.
64 pro-tumorigenic factors that participate in oncogenesis.
65 g a number of cellular pathways critical for oncogenesis.
66 n normal cellular metabolism plays a role in oncogenesis.
67 in the MCPyV life cycle and virus-associated oncogenesis.
68 during embryogenesis would also be used for oncogenesis.
69 ression of genes involved in cell growth and oncogenesis.
70 o dissect developmental pathways involved in oncogenesis.
71 and promotes G1/S cell-cycle progression and oncogenesis.
72 velopment, homeostasis, innate immunity, and oncogenesis.
73 g genomic instability and thereby initiating oncogenesis.
74 signaling to senescence, tissue-fibrosis and oncogenesis.
75 ng of Rb mutant phenotypes and Rb's roles in oncogenesis.
76 of FAT1 function is a frequent event during oncogenesis.
77 h encodes a transcription factor involved in oncogenesis.
78 ere is aberrant epigenetic regulation in ACC oncogenesis.
79 n somatic cells that can be de-repressed for oncogenesis.
80 contribute to beta-HPV replication and viral oncogenesis.
81 MSET, that have established genetic links to oncogenesis.
82 cesses ranging from embryonic development to oncogenesis.
83 eins that promote cell cycle progression and oncogenesis.
84 iferation and apoptosis during c-Myc-induced oncogenesis.
85 rangements are considered a driving force of oncogenesis.
86 m cells, cellular reprogramming, growth, and oncogenesis.
87 ession of these and other genes that promote oncogenesis.
88 I3K-Akt pathways, which are essential for EN oncogenesis.
89 also offers a biochemical mechanism for BRAF oncogenesis.
90 arburg effect, which is a general feature of oncogenesis.
91 s hypothesized to be a driving event of DIPG oncogenesis.
92 ate, target, and intercept events that drive oncogenesis.
93 erts significant regulatory effects on tumor oncogenesis.
94 ion, which, when dysregulated, could lead to oncogenesis.
95 ing crucial for DNA repair, pluripotency and oncogenesis.
96 regulatory molecules may also contribute to oncogenesis.
97 have crucial roles in immune regulation and oncogenesis.
98 uclease activities of MRE11 are required for oncogenesis.
99 the same degree, potentially contributing to oncogenesis.
100 ell differentiation as an initiating step in oncogenesis.
101 r integration is required for HPV-associated oncogenesis.
102 Thus, we examined the role this may play in oncogenesis.
103 and a tumor suppressor respectively in human oncogenesis.
104 itches that determine normal development and oncogenesis.
105 stress barriers, providing a causal link to oncogenesis.
106 me genetically or pharmacologically inhibits oncogenesis.
107 ue levels to better understand breast cancer oncogenesis.
108 ave overlapping risk factors and pathways of oncogenesis.
109 cking cellular differentiation and promoting oncogenesis.
110 raditional understanding of NR activities in oncogenesis.
111 activation of target genes and neuroblastoma oncogenesis.
112 ploring a potential role for this pathway in oncogenesis.
113 the activity of the complex plays a role in oncogenesis.
114 e of significant interest in development and oncogenesis.
115 function of CDK12 in genome maintenance and oncogenesis.
116 defining the function of HSF1 as a driver of oncogenesis.
117 heterogeneity as an accidental byproduct of oncogenesis.
118 ranged and plays a critical role in prostate oncogenesis.
119 Inflammation is paramount in pancreatic oncogenesis.
120 ling has been implicated in BRCA1-associated oncogenesis.
121 t EMT strips Sox4 of an essential partner in oncogenesis.
122 em cells that likely reflects their risk for oncogenesis.
123 d supply to human tissue be an early step in oncogenesis?
124 and abnormal cell-cycle control can lead to oncogenesis, aberrancies within the UPS pathway can resu
125 egulator of Wnt signaling in development and oncogenesis, acts in the destruction complex with the sc
126 e loci, thereby representing a key player in oncogenesis and a viable target for cancer therapy.
128 ers, frequently disrupting genes involved in oncogenesis and amplifying HPV oncogenes E6 and E7.
131 DGFRs as critical mediators of breast cancer oncogenesis and chemoresistance driven by Foxq1, with po
132 on cancers, tested its contribution to colon oncogenesis and determined the mechanism of eIF3i action
134 R) provides insight into genome instability, oncogenesis and genome engineering, including disease ge
135 I1 requires RHA to enable Ewing sarcoma (ES) oncogenesis and growth; a small molecule, YK-4-279 disru
136 n protein glycosylation are a key feature of oncogenesis and have been shown to affect cancer cell be
137 w elucidates the role of AXL in EMT-mediated oncogenesis and highlights the reciprocal control betwee
142 er than 1 cm(3) MYC is a protein involved in oncogenesis and is overexpressed in triple-negative brea
144 ide novel mechanisms underlying EBV-mediated oncogenesis and may have a broad impact on IRF7-mediated
145 transcriptional repression, activation, and oncogenesis and may represent an attractive therapeutic
146 whereas deletion of Mincle protected against oncogenesis and phenocopied the immunogenic reprogrammin
147 ribution of the non-kinase fusion partner to oncogenesis and potential therapeutic strategies against
151 s (Sam68; 68 kDa) has been implicated in the oncogenesis and progression of several human cancers.
154 t 30% of human cancers, are major drivers of oncogenesis and render tumors unresponsive to standard t
155 ignaling through Rab1A overexpression drives oncogenesis and renders cancer cells prone to mTORC1-tar
156 rigenesis that promotes mutant KRAS-mediated oncogenesis and reveals that miR-31 directly targets and
158 erates with PTEN loss to accelerate prostate oncogenesis and that loss of component genes correlates
159 regulatory mechanisms relevant to pancreatic oncogenesis and the maintenance of the exocrine phenotyp
161 normal cell differentiation are required for oncogenesis and tumor cell survival in certain cancers.
166 of translational control that contributes to oncogenesis and underlies the anticancer effects of silv
168 T, and ErbB pathways, which are critical for oncogenesis and/or include signaling mediators involved
169 mechanism controlling cell proliferation and oncogenesis, and it mainly occurs in the initiation step
170 ed a critical role for altered metabolism in oncogenesis, and the neomorphic, oncogenic function of I
171 germline (including meiosis) functions drive oncogenesis, and we extend this to propose that meiotic
172 which mutations are drivers - play a role in oncogenesis, and which are passengers - do not play a ro
173 ght into the contribution of splicing toward oncogenesis, and, reciprocally, EWS-FLI1 interactions wi
174 d chronologically early somatic mutations in oncogenesis- and immune-related genes that may represent
175 ontrolling chemotaxis, growth, survival, and oncogenesis are activated by receptor tyrosine kinases a
177 erturbation of the SWI/SNF complexes promote oncogenesis are not fully elucidated; however, alteratio
180 ation-specific routes that cells take during oncogenesis are stochastic, genetic trajectories may be
181 important roles in embryonic development and oncogenesis, but how it affects metabolism is less clear
182 hh) signaling is critical in development and oncogenesis, but the mechanisms regulating this pathway
183 fferentiation during development can lead to oncogenesis, but the underlying mechanisms remain poorly
184 ork deepens understanding of how TAM promote oncogenesis by altering the molecular oncogenic program
186 nts, immunosuppression plays a major role in oncogenesis by both impairement of immunosurveillance, e
187 R1), when inappropriately regulated, induces oncogenesis by causing RNA processing defects, for examp
189 eIF3i in intestinal epithelial cells causes oncogenesis by directly upregulating the synthesis of cy
190 aintains stem cell self-renewal and promotes oncogenesis by enhancing cell proliferation in hematopoi
191 ors, our findings raise the possibility that oncogenesis by ErbB2 involves previously unexplored PKC-
193 naling that promotes hepatocyte survival and oncogenesis by inducing Mdm2-mediated Rb degradation.
195 lls and their microenvironment, thus driving oncogenesis by shaping cellular electrical activity in r
196 end our investigation of Mule's influence on oncogenesis by showing that Mule interacts directly with
197 eIF3i is a proto-oncogene that drives colon oncogenesis by translationally upregulating COX-2 and ac
198 erotrimeric G proteins, drive uveal melanoma oncogenesis by triggering multiple downstream signaling
199 Autophagy plays key roles in development, oncogenesis, cardiovascular, metabolic, and neurodegener
200 , these results reveal a role for SMARCA2 in oncogenesis caused by SMARCA4 loss and identify the ATPa
202 nylated proteins are often key effectors for oncogenesis, congenital disorders, and microbial pathoge
203 tial contributions in the area of retroviral oncogenesis, delineated mechanisms that control retrovir
204 have protective or protumorigenic effects on oncogenesis depending on the cancer subtype and on speci
206 erated from human fetal pancreas by targeted oncogenesis followed by in vivo cell differentiation in
207 ese findings have important implications for oncogenesis following either physiological or therapeuti
209 ments that contribute to different stages of oncogenesis, from predisposition to disease manifestatio
211 he microRNA (miR) 15a/16-1 cluster in B-cell oncogenesis has been extensively demonstrated, with over
212 nding of the mechanism of action of CARM1 in oncogenesis has been limited by a lack of selective tool
215 This reflects the multistep nature of viral oncogenesis, host genetic variability, and the fact that
216 d aberrant miR expression has been linked to oncogenesis; however, little is understood about their c
221 alternate means of enabling SS18-SSX-driven oncogenesis in cells as differentiated as preosteoblasts
223 nt sites and has been shown to contribute to oncogenesis in endometrial and cervical carcinomas.
224 her and how the piRNA pathway contributes to oncogenesis in human neoplasms remain poorly understood.
226 eins activate signaling molecules that drive oncogenesis in multiple human tumors including acute mye
230 icate that IER3 supports KRASG12D-associated oncogenesis in the pancreas by sustaining ERK1/2 phospho
231 Moreover, IER3 enhanced KrasG12D-dependent oncogenesis in the pancreas, as both PanIN and PDAC deve
232 ns would be an important mechanism for viral oncogenesis in the presence of a functional immune syste
233 e a novel role for IL2Rgamma in potentiating oncogenesis in the setting of JAK3-mutation-positive leu
234 nificant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown of eithe
237 ant functions in developmental processes and oncogenesis, including Notch proteins, which are functio
239 ch Wnt signaling drives proliferation during oncogenesis is attributed to its regulation of the cell
248 6a/G to activate Notch signaling and promote oncogenesis is substantially higher than that of pre-miR
251 mportance of the t(X;18) translocation in SS oncogenesis is well established, the genetic basis of SS
252 nerves of the PanIN microenvironment promote oncogenesis, likely via direct signaling to neoplastic n
253 that contribute to the biology of multistep oncogenesis mediated by established human oncoviruses.
255 with many physiological functions including oncogenesis, obesity, stem cell youth, human height, and
256 sal and luminal markers, indicating prostate oncogenesis occurs through disruption of an intermediate
258 l migration, invasion and contributes to the oncogenesis of anaplastic large cell lymphoma (ALCL) are
259 Hh) signaling plays an important role in the oncogenesis of B-cell malignancies such as multiple myel
262 ENP1, Maf1, and RNA pol III transcription in oncogenesis, our studies support the idea that deSUMOyla
263 mplicated the APOBEC3 cytosine deaminases in oncogenesis, possibly offering a therapeutic vulnerabili
264 This implies that at least in some cases, oncogenesis proceeds along with a temporary inhibition o
273 ell therapies, gene and oncoviral therapies, oncogenesis, signal pathway monitoring, and imaging drug
274 28B-RAN-AURKA signaling drives neuroblastoma oncogenesis, suggesting that this pathway may be amenabl
275 e for tumorigenesis, including those driving oncogenesis, survival, proliferation and death of cells,
276 Telomere biology is complexly related to oncogenesis: telomere attrition is protective by enforci
277 is linked to specific signaling cascades and oncogenesis, the cellular roles of its paralog, CDK19, a
278 zation of chromatin is frequently altered in oncogenesis, this work provides evidence pairing molecul
279 ressed in liver cancer and known to regulate oncogenesis through chromatin structure remodeling and c
282 anging from blood coagulation to embryo- and oncogenesis, tissue regeneration, and immune response re
284 ubule destabilizing factors can occur during oncogenesis to support enhanced migration and invasion o
285 with potential to study early stages of NBL oncogenesis, to functionally assess NBL oncogenic driver
286 ys important roles in mammalian development, oncogenesis, treatment response, and responses to the en
289 in contributes to stem cell pluripotency and oncogenesis via multiple functions, including its newly
290 /2/3) have been shown to modulate Ras-driven oncogenesis, we asked if these enzymes might regulate si
291 how these antagonistic activities influence oncogenesis, we dissected the nuclear and cytoplasmic fu
293 utative roles in both neuronal apoptosis and oncogenesis, we sought to determine their behavior under
294 mor microenvironment is vital for subsequent oncogenesis, we tested for miR-874 and CCNE1 interdepend
295 C by itself, nor does it enhance HIF1alphaM3 oncogenesis when coexpressed with constitutively active
296 controls self-renewal and is hijacked during oncogenesis, whereas another signal controls reprogrammi
299 orders and the molecular mechanisms of viral oncogenesis will lead to better prevention, diagnosis, a
300 at ASEs represent a significant mechanism of oncogenesis with untapped potential for understanding co
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