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1 fferent cellular states (such as observed in oncogenesis).
2 bution of heterochromatin hypomethylation to oncogenesis.
3 (RBLs) is a useful model system to study EBV oncogenesis.
4 ral reactivation from latency often precedes oncogenesis.
5 pathologic stabilization of beta-catenin and oncogenesis.
6 oylation and may contribute to LMP1-mediated oncogenesis.
7 t in gene regulation, cell proliferation and oncogenesis.
8 etic regulator implicated in development and oncogenesis.
9 s have been increasingly implicated in human oncogenesis.
10 specific, activated pathways is important in oncogenesis.
11 ression in cancer and broadly contributes to oncogenesis.
12 as well as mammalian organ regeneration and oncogenesis.
13 uminal androgen-receptor program of prostate oncogenesis.
14 peat-mediated rearrangements associated with oncogenesis.
15 ting distinct roles in tumor suppression and oncogenesis.
16 herapeutics in treating hepatic fibrosis and oncogenesis.
17 ring latent EBV infections, which can affect oncogenesis.
18 d, representing a genomic signature of early oncogenesis.
19 ting mutations are initiating events in lung oncogenesis.
20 s hypothesized to be a driving event of DIPG oncogenesis.
21 uclease activities of MRE11 are required for oncogenesis.
22 itches that determine normal development and oncogenesis.
23 cking cellular differentiation and promoting oncogenesis.
24 e of significant interest in development and oncogenesis.
25 ranged and plays a critical role in prostate oncogenesis.
26 ng, inflammation, allergy, autoimmunity, and oncogenesis.
27 ral immune infiltration, thereby diminishing oncogenesis.
28 loid cell division, genomic instability, and oncogenesis.
29 tor with PDZ-binding motif), as key steps in oncogenesis.
30 signaling to senescence, tissue-fibrosis and oncogenesis.
31 n somatic cells that can be de-repressed for oncogenesis.
32 eins that promote cell cycle progression and oncogenesis.
33 ate, target, and intercept events that drive oncogenesis.
34 erts significant regulatory effects on tumor oncogenesis.
35 ion, which, when dysregulated, could lead to oncogenesis.
36 ing crucial for DNA repair, pluripotency and oncogenesis.
37 regulatory molecules may also contribute to oncogenesis.
38 have crucial roles in immune regulation and oncogenesis.
39 l differentiation, leading to suppression of oncogenesis.
40 the same degree, potentially contributing to oncogenesis.
41 ell differentiation as an initiating step in oncogenesis.
42 r integration is required for HPV-associated oncogenesis.
43 Thus, we examined the role this may play in oncogenesis.
44 and a tumor suppressor respectively in human oncogenesis.
45 stress barriers, providing a causal link to oncogenesis.
46 of HUWE1 significantly reduces RET-mediated oncogenesis.
47 me genetically or pharmacologically inhibits oncogenesis.
48 ue levels to better understand breast cancer oncogenesis.
49 ave overlapping risk factors and pathways of oncogenesis.
50 raditional understanding of NR activities in oncogenesis.
51 activation of target genes and neuroblastoma oncogenesis.
52 ploring a potential role for this pathway in oncogenesis.
53 the activity of the complex plays a role in oncogenesis.
54 asure their network change (rewiring) during oncogenesis.
55 function of CDK12 in genome maintenance and oncogenesis.
56 defining the function of HSF1 as a driver of oncogenesis.
57 heterogeneity as an accidental byproduct of oncogenesis.
58 Inflammation is paramount in pancreatic oncogenesis.
59 ling has been implicated in BRCA1-associated oncogenesis.
60 t EMT strips Sox4 of an essential partner in oncogenesis.
61 em cells that likely reflects their risk for oncogenesis.
62 se transition and their deregulation induces oncogenesis.
63 7 to promote tumor growth during lung cancer oncogenesis.
64 se to DNA damage and an important barrier to oncogenesis.
65 cer can also exploit geometry to orchestrate oncogenesis.
66 ssion of regulatory genes, together, lead to oncogenesis.
67 y cellular processes, and play a key role in oncogenesis.
68 nd enhanced opportunities for virus-mediated oncogenesis.
69 ifferentiation, apoptosis, inflammation, and oncogenesis.
70 to aid in infection of endothelial cells and oncogenesis.
71 metimes associated with clonal expansion and oncogenesis.
72 help explain HTLV-1-related pathogenesis and oncogenesis.
73 elopment, its dysregulation can also promote oncogenesis.
74 PTMs to gene expression changes that promote oncogenesis.
75 -has the potential to limit aging-associated oncogenesis.
76 nes at the level of transcription to mediate oncogenesis.
77 leukemias and highlight a role for Tspan3 in oncogenesis.
78 help advance our knowledge of virus-induced oncogenesis.
79 lecular networks under selective pressure in oncogenesis.
80 ronmental factors likely interact to promote oncogenesis.
81 to acquire genetic alterations that promote oncogenesis.
82 ts the role of inflammatory cytokines in CCA oncogenesis.
83 ions suggests that they have unique roles in oncogenesis.
84 expand our understanding of virus-associated oncogenesis.
85 progenitors and prevented NRAS(V12)-mediated oncogenesis.
86 he regulation of genes participating in KSHV oncogenesis.
87 miR181ab1 is a key modulator of KRAS-driven oncogenesis.
88 e fusion product is a key driver of prostate oncogenesis.
89 osition of rodent and human MECs to initiate oncogenesis.
90 ional-repression and impedes SPINK1-mediated oncogenesis.
91 ical pathways controlling the cell cycle and oncogenesis.
92 th MYC both during normal development and in oncogenesis.
93 nificantly accelerates mutant Kras-dependent oncogenesis.
94 er transcription factors with known roles in oncogenesis.
95 se variants as driver events contributing to oncogenesis.
96 e frequently co-activated and altered during oncogenesis.
97 plore here the roles that chromatin plays in oncogenesis.
98 SEs play pivotal roles in development and oncogenesis.
99 es Mst1/2-mutant-driven liver overgrowth and oncogenesis.
100 other proteins are frequently altered during oncogenesis.
101 promote the genomic instability that drives oncogenesis.
102 It can also promote or inhibit oncogenesis.
103 us (MDV), respectively, are also involved in oncogenesis.
104 way and is an essential factor in RAS-driven oncogenesis.
105 da, Saccharomyces or Aspergillus-accelerated oncogenesis.
106 r fusions are all now known to be drivers of oncogenesis.
107 and may be implicated in pathologies such as oncogenesis.
108 ex functions with a focus on how it promotes oncogenesis.
109 vidual contributions of these alterations to oncogenesis.
110 ype I IFN, it mediates mTORC1 activation and oncogenesis.
111 e "driver" mutations, causally implicated in oncogenesis.
112 the COMPASS family during development and in oncogenesis.
113 d this microRNA regulates several aspects of oncogenesis.
114 us to examine the involvement of Aldh1b1 in oncogenesis.
115 f the virus is known to drive EBV-associated oncogenesis.
118 egulator of Wnt signaling in development and oncogenesis, acts in the destruction complex with the sc
119 e loci, thereby representing a key player in oncogenesis and a viable target for cancer therapy.
122 elta; V653A Kit mutation had increased tumor oncogenesis and associated KIT-dependent STAT activation
125 DGFRs as critical mediators of breast cancer oncogenesis and chemoresistance driven by Foxq1, with po
128 lls in numerous examples of childhood cancer oncogenesis and emerging therapeutic opportunities aimed
130 mportant for rationalizing the mechanisms of oncogenesis and for individualizing anticancer treatment
131 R) provides insight into genome instability, oncogenesis and genome engineering, including disease ge
133 n protein glycosylation are a key feature of oncogenesis and have been shown to affect cancer cell be
134 w elucidates the role of AXL in EMT-mediated oncogenesis and highlights the reciprocal control betwee
137 found in these gene fusions as critical for oncogenesis and implicate these YAP functions as potenti
139 er than 1 cm(3) MYC is a protein involved in oncogenesis and is overexpressed in triple-negative brea
141 ide novel mechanisms underlying EBV-mediated oncogenesis and may have a broad impact on IRF7-mediated
142 whereas deletion of Mincle protected against oncogenesis and phenocopied the immunogenic reprogrammin
143 ribution of the non-kinase fusion partner to oncogenesis and potential therapeutic strategies against
146 t 30% of human cancers, are major drivers of oncogenesis and render tumors unresponsive to standard t
147 rigenesis that promotes mutant KRAS-mediated oncogenesis and reveals that miR-31 directly targets and
148 erates with PTEN loss to accelerate prostate oncogenesis and that loss of component genes correlates
154 ignaling through this cascade contributes to oncogenesis and underlies the RASopathies, a family of c
159 unctions in regulating both pluripotency and oncogenesis, and suggest that sGRP78 marks a stem-like p
160 germline (including meiosis) functions drive oncogenesis, and we extend this to propose that meiotic
161 which mutations are drivers - play a role in oncogenesis, and which are passengers - do not play a ro
162 d chronologically early somatic mutations in oncogenesis- and immune-related genes that may represent
163 ontrolling chemotaxis, growth, survival, and oncogenesis are activated by receptor tyrosine kinases a
165 erturbation of the SWI/SNF complexes promote oncogenesis are not fully elucidated; however, alteratio
168 ation-specific routes that cells take during oncogenesis are stochastic, genetic trajectories may be
171 ribe the critical cellular events that drive oncogenesis as well as a comprehensive map of the molecu
173 criptional changes, only some of which drive oncogenesis at certain times during cancer evolution.
174 man MPNST illustrates how PRC2 loss promotes oncogenesis but renders tumors vulnerable to pharmacolog
175 important roles in embryonic development and oncogenesis, but how it affects metabolism is less clear
176 ons of the EBV and KSHV genomes that mediate oncogenesis, but the detailed mechanisms are not fully u
177 hh) signaling is critical in development and oncogenesis, but the mechanisms regulating this pathway
178 nts, immunosuppression plays a major role in oncogenesis by both impairement of immunosurveillance, e
179 R1), when inappropriately regulated, induces oncogenesis by causing RNA processing defects, for examp
180 e ternary complex regulates pluripotency and oncogenesis by controlling processing of the let-7 famil
181 ction is necessary for B-cell maturation and oncogenesis by E2A-PBX1 and occurs through conserved Phi
182 aintains stem cell self-renewal and promotes oncogenesis by enhancing cell proliferation in hematopoi
183 uggest that cohesin mutations could progress oncogenesis by enhancing Wnt signaling, and that targeti
185 naling that promotes hepatocyte survival and oncogenesis by inducing Mdm2-mediated Rb degradation.
186 Our findings support a multi-step model of oncogenesis by miR-155 in which miR-155 promotes both a
188 cy, we describe here a multi-step process of oncogenesis by miR-155, which involves cooperation betwe
190 lls and their microenvironment, thus driving oncogenesis by shaping cellular electrical activity in r
191 end our investigation of Mule's influence on oncogenesis by showing that Mule interacts directly with
193 erotrimeric G proteins, drive uveal melanoma oncogenesis by triggering multiple downstream signaling
194 Autophagy plays key roles in development, oncogenesis, cardiovascular, metabolic, and neurodegener
196 tial contributions in the area of retroviral oncogenesis, delineated mechanisms that control retrovir
197 have protective or protumorigenic effects on oncogenesis depending on the cancer subtype and on speci
199 firms the central role of FOXA1 in mediating oncogenesis driven by the androgen receptor, and provide
200 spite the role of STAT3 as a known driver of oncogenesis, efforts to develop therapeutic STAT3 inhibi
201 AF complex, including ARID1A, play a role in oncogenesis, either as tumor suppressors or oncogenes.
202 n cell-surface glycosylation associated with oncogenesis enhances AML blast binding to E-selectin and
203 n real time, and gene expression analysis of oncogenesis, epithelial to mesenchymal transition and ap
205 w microbe-induced immune activation promotes oncogenesis, focusing particularly on pancreatic carcino
206 ese findings have important implications for oncogenesis following either physiological or therapeuti
207 ments that contribute to different stages of oncogenesis, from predisposition to disease manifestatio
208 minate the way cancer biologists think about oncogenesis, growing evidence suggests that systemic fac
210 he microRNA (miR) 15a/16-1 cluster in B-cell oncogenesis has been extensively demonstrated, with over
211 The contribution of coding mutations to oncogenesis has been largely clarified, whereas little i
212 nding of the mechanism of action of CARM1 in oncogenesis has been limited by a lack of selective tool
213 pamycin (mTOR) in the positive regulation of oncogenesis has been well documented and thus mTOR has e
216 ry causes replication stress, DNA damage and oncogenesis, highlighting the need for strict regulation
217 d aberrant miR expression has been linked to oncogenesis; however, little is understood about their c
218 cell dysfunctional status seen in this viral oncogenesis humanized model replicates observations obta
219 Emerging evidence suggests that during early oncogenesis IL-17 supports tumor growth, whereas in esta
220 tentially deepening our understanding of eBL oncogenesis.IMPORTANCE Improved viral enrichment methods
221 netically reactivated in cancer to influence oncogenesis in a process termed onco-exaptation(4).
224 alternate means of enabling SS18-SSX-driven oncogenesis in cells as differentiated as preosteoblasts
225 nt sites and has been shown to contribute to oncogenesis in endometrial and cervical carcinomas.
226 -1) signaling network has been implicated in oncogenesis in GBM, making it an appealing target for ad
227 , we described a robust protocol of targeted oncogenesis in human fetal pancreas and produced the fir
228 her and how the piRNA pathway contributes to oncogenesis in human neoplasms remain poorly understood.
231 Gain-of-function PTPN11 mutations drive oncogenesis in several leukemias and cause developmental
234 ns would be an important mechanism for viral oncogenesis in the presence of a functional immune syste
235 e a novel role for IL2Rgamma in potentiating oncogenesis in the setting of JAK3-mutation-positive leu
237 nificant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown of eithe
238 he dissemination of the virus but also viral oncogenesis, in which the effect of RTA on the host tran
239 that the genomic events central to childhood oncogenesis include mutations resulting in broad epigene
240 of several biological processes important to oncogenesis, including control of cell proliferation, di
241 s Avastin, effectively abrogated the EMT and oncogenesis induced by the acetylated SPZ1-TWIST1 comple
256 le serves two opposing roles; earlier during oncogenesis it suppresses neoplastic transformation and
257 nerves of the PanIN microenvironment promote oncogenesis, likely via direct signaling to neoplastic n
258 hanisms of action of PAX8 in development and oncogenesis may identify new vulnerabilities in malignan
260 ogical gene expression programs that support oncogenesis.Objectives: To identify molecular mechanisms
262 l migration, invasion and contributes to the oncogenesis of anaplastic large cell lymphoma (ALCL) are
266 olycomb repressive complex 2 (PRC2) promotes oncogenesis partly through its enzymatic function for in
267 mplicated the APOBEC3 cytosine deaminases in oncogenesis, possibly offering a therapeutic vulnerabili
276 demonstrate miR-644a mediated fine-tuning of oncogenesis, stimulating pathways and resultant potentia
277 28B-RAN-AURKA signaling drives neuroblastoma oncogenesis, suggesting that this pathway may be amenabl
278 is linked to specific signaling cascades and oncogenesis, the cellular roles of its paralog, CDK19, a
279 m cell differentiation, in vivo development, oncogenesis, the emergence of drug resistance and cell s
280 zation of chromatin is frequently altered in oncogenesis, this work provides evidence pairing molecul
281 ressed in liver cancer and known to regulate oncogenesis through chromatin structure remodeling and c
285 anging from blood coagulation to embryo- and oncogenesis, tissue regeneration, and immune response re
286 with potential to study early stages of NBL oncogenesis, to functionally assess NBL oncogenic driver
287 ys important roles in mammalian development, oncogenesis, treatment response, and responses to the en
288 es in the biology of solid tumors, including oncogenesis, tumor growth, invasion and metastasis, and
290 se coregulators are frequently implicated in oncogenesis via causal roles in dysregulated, malignant
291 plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differen
293 /2/3) have been shown to modulate Ras-driven oncogenesis, we asked if these enzymes might regulate si
295 mor microenvironment is vital for subsequent oncogenesis, we tested for miR-874 and CCNE1 interdepend
298 e discovery of aberrant splicing patterns in oncogenesis, while more recent advances have uncovered n
300 at ASEs represent a significant mechanism of oncogenesis with untapped potential for understanding co