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1 +) mice (an animal model of human intestinal tumorigenesis).
2 primary cilia formation during Hh-dependent tumorigenesis.
3 ons to the p53 pathway during retinoblastoma tumorigenesis.
4 of MED1 to evaluate its role in HER2-driven tumorigenesis.
5 the crucial role of epigenetic mechanisms in tumorigenesis.
6 epigenetic regulation and its role in breast tumorigenesis.
7 chromatin alterations that drive HPV-related tumorigenesis.
8 have been identified as bona fide drivers of tumorigenesis.
9 reased telomerase levels are associated with tumorigenesis.
10 ronic intestinal inflammation and colorectal tumorigenesis.
11 r development, indicating a causal effect in tumorigenesis.
12 euploidy and centrosome defects and enhances tumorigenesis.
13 ing regions of the genome is a key driver of tumorigenesis.
14 ted suppressive effect of gga-miR-219b on MD tumorigenesis.
15 cancer cell energy metabolic homeostasis and tumorigenesis.
16 inent oncogene that has been proven to drive tumorigenesis.
17 mmunity, persist lifelong, and contribute to tumorigenesis.
18 ) expression is necessary to protect against tumorigenesis.
19 tenin and provides insights into its role in tumorigenesis.
20 transduction, especially in viral-associated tumorigenesis.
21 mmunological roles and off-target effects in tumorigenesis.
22 le for the oxidative stress response in lung tumorigenesis.
23 he context of somatic cell reprogramming and tumorigenesis.
24 em cell pluripotency, cancer metastasis, and tumorigenesis.
25 on of Dnmt3b is thought to generally promote tumorigenesis.
26 gnificant suppression in spontaneous mammary tumorigenesis.
27 of aging, but was also insufficient to drive tumorigenesis.
28 tivated, proinflammatory state that promotes tumorigenesis.
29 ocking lipogenesis in vivo can prevent liver tumorigenesis.
30 imulation with CXCL12 supports neuroblastoma tumorigenesis.
31 he key regulator of MaSC activity and breast tumorigenesis.
32 ss of E2f1 did not rescue, but worsened skin tumorigenesis.
33 ons fully explains the cell lineage-specific tumorigenesis.
34 otherwise promote genome instability to fuel tumorigenesis.
35 and triggers apoptosis, thereby suppressing tumorigenesis.
36 ion coordinately acts with CDK4 to drive GBM tumorigenesis.
37 osis, both of which are important drivers of tumorigenesis.
38 ammation, the severity of colitis, and colon tumorigenesis.
39 ethyltransferases and are thought to promote tumorigenesis.
40 inhibitory role of atherogenic diet on lung tumorigenesis.
41 vel axis involved in skin stratification and tumorigenesis.
42 lopment and pathologic conditions such as NB tumorigenesis.
43 tin, malignant gene expression programs, and tumorigenesis.
44 /c-Jun signaling pathway contributes to TNBC tumorigenesis.
45 ibute to the observed dual roles of SIRT1 in tumorigenesis.
46 tasis and, when unrestricted, it can lead to tumorigenesis.
47 orward loop between both cell types in liver tumorigenesis.
48 ic copy number alterations (CNAs), can drive tumorigenesis.
49 hereby serving as an immunological driver of tumorigenesis.
50 of this splice variant on the progression of tumorigenesis.
51 in the Apc (Min/+) mouse model of intestinal tumorigenesis.
52 nase activity and reduces BRAF(V600E)-driven tumorigenesis.
53 on leads to CRC cell proliferation, EMT, and tumorigenesis.
54 lays key roles in stem cell self-renewal and tumorigenesis.
55 ted cancer and Apc(Min)-dependent intestinal tumorigenesis.
56 s, thus promoting cell cycle progression and tumorigenesis.
57 while exogenous TRIM14 expression attenuated tumorigenesis.
58 glucose signal to the Hippo-YAP pathway and tumorigenesis.
59 at RET expression is upregulated during PDAC tumorigenesis.
60 l GBM specimens and required for EGFR-driven tumorigenesis.
61 eam signaling, thereby enhancing EGFR-driven tumorigenesis.
62 ecule involved in cell-cell interactions and tumorigenesis.
63 of PTK6 Y342, and disruption of Ptk6 impairs tumorigenesis.
64 dual infection enhanced KSHV persistence and tumorigenesis.
65 TNFR1 signaling to promote DEN-induced liver tumorigenesis.
66 kinesin KIF23, a key target gene of MMB, in tumorigenesis.
67 homeostasis, and regeneration, as well as in tumorigenesis.
68 ses developmental disorders or has a role in tumorigenesis.
69 part in lung cancer cell growth and in vivo tumorigenesis.
70 tability are the two key events required for tumorigenesis.
71 rotein level and thus potentially affect ACC tumorigenesis.
72 of IBD and prevention of colitis-associated tumorigenesis.
73 re thought to be involved in early stages of tumorigenesis.
74 the concept that inflammation promotes colon tumorigenesis.
75 ne fusion has not been shown to induce liver tumorigenesis.
76 hich plays a crucial role in development and tumorigenesis.
77 NPM signaling axis that is required for lung tumorigenesis.
78 fate decision and has an ambivalent role in tumorigenesis.
79 tion and P50 phosphorylation causing mammary tumorigenesis.
80 hymus, the colon submucosa, and during early tumorigenesis.
81 tiation of genome instability permissive for tumorigenesis.
82 ed with liver development, regeneration, and tumorigenesis.
83 s-a novel, potential pathway of VAT-enhanced tumorigenesis.
84 tion and role of MEG3 in nickel-induced lung tumorigenesis.
85 al tumor suppressor genes, can contribute to tumorigenesis.
86 ed apoptotic signaling is a prerequisite for tumorigenesis.
87 lopment and exert oncogenic functions during tumorigenesis.
88 f hepatic PPARgamma expression and promoting tumorigenesis.
89 icient to drive ICC hyperplasia but not GIST tumorigenesis.
90 he favoring cholangiocellular overgrowth and tumorigenesis.
91 EG3 in environmental carcinogen-induced lung tumorigenesis.
92 ture for processes frequently altered during tumorigenesis.
93 ation of NFAT3 has an important role in skin tumorigenesis.
94 d in adult somatic cells, is critical during tumorigenesis.
95 ctional in vivo role for Bcor in suppressing tumorigenesis.
96 transcriptional program essential for NSCLC tumorigenesis.
97 altered epigenetic state that contribute to tumorigenesis.
98 ey promoter of cancer cell proliferation and tumorigenesis.
99 c mouse lines to examine the role of Plk1 in tumorigenesis.
100 tumoral genomic heterogeneity evolves during tumorigenesis.
101 s in tumor cells involved in development and tumorigenesis.
102 functions in SCC and to examine its role in tumorigenesis.
103 ve cancers and may influence early stages of tumorigenesis.
104 plicated as an underlying cause of aging and tumorigenesis.
105 them are likely to have functional roles in tumorigenesis.
106 in cancer and describe the role of Daam2 in tumorigenesis.
107 lation patterns have been widely observed in tumorigenesis, ageing and neurodegenerative diseases, hi
109 hat combined inactivation of E2f7/8 enhanced tumorigenesis and accelerated malignant progression.
111 cosal barrier components in regulating colon tumorigenesis and cancer progression remains unclear.
115 med a long-term diet study in mice to follow tumorigenesis and characterize structural and metabolic
116 lator of AKT pathway with a critical role in tumorigenesis and chemo-response in pancreatic cancer.
117 ew hypotheses of the cell of origin of liver tumorigenesis and clarify the classes of liver cancer ba
118 tinocytes significantly restrains murine BCC tumorigenesis and demonstrate the counterintuitive concl
119 and gene regulatory networks associated with tumorigenesis and EMT that correlate with accessibility
120 et al. report that Ect2 is required for lung tumorigenesis and identified a role for this GEF in ribo
121 ption of Pten in the mouse prostate leads to tumorigenesis and increased phosphorylation of PTK6 Y342
123 hat IRE1alpha has a critical role in colonic tumorigenesis and IRE1alpha targeting might be a strateg
124 show that RET is upregulated during pancreas tumorigenesis and its activation induces cancer perineur
125 is between female and male fish during early tumorigenesis and long-term tumor progression in our pre
126 d the associated BFB-mediated instability in tumorigenesis and may shed light on the early consequenc
127 n breast cancer cells-mechanisms critical to tumorigenesis and metastasis-through a TLR4/nuclear fact
131 iR-140-5p/Pin1 axis may play a major role in tumorigenesis and offer promising therapeutic targets fo
132 o determine how the epigenome changes during tumorigenesis and reprogramming, we performed integrated
133 knockout mice showed a shortened latency of tumorigenesis and significantly increased numbers of tum
134 by single-chromosome gains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for
135 uggest that INTU is indispensable during BCC tumorigenesis and that its aberrant upregulation is like
136 Dnmt3a and Dnmt3b protect the epidermis from tumorigenesis and that squamous carcinomas are sensitive
138 uses on advances in our understanding of the tumorigenesis and treatment of poorly differentiated neu
143 tream of TBK1 in control of innate immunity, tumorigenesis, and disorders linked to chronic inflammat
144 atic cholesterol level, is important in lung tumorigenesis, and LXR activation might partly contribut
146 promoting oncogenic transcription and NSCLC tumorigenesis, and reveals a potential treatment strateg
147 that ERalpha and ERbeta expression, mammary tumorigenesis, and survival are energy balance dependent
148 link between mammary epithelial involution, tumorigenesis, and the phenomenon of chemoresistance.
149 a profound impact on the genetic history of tumorigenesis, and to adapt to the multiple constraints
150 o investigate CtBP's contribution to in vivo tumorigenesis, Apc(min/+) mice, which succumb to massive
152 The contributions of coding mutations to tumorigenesis are relatively well known; however, little
156 pRb and p53 doubly deficient (DKO) prostate tumorigenesis as a context in which p27 ubiquitination b
157 tep process leading to transformation and/or tumorigenesis, as either a tumor suppressor or tumor pro
158 at p62 is a critical mediator of TSC2-driven tumorigenesis, as Tsc2(+/-) and Tsc2f/f Ksp-CreERT2(+) m
159 ypes, including tumorspheres, cell motility, tumorigenesis, as well as in vitro and in vivo responses
160 g/kg body weight) were established and lung tumorigenesis assessments were taken after 15 weeks late
161 iciency in liver parenchymal cells triggered tumorigenesis at 18 months of age preceded by spontaneou
162 omatin marks and reduced expression prior to tumorigenesis, at a time point coinciding with peak leve
163 neered mouse model of gastric adenocarcinoma tumorigenesis based on Kras(G12D) expression plus inacti
164 opment and potential contributions to breast tumorigenesis, based on coamplification of MED1 and HER2
165 of HCC, we compared the difference of liver tumorigenesis between female and male fish during early
166 stigation revealed that MAGEs not only drive tumorigenesis but also regulate pathways essential for d
167 refore, defects in BRCA2 are associated with tumorigenesis but also with increased susceptibility to
168 presses malignant growth early in epithelial tumorigenesis but promotes metastasis at later stages.
169 wo oncogenes KRas and Myc cooperate to drive tumorigenesis, but the mechanism underlying this remains
170 IDH1 induces epigenetic changes that promote tumorigenesis, but the scale and reversibility of these
172 viability in vitro by 11% to 19% and reduced tumorigenesis by 50% when preincubated MCF-7 breast canc
173 's ability to promote cell proliferation and tumorigenesis by altering the subcellular localization o
175 s due to inactivation of STAG2 could promote tumorigenesis by extending the period during which tumor
176 This suggests that MMB could contribute to tumorigenesis by mediating overexpression of mitotic gen
177 ay serve to adjust liver repair and to block tumorigenesis by modulating stem-like cells and beta-Cat
178 our data demonstrate that JNK regulates TNBC tumorigenesis by promoting CSC phenotype through Notch1
179 These data suggest that TPMs contribute to tumorigenesis by promoting immortalization and genomic i
180 air suggests HPV oncogenes may contribute to tumorigenesis by promoting the integration of the HPV ge
181 BRD4 has emerged as an important factor in tumorigenesis by promoting the transcription of genes in
182 pool of active EGFRs is sufficient to drive tumorigenesis by signaling primarily through the Ras-MAP
184 ially rescues normal mitosis and impairs the tumorigenesis exerted by miR-26a, indicating that CHFR r
186 of JAK/STAT3 is critical in gastrointestinal tumorigenesis following Lkb1 mutations and suggest that
187 bition of IL6 signaling dramatically impedes tumorigenesis following partial hepatectomy without comp
188 study, we generated a mouse model of mammary tumorigenesis harboring the MMTV-HER2 oncogene and mutat
191 e relationship between IGF2 LOI and prostate tumorigenesis has not been established functionally.
195 orectal cancer (CRC) and its contribution to tumorigenesis have not been comprehensively analyzed.
196 ne kinases (RTKs) are frequent events during tumorigenesis; however, the cellular vulnerability to no
200 aling inhibited epithelial proliferation and tumorigenesis in an ACh muscarinic receptor-3 (M3R)-depe
201 ne can restrain mitochondrial metabolism and tumorigenesis in an LFS model, supporting its further co
205 et not only accelerated Src-induced prostate tumorigenesis in mice but also compromised the inhibitor
207 hat Foxp1-Shq1 deletion accelerates prostate tumorigenesis in mice in combination with Pten loss, con
208 ws that lipogenesis is dispensable for liver tumorigenesis in mice treated with DEN, and identifies a
212 The DNA methyltransferase Dnmt3a suppresses tumorigenesis in models of leukemia and lung cancer.
213 tly, oral administration of KPT-9274 reduces tumorigenesis in mouse models of human triple negative b
214 tant Ras is insufficient to initiate thyroid tumorigenesis in murine models, indicating that addition
216 ayed a potential oncogenic role in mediating tumorigenesis in non-small cell lung cancer (NSCLC).
217 Vgll4-4A (S58A/S155A/T159A/S280A) suppressed tumorigenesis in pancreatic cancer cells in vitro and in
218 pressor kinase LKB1 lead to gastrointestinal tumorigenesis in Peutz-Jeghers syndrome (PJS) patients a
219 xpression and activity, chemoresistance, and tumorigenesis in subcutaneous and intrabursal mouse xeno
222 LECT and demonstrate that Vitamin E promotes tumorigenesis in the early stages of prostate cancer evo
223 anscription factor was equally important for tumorigenesis in the intrabursal model, but had no effec
225 lish the mechanism underlying UBE3A-mediated tumorigenesis in this disease.Significance: These findin
227 ngly, loss of Atf3 also promoted spontaneous tumorigenesis in Trp53(+/-) mice, but did not affect tum
228 lar membrane, blocks dietary fat-accelerated tumorigenesis in vivo Our findings uncover the molecular
229 damage, a mutator phenotype associated with tumorigenesis in vivo Thus, these studies demonstrate a
237 p53 but also gain new activities to promote tumorigenesis independently of wild-type p53, termed gai
238 ogated Hippo signal deficiency-induced liver tumorigenesis, indicating their epistatic interaction.
240 ll fate determination factor, contributes to tumorigenesis, invasion, metastasis of human breast neop
244 ation of the function of genes implicated in tumorigenesis is limited by the need to generate and cro
249 ation of developmental gene promoters during tumorigenesis may therefore reflect the misappropriation
251 eta-catenin signaling-mediated breast cancer tumorigenesis, metastasis, and cancer stem cell (CSC) ma
252 hybrid cells exhibited increased migration, tumorigenesis, metastasis, red blood cell recruitment to
253 nesis, neuronal maturation and survival, and tumorigenesis, mostly through regulating cell cycle prog
257 genetic and epigenetic determinants of BTIC tumorigenesis offer novel opportunities for RNAi-mediate
258 tumoral contexts and shown to promote breast tumorigenesis or to trigger the tumoral angiogenic switc
260 e lineage-specific function of CDC42 in lung tumorigenesis potentially through the regulation of cell
261 ncidence and mortality, and as a result, CRC tumorigenesis, progression and metastasis have been heav
262 that CTNNB1 mutations may be more related to tumorigenesis rather than excessive aldosterone producti
263 of gene isoform ASE is widespread, including tumorigenesis relevant genes and pluripotency markers.
268 fully penetrant and slowly evolving prostate tumorigenesis showed that a high calcium diet dramatical
269 ting epithelial cancer stem cells with rapid tumorigenesis signatures in future might help to combat
271 d an E2F1-p73-apoptosis axis in DKO prostate tumorigenesis, slowed disease progression and significan
272 resents a therapeutic opportunity to inhibit tumorigenesis specifically in the context of PTEN deleti
274 echanism by which inflammation impacts colon tumorigenesis, STEAP4 expression, function, and mitochon
275 that MED1 is critical for HER2-driven breast tumorigenesis, suggesting its candidacy as a disease-sel
276 as a critical mediator of HER2-driven breast tumorigenesis, suggesting its candidacy as a disease-sel
277 ethylnitrosamine-induced (DEN-induced) liver tumorigenesis that correlated with increased DEN-induced
278 ring the decades required for HPV-associated tumorigenesis, the cellular genome becomes significantly
280 transduction pathways emanating from KIT for tumorigenesis, the oncogenic Kit(V558Delta) mutation was
281 s and mice reveal that Akt2 controls hepatic tumorigenesis through crosstalk between HNF1alpha and PP
282 , pharmacological blockade of UBE2O inhibits tumorigenesis through the restoration of AMPKalpha2, sug
283 ta-catenin, a key factor that drives colonic tumorigenesis, through activating pancreatic ER kinase/e
284 ifier of both p53-dependent and -independent tumorigenesis, underscoring the complexity of MDM2 postt
287 ta suggest that KSHV augments EBV-associated tumorigenesis via stimulation of lytic EBV replication.
289 The role of mesenchymal-derived cells in TSC tumorigenesis was investigated through disruption of Tsc
291 ute 2 (MDM2)-p53 pathway to APC loss-induced tumorigenesis, we crossed mice bearing MDM2(C305F) mutat
292 er the mechanism by which SLFN5 promotes GBM tumorigenesis, we found that this protein is a transcrip
293 Using a murine model of inflammation-induced tumorigenesis, we tested the hypothesis that inflammatio
295 and critical mechanism for mutant p53 GOF in tumorigenesis, which could be targeted for therapy in tu
296 way and chronic inflammation in KSHV-induced tumorigenesis, which helps explain why HIV-infected pati
299 ecule JAK inhibitor, abolishes FGF19-induced tumorigenesis, while the regulatory functions of FGF19 i
300 uman ubiquitin ligase HUWE1 has key roles in tumorigenesis, yet it is unkown how its activity is regu
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