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1 ycle and self-renewal regulation to restrain tumorigenesis.
2 nome-wide redistribution and couples BRAF to tumorigenesis.
3 in proliferating cells, predisposing them to tumorigenesis.
4 ts, partly because of its documented role in tumorigenesis.
5 ation of APC significantly contribute to CRC tumorigenesis.
6 fication of the role of 'oncometabolites' in tumorigenesis.
7 portant role in governing stem cell fate and tumorigenesis.
8 ll growth during intestinal regeneration and tumorigenesis.
9 tasis, whereas its dysregulation can lead to tumorigenesis.
10 Avoiding immune destruction is essential for tumorigenesis.
11 ssue stem cells to promote tissue repair and tumorigenesis.
12 y an emerging role in cancer progression and tumorigenesis.
13 ice caused increased H(2)O(2) production and tumorigenesis.
14 in murine colon and liver tissues increases tumorigenesis.
15 inal diseases such as colitis and intestinal tumorigenesis.
16 nd epithelium during tissue regeneration and tumorigenesis.
17 gulatory domains and these features impacted tumorigenesis.
18 etraploidization are responsible for driving tumorigenesis.
19 ffect of defined allelic variants on mammary tumorigenesis.
20 Wnt/beta-catenin signaling-mediated prostate tumorigenesis.
21 to be crucial integrators in the pathways of tumorigenesis.
22 a indicate that adiponectin suppresses colon tumorigenesis.
23 cluding neurodevelopment, embryogenesis, and tumorigenesis.
24 le for TGFbeta signaling on myeloid cells in tumorigenesis.
25 jacked in cancer and play a critical role in tumorigenesis.
26 r deregulation is frequently associated with tumorigenesis.
27 nd bacterial factors responsible for gastric tumorigenesis.
28 tion also seems to confer protection against tumorigenesis.
29 enome integrity and typically deregulated in tumorigenesis.
30 ional association of LKB1 dosage to prostate tumorigenesis.
31 if the secretome was involved in BRF1-driven tumorigenesis.
32 ing metabolic and inflammatory disorders and tumorigenesis.
33 uggesting regulatory network rewiring during tumorigenesis.
34 anistic insight into hTERT activation during tumorigenesis.
35 e constrains the mutational landscape during tumorigenesis.
36 s, aneuploidy is not a universal promoter of tumorigenesis.
37 rs ERMS differentiation, contributing to RMS tumorigenesis.
38 ss), and these splicing errors contribute to tumorigenesis.
39 retory pathway are often dysregulated during tumorigenesis.
40 cell overproliferation due to aging or even tumorigenesis.
41 e that restricts cell lineage progression in tumorigenesis.
42 ote cancer cell proliferation, invasion, and tumorigenesis.
43 modification in mRNA, has been implicated in tumorigenesis.
44 destruction complex in Wnt-driven intestinal tumorigenesis.
45 different models of sporadic, autochthonous tumorigenesis.
46 ortant for viral life cycle and HPV-mediated tumorigenesis.
47 activity of the chaperonin and is needed for tumorigenesis.
48 ) have biallelic NF1 mutations necessary for tumorigenesis.
49 to inhibit proliferation, clonogenicity, and tumorigenesis.
50 microenvironment may play an active role in tumorigenesis.
51 their implications for our understanding of tumorigenesis.
52 umor subpopulation-enriched gene networks in tumorigenesis.
53 n accumulation of mutations that can promote tumorigenesis.
54 secondary concomitant alterations to promote tumorigenesis.
55 otes oncogenic Kras-driven pancreatic ductal tumorigenesis.
56 sion gene and stem cell marker that controls tumorigenesis.
57 Aneuploidy can instigate tumorigenesis.
58 match repair propels colorectal cancer (CRC) tumorigenesis.
59 es in adaptation, evolution, senescence, and tumorigenesis.
60 n activated coagulation system implicated in tumorigenesis.
61 d in NSCLC and other cancers, in KRAS-driven tumorigenesis.
62 ial cells during intestinal regeneration and tumorigenesis.
63 he genotoxic stress response and suppressing tumorigenesis.
64 y key roles in MYC regulation and RAS-driven tumorigenesis.
65 in, a driver of proliferation and colorectal tumorigenesis.
66 ggesting that condensates play a key role in tumorigenesis.
67 lation in the number of centrosomes triggers tumorigenesis.
68 to be understood about how it contributes to tumorigenesis.
69 region that potentially contributes to ERMS tumorigenesis.
70 of STAT3 and ERK during the later stages of tumorigenesis.
71 uncover the key miRNAs during the process of tumorigenesis.
72 y contribute to aging and favorably suppress tumorigenesis.
73 most well-characterized drivers of prostate tumorigenesis.
74 and its metabolites play a critical role in tumorigenesis.
75 tential to fight the tumor without promoting tumorigenesis.
76 athways that are therapeutically involved in tumorigenesis.
77 -modulatory program that supports pancreatic tumorigenesis.
78 , in turn influencing contact inhibition and tumorigenesis.
79 0 genes that are implied in all steps of CRC tumorigenesis.
80 of noncoding somatic mutations in promoting tumorigenesis.
81 ontribute to aberrant cell proliferation and tumorigenesis.
82 gated in gastric epithelial cells or gastric tumorigenesis.
83 ole as founding mutations in UV-induced skin tumorigenesis.
84 model for studying the role of aneuploidy in tumorigenesis.
85 nanticipated consequences of injury, such as tumorigenesis.
86 and revealed genes that contribute to breast tumorigenesis.
87 omology-directed repair pathway and prostate tumorigenesis.
88 for immune responses against infections and tumorigenesis.
89 only for H. pylori pathogenesis but for host tumorigenesis.
90 TSGs) were observed to alter the dynamics of tumorigenesis.
91 blation inhibits PTEN heterozygosity-induced tumorigenesis.
92 their effects on cell cycle progression and tumorigenesis.
93 loss of BCCIP functions is more relevant to tumorigenesis.
94 green swordtails leads to lethal melanocyte tumorigenesis.
95 n mice; IL22 increased with pancreatitis and tumorigenesis.
96 ufficient to trigger genomic instability and tumorigenesis.
97 grees have been reported to be implicated in tumorigenesis.
98 ies related to mammary gland development and tumorigenesis.
99 ckdown of ADAR1 attenuates proliferation and tumorigenesis.
100 ), whose activating mutations underlie human tumorigenesis.
101 or microenvironment and its putative role in tumorigenesis.
102 TX in TSC2-deficient cell fitness and in TSC tumorigenesis.
103 lastoma microenvironment that contributes to tumorigenesis.
104 bolism, and the susceptibility to colorectal tumorigenesis.
105 and limits tetraploidy, a starting point for tumorigenesis.
106 ts in chronic inflammation, often leading to tumorigenesis.
107 be indicative of metabolic abnormalities or tumorigenesis.
108 maintain a balance between inflammation and tumorigenesis.
110 ulation of this homeostasis is implicated in tumorigenesis and acquired resistance to treatments.
111 e been reported to have an important role in tumorigenesis and an inverse association with tumor prog
112 erred an increased risk of spontaneous liver tumorigenesis and B-cell lymphoma development at old age
113 cell stemness during Kras-driven pancreatic tumorigenesis and can be targeted for development of a n
114 posttranslational modifications important to tumorigenesis and cancer cell growth, here we report a c
117 proteins, the ubiquitin ligase RNF4 promotes tumorigenesis and confers resistance to targeted therapy
119 en made in the past decade to understand the tumorigenesis and genetic landscape of each biliary trac
120 tive lipids associated to various aspects of tumorigenesis and have been extensively studied in cance
121 aberrant expression of PLK1 triggers CIN and tumorigenesis and highlights potential therapeutic oppor
122 -in mice showed markedly reduced spontaneous tumorigenesis and increased resistance to Myc-driven lym
124 t to the significance of epigenetic aging in tumorigenesis and its potential use for cancer risk pred
128 ctor NFE2-related factor 2 (NRF2) influences tumorigenesis and metastasis, and where the current gaps
129 ) mice are susceptible to lung inflammation, tumorigenesis and metastasis, which resembles the pathol
131 es, from senescent stromal cells can promote tumorigenesis and multidrug resistance in prostate or br
132 chaperone FACT is upregulated during mammary tumorigenesis and necessary for the viability and growth
135 endothelial cells, supporting Kaposi sarcoma tumorigenesis and representing attractive therapeutic ta
137 ociated DNA polymerase e (Pole) mutations on tumorigenesis and response to immune checkpoint blockade
138 mation by TNF-alpha neutralization inhibited tumorigenesis and reversed MHC-II upregulation on tumor
139 els to uncover the mechanism of ERG-mediated tumorigenesis and subsequent oncogenic dependencies in p
140 adictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferatio
141 tant donor cells increases proliferation and tumorigenesis and that knockdown of Rab13 blocks these e
142 sis is selectively relaxed relative to early tumorigenesis and that metastasis-private mutations are
144 that there is no direct correlation between tumorigenesis and viral load and consequently no evidenc
145 7M-driven transcriptome remodelling promotes tumorigenesis and will be critical for targeting cancers
146 step to uncover the epigenetic mechanism of tumorigenesis, and identify biomarkers for cancer subtyp
149 s-induced chromosomal alterations in ovarian tumorigenesis, and they add new genes to known cancer pa
152 The mechanisms of AIP-dependent pituitary tumorigenesis are still under investigation and evidence
153 studied extensively, as frequent drivers of tumorigenesis as well as potential therapeutic targets.
155 ghly expressed in neuroblastoma and promotes tumorigenesis, at least, in part, through inhibition of
156 lterations are located in genes important in tumorigenesis (ATRX, BCOR, CDKN2B, MAP3K1, MAP3K4, MDM2,
157 oliferation and progression in mTORC1-driven tumorigenesis but the picture of the relevant FoxO targe
158 tially be valuable in not only understanding tumorigenesis, but also developing effective diagnosis,
160 receptor tyrosine kinase ligand enhancer in tumorigenesis, but the impact of endocan on EGFR-driven
161 entiation have been implicated in pancreatic tumorigenesis, but the molecular mechanisms are poorly u
162 on factors (TFs) are important regulators of tumorigenesis, but their biological functions are often
163 ylation cooperate with active Ras to promote tumorigenesis by abolishing the inhibitory function of R
164 te that organismal hyperinsulinemia promotes tumorigenesis by abrogating local cell competition.
165 by which diet and antibiotic use can promote tumorigenesis by colon cancer cells at the anastomosis a
167 s that gives rise to aneuploidy, can promote tumorigenesis by increasing genetic heterogeneity and pr
170 that a novel lncRNA SCIRT counteracts breast tumorigenesis by opposing transcriptional networks assoc
171 CAV1 expression to promote angiogenesis and tumorigenesis by regulating the formation of STAT3-DNMT1
172 and RNA splicing, plays an important role in tumorigenesis by supporting cancer cell growth and suppr
173 ET and Wnt/beta-catenin cascades in prostate tumorigenesis by using a newly generated mouse model in
174 naling integrates the two tissues to promote tumorigenesis, by co-opting a normal regulatory mechanis
176 ufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to c
178 vates tumor Akt, exacerbating ErbB2-mediated tumorigenesis, curbed by pharmacological reduction of th
179 nary process, there are repeated patterns in tumorigenesis defined by recurrent driver mutations and
180 yet RAS mutation itself is insufficient for tumorigenesis, due in part to profound metabolic stress
181 -PD-1 axis and were sufficient to accelerate tumorigenesis, even in the absence of endogenous PD-L1;
183 r with pathway and lineage analyses to study tumorigenesis from a developmental perspective in a mous
184 ay fundamental roles in multistep process of tumorigenesis, from cellular transformation, disease pro
186 yet questions remain regarding mechanisms of tumorigenesis, genotype-phenotype correlation, and thera
187 ) to degrade proteins that are important for tumorigenesis has emerged as a potential therapeutic str
189 nd consequences of lineage plasticity during tumorigenesis have remained mysterious due to the limits
190 our understanding of molecular mechanisms of tumorigenesis have translated into knowledge-based thera
191 vitally involved in tissue inflammation and tumorigenesis, here we employed a genome-wide CRISPR kno
192 est that extracellular ATP may promote liver tumorigenesis, however, the underlying mechanisms are po
193 es a hypermutator phenotype that can lead to tumorigenesis; however, the functional impact of the hig
197 nduced cell proliferation and promotes colon tumorigenesis in a preclinical colitis-associated tumor
198 d in DNA repair, chromocenter formation, and tumorigenesis in addition to changes in chromatin access
199 enin in the intestinal crypt, augmenting CRC tumorigenesis in an adenomatous polyposis coli (APC(Delt
203 ve mode, mutant p53 eliminated dysplasia and tumorigenesis in Csnk1a1-deficient and Apc(Min/+) mice,
205 n SmgGDS promotes cell-cycle progression and tumorigenesis in human breast and nonsmall cell lung can
207 ies against IL27 and an FFAR2 agonist reduce tumorigenesis in mice and might be developed for the tre
208 at lung-specific loss of Kmt2d promotes lung tumorigenesis in mice and upregulates pro-tumorigenic pr
211 We have demonstrated that TCS promotes liver tumorigenesis in mice, yet the biological and molecular
216 hosphorylation to glycolysis is required for tumorigenesis in order to provide cancer cells with ener
218 te that IEC-specific PHB1 combats intestinal tumorigenesis in the Apc(Min/+) mouse model by inhibitin
220 nd that deletion of Gcn5 delays or abrogates tumorigenesis in the Emu-Myc mouse model of B-cell lymph
221 that oral dysbiotic states can contribute to tumorigenesis in the oral cavity as well as in distant b
222 gGDS splicing in the mammary gland and slows tumorigenesis in this aggressive model of breast cancer.
227 alyses were performed at different stages of tumorigenesis in vivo, as well as in primary mouse hepat
228 e self-renewal of ovarian CSC and suppressed tumorigenesis in vivo, both of which required FTO demeth
230 mon genes implicated in biliary tract cancer tumorigenesis include IDH1, IDH2, FGFR1, FGFR2, FGFR3, E
231 to form skin tumors during two-step chemical tumorigenesis, indicating a protumorigenic role for inte
241 prostate epithelium was inconsequential for tumorigenesis, its combination with an oncogenic insult,
242 ticity to human health, covering its role in tumorigenesis, its crosstalk with innate immunity respon
243 on of the antiviral factor ZAP in colorectal tumorigenesis, linking intrinsic immunity to tumor patho
244 nd a better understanding of its function in tumorigenesis may further the development of new therape
246 f the transcriptional repressor BCL6 enables tumorigenesis of germinal center B-cells, and hence BCL6
249 a crucially important metabolic network for tumorigenesis, of unanticipated complexity, and with imp
250 Here, we investigate the consequences of tumorigenesis on the microbiome using a Drosophila intes
251 hile Bcor (DeltaE9-10) alone did not promote tumorigenesis or affect GNP differentiation, Bcor (Delta
253 thelial-to-mesenchymal transition signature, tumorigenesis proceeds through Wnt-differential cancer s
254 drogenase (ALDH) have been implicated in key tumorigenesis processes including cancer initiating cell
255 Taken together, our results reveal a unique tumorigenesis profile for PRD mutations that is distinct
256 onmental consequences of obesity that foster tumorigenesis rather than new driver gene mutations, inc
257 r potential clinical application and role in tumorigenesis, recent studies have shown that MAGE prote
258 c-Cbl(+/-) alone was insufficient to induce tumorigenesis regardless of an increase in the number of
268 ncreased in villin-TLR4 mice; TLR4-dependent tumorigenesis required the presence of DUOX2 and a micro
269 hese findings demonstrate that KRAS-mediated tumorigenesis requires PKCe expression and highlight the
270 s illustrated the hub genes involved in KIRC tumorigenesis, shedding light on the development of prog
271 idermal growth factor receptor (EGFR)-driven tumorigenesis similarly relies on the interaction betwee
272 DNA damage, genome instability, and further tumorigenesis so that LRPPRC knockout mice develop more
274 this Review, we discuss systemic effects of tumorigenesis that are now being appreciated in epimorph
276 ling axis as a critical mechanism for glioma tumorigenesis that may serve as a new therapeutic target
277 with oncogenic PI3K to promote rapid mammary tumorigenesis, the additional loss of PTEN protein-phosp
278 lease stimulatory factors to accelerate PDAC tumorigenesis, the metabolic contribution of peripheral
279 nd examine the effects of these mutations on tumorigenesis, the tumor mutational landscape, and the t
280 While kinases often play key roles driving tumorigenesis, there are strikingly few kinases known to
282 model, Deptor knockout accelerated prostate tumorigenesis triggered by Pten loss via the activation
284 B4GALNT1, and consequently GM2/GD2, enhanced tumorigenesis via induction of angiogenesis, AIG, and ce
285 in the prostate, and its depletion promotes tumorigenesis via the activation of mTORC1 and mTORC2 si
286 te with KRAS mutations to promote multi-step tumorigenesis via the Wnt-Ras-p53 axis in human colon ca
288 w ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murin
289 determine whether Plk1 overexpression drives tumorigenesis, we established transgenic mouse lines tha
290 nderstand the impact of EBV variation in eBL tumorigenesis, we improved viral DNA enrichment methods
291 ress the role that BRG1 loss plays in SCCOHT tumorigenesis, we performed integrative multi-omic analy
292 f differentially regulated genes involved in tumorigenesis were expressed in a highly coordinated man
293 rotected obese/diabetic mice against hepatic tumorigenesis, whereas lean/nondiabetic mice developed t
294 delta-catenin promoted Myc-induced prostate tumorigenesis while increasing bFGF-p38 MAP kinase signa
295 proliferation, thus restraining HRAS-driven tumorigenesis while maintaining normal tissue growth.
296 cer, oncogenic KRAS is insufficient to drive tumorigenesis, while addition of modest MYC overexpressi
297 sion, showing that obesity markedly enhances tumorigenesis, while genetic or dietary induction of wei
298 on were resistant to spontaneous and induced tumorigenesis, while they had shortened lifespan, but di
299 out in urethane- and KRAS(G12D)-induced lung tumorigenesis with decreased pAKT levels observed in the
300 iption of Wnt target genes and regulation of tumorigenesis, with important clinical implications.