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1 induce mutations, chronic liver damage, and carcinogenesis.
2 ns and have been suggested to play a role in carcinogenesis.
3 umor suppressor function of TGFbeta in liver carcinogenesis.
4 it has also been intimately associated with carcinogenesis.
5 tion contribute to differences in colorectal carcinogenesis.
6 m for downregulating Notch during UV-induced carcinogenesis.
7 bility, which can both lead to cell death or carcinogenesis.
8 ation that in turn mean an increased risk of carcinogenesis.
9 ys in mediating the observed effects on lung carcinogenesis.
10 ls play a major role in nearly every step of carcinogenesis.
11 h the occurrence of gastric inflammation and carcinogenesis.
12 urogenital schistosomiasis promotes bladder carcinogenesis.
13 ress replication stress, and protect against carcinogenesis.
14 so plays an understudied role in suppressing carcinogenesis.
15 enhances human papillomavirus (HPV)-induced carcinogenesis.
16 nderstand the etiology of this virus-induced carcinogenesis.
17 intestinal microbiome to promote colorectal carcinogenesis.
18 oprotein is a primary driver of HPV-mediated carcinogenesis.
19 isorders beyond the well-established role in carcinogenesis.
20 o the understanding of EBV infection-related carcinogenesis.
21 rand breaks prevents genomic instability and carcinogenesis.
22 ays contributing to gastric inflammation and carcinogenesis.
23 heir emergence, offering a window into early carcinogenesis.
24 role for adenosine-to-inosine RNA editing in carcinogenesis.
25 mbedded noncoding somatic mutations in human carcinogenesis.
26 promote regeneration, likely independent of carcinogenesis.
27 ronic inflammation as a mechanism of ovarian carcinogenesis.
28 define cancer-specific SEs and their role in carcinogenesis.
29 c thyroid cancer cells contribute to thyroid carcinogenesis.
30 d digestion, metabolic processes and gastric carcinogenesis.
31 A methylation alterations happening early in carcinogenesis.
32 w a gut microbe may contribute to colorectal carcinogenesis.
33 hallmarks of cell proliferation and hepatic carcinogenesis.
34 stance and consequently contributes to colon carcinogenesis.
35 l transduction network, critical to melanoma carcinogenesis.
36 brafish development, liver regeneration, and carcinogenesis.
37 l to lead to new insights into mechanisms of carcinogenesis.
38 C2 axis, which is essential for ErbB2-driven carcinogenesis.
39 l transition, a key event in development and carcinogenesis.
40 nyl electrophiles in inflammation-associated carcinogenesis.
41 rine/threonine kinase recently implicated in carcinogenesis.
42 is important for understanding mechanisms of carcinogenesis.
43 ncer risk in order to identify mechanisms of carcinogenesis.
44 on to induce VGPC transformation and gastric carcinogenesis.
45 s of the METTL3-m(6)A-CDCP1 axis in chemical carcinogenesis.
46 DNA methylation is associated with anal carcinogenesis.
47 radiation-induced cardiovascular disease and carcinogenesis.
48 tigation of epithelial cell polarization and carcinogenesis.
49 effector protein that contributes to gastric carcinogenesis.
50 e H2 activity is disrupted during intestinal carcinogenesis.
51 suppressing colonic mucosal inflammation and carcinogenesis.
52 echanisms during thyroid differentiation and carcinogenesis.
53 ortant downstream mechanism of PRC2-mediated carcinogenesis.
54 udy the roles of RNase H2 in tissue-specific carcinogenesis.
55 ) transcription factors plays vital roles in carcinogenesis.
56 mmune response to H. pylori colonization and carcinogenesis.
57 promoter, activate gene expression to drive carcinogenesis.
58 pathway plays a critical role in colorectal carcinogenesis.
59 against primary 3-methylcholantrene-induced carcinogenesis.
60 ate between pre-cancer and cancer in gastric carcinogenesis.
61 ation, may protect against UVB-mediated skin carcinogenesis.
62 with tumor pathogenesis during all stages of carcinogenesis.
63 ape powder-fortified diet (3% or 5%) on skin carcinogenesis.
64 emonstrated that YES1 is essential for NSCLC carcinogenesis.
65 n the early stages of prostate tumorigenesis carcinogenesis.
66 al, suggesting an important role in cervical carcinogenesis.
67 as an essential mechanism to increase colon carcinogenesis.
68 hemselves, contributes to suppression of BCC carcinogenesis.
69 ode long non-coding RNAs implicated in human carcinogenesis.
70 gulate gene-environment interaction in human carcinogenesis.
71 gesting that GalNAc-T6 plays a role in colon carcinogenesis.
72 ich represent important initiating events in carcinogenesis.
73 complex relationships between aneuploidy and carcinogenesis.
74 rning how vascular morphology evolves during carcinogenesis.
75 promotion-malignant-conversion hypothesis of carcinogenesis.
76 latter is due to its viral or UV-associated carcinogenesis.
77 uced DNA damage and repair and ultimately UV carcinogenesis.
78 in breast tissue with implications in breast carcinogenesis.
79 us to hypothesize that it may play a role in carcinogenesis.
80 oprotein is a primary driver of HPV-mediated carcinogenesis.
81 gene mutations play only part of the role in carcinogenesis.
82 ated by SUV irradiation and involved in skin carcinogenesis.
83 rimary target for HPV infection and cervical carcinogenesis.
84 to chronic inflammation and promotes hepatic carcinogenesis.
85 rategy to prevent schistosomiasis-associated carcinogenesis.
86 ive pS-STAT3 in Helicobacter-induced gastric carcinogenesis.
87 provide clues to the roles bacteria play in carcinogenesis.
88 teomic alteration that supports BRCA1-mutant carcinogenesis.
89 ed mutations in viral clearance and cervical carcinogenesis.
90 intestinal microbiome to promote colorectal carcinogenesis.
91 ial cancer is associated with aneuploidy and carcinogenesis.
92 osphatidylglycerols contribute to esophageal carcinogenesis.
93 o function as a tumor suppressor during skin carcinogenesis.
94 the calculation of the risk of developing a carcinogenesis.
95 d the early clonal evolutionary hallmarks of carcinogenesis.
96 tumour stroma regulates nearly all stages of carcinogenesis.
97 me-wide epigenetic aberrations in urothelial carcinogenesis.
98 t schistosomiasis can promote hepatocellular carcinogenesis.
99 nd the mechanisms of environmentally induced carcinogenesis.
100 tant role in inflammation-associated gastric carcinogenesis.
101 mplicating the complement system in prostate carcinogenesis.
102 ointestinal tract and is dysregulated during carcinogenesis.
103 link between incessant ovulation and ovarian carcinogenesis.
104 tect against UVB-induced DNA damage and skin carcinogenesis.
105 may directly and/or indirectly contribute to carcinogenesis.
106 r oncogenic AR transcription during prostate carcinogenesis.
107 standing squamous epithelial homeostasis and carcinogenesis.
108 types require different numbers of hits for carcinogenesis?
110 genes susceptible to mutagenic insults, with carcinogenesis accelerated by germline DNA repair gene d
114 posure denotes an early process occurring in carcinogenesis analogous to the oxidative events surfaci
115 asopharyngeal, breast, melanoma, and bladder carcinogenesis and are regulated by the epigenetic lands
116 d groupings of tumors differentiate early in carcinogenesis and are, therefore, appropriate targets f
117 TOPK-032 suppressed chronic SSL-induced skin carcinogenesis and c-Jun phosphorylation levels in SKH1
118 ication of histone is extensively studied in carcinogenesis and cancer cell's response to chemotherap
119 ring early neoplastic events and its role in carcinogenesis and cancer progression is not fully under
120 standing the molecular mechanisms underlying carcinogenesis and cellular events during cancer progres
121 oncoprotein plays a crucial role in cervical carcinogenesis and commonly cause the dysregulation of t
122 s on recent advances in elucidating prostate carcinogenesis and explore novel therapeutic and prevent
123 herapy, we exposed K5.Smad7 skin to chemical carcinogenesis and found reduced myeloid leukocyte infil
124 nctional fusions, identifying new drivers of carcinogenesis and fusions that could have clinical impl
125 un at Ser63 and Ser73 in the process of skin carcinogenesis and HI-TOPK-032 could be used as a potent
126 genetic mechanisms contributing to pulmonary carcinogenesis and highlight ASXL3 as a novel candidate
127 vides an elegant model for neutrophil-driven carcinogenesis and identifies potential targets for immu
129 golian gerbils as models of H pylori-induced carcinogenesis and in C57BL/6 mice treated with azoxymet
130 with IgA(+) cell generation attenuates liver carcinogenesis and induces cytotoxic T-lymphocyte-mediat
131 microbiota at different stages of Barrett's carcinogenesis and investigate the Cytosponge as a minim
132 ls are important in alveolar maintenance and carcinogenesis and may be a therapeutic target against p
135 thway controlling the REGgamma-proteasome in carcinogenesis and offer a novel approach to drug-resist
136 )R and ET(B)R play dichotomous roles in oral carcinogenesis and pain, such that ET(A)R activation and
138 As (miRNAs) are implicated in every stage of carcinogenesis and play an essential role as genetic bio
139 cantly reduced numbers of tumors during skin carcinogenesis and presented a prolonged latency of tumo
140 olecular and cellular heterogeneity of field carcinogenesis and propose directions to tackle these vo
141 ysregulated translation that is a feature of carcinogenesis and propose dysregulated translation as a
142 current science in relation to environmental carcinogenesis and recommends improvements to protect pu
144 tion may further our understanding of breast carcinogenesis and reveal new therapeutic opportunities.
145 ole for hormone-related exposures in ovarian carcinogenesis and risk factor differences by histologic
147 ng evidence that CRP plays a role in ovarian carcinogenesis and suggests that inflammation may be par
148 nset of cDC1 dysregulation during pancreatic carcinogenesis and suggests therapeutically tractable st
150 a and fungi have been shown to contribute to carcinogenesis and therapeutic responses, both positivel
152 mportance of genomic instability in prostate carcinogenesis and tumor progression, we performed ultra
154 , there are many gaps about the diffuse-type carcinogenesis and, as a result, its epidemiologic and p
155 C-reactive protein is involved in ovarian carcinogenesis, and chronic inflammation may be particul
156 Notch signaling plays a complex role in carcinogenesis, and its signaling pathway has both tumor
157 Aberrant stem cell activation is linked to carcinogenesis, and Lrig1 (leucine-rich repeats and Ig-l
158 genesis, focusing particularly on pancreatic carcinogenesis, and show that modulation of the microbio
160 ble exposed cells immune escape resulting in carcinogenesis, and why patients who smoke respond bette
161 model the level of risk of developing fatal carcinogenesis; and third, test whether pattern of injur
162 MC), developed in the 1950 s-70s, postulated carcinogenesis as a Darwinian somatic selection process.
165 onses; evaluate biological events leading to carcinogenesis both spatially and temporally; examine th
166 ta HPVs appear to be not the main drivers of carcinogenesis but rather facilitators of the accumulati
167 As (miRNAs) have been implicated in cervical carcinogenesis, but have never been assessed in anal pre
168 ther light into the complexity of colorectal carcinogenesis, but it also puts forward a potential nov
169 The AhR and its ligands also inhibit colon carcinogenesis, but it has been reported that the AhR an
170 lesion associated with an increased risk for carcinogenesis, but the mechanism(s) by which inflammati
171 ithelial cells meet, are high-risk sites for carcinogenesis, but the underlying mechanism remains lar
173 Here, we studied its involvement in thyroid carcinogenesis by analyzing its expression in cancer tis
174 ndicate that SMOX promotes H. pylori-induced carcinogenesis by causing inflammation, DNA damage, and
175 mor initiators, and that they stimulate skin carcinogenesis by elevating p38MAPK and MAPK/ERK signali
177 essed MCPs can support multiple hallmarks of carcinogenesis by interacting with various cellular comp
178 nsulin receptor plays a central role in skin carcinogenesis by regulating cytoskeleton assembly.
182 l the acquisition of aneuploidy during early carcinogenesis, chromosome missegregation was induced in
183 e infiltration in tumors but not accelerated carcinogenesis compared with wild-type littermates.
184 e, we review recent evidence on how serrated carcinogenesis contributes to the subtype of CRC with th
185 rogression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modific
187 ich genomic and non-genomic factors initiate carcinogenesis, drive cell invasion and metastasis, and
188 m the AR cistrome in the process of prostate carcinogenesis, ERG knockout in established prostate can
190 golipid deterioration in inflammation versus carcinogenesis for the pathophysiology of colitis-associ
192 f glucose metabolism to favor hepatocellular carcinogenesis (HCC), but the upstream signaling events
193 on of biomarkers expressed at early onset of carcinogenesis, hold promise for the identification of s
194 fection is the vital factor driving cervical carcinogenesis; however, other features of the local cer
195 We also identified a primordial marker of carcinogenesis in a cancer-predisposed strain of mice, a
197 is one of the first events in the process of carcinogenesis in cervical and head and neck cancers.
200 ns, we deepen the molecular understanding of carcinogenesis in head and neck squamous cell carcinoma.
203 e results indicate that mutagenesis and skin carcinogenesis in IGF-1-deficient geriatric skin may be
207 r chromatin folding throughout all stages of carcinogenesis in multiple tumor types, and prior to tum
208 me-derived metabolome, potentially promoting carcinogenesis in organs that are distal to the gut.
209 genic pathways, including BMP4, and promotes carcinogenesis in patients and in animal models with ZFP
213 ther inhibiting autophagy affects colorectal carcinogenesis in susceptible mice infected with CoPEC.
216 ate cell proliferation, differentiation, and carcinogenesis in the endometrium by controlling gene tr
220 ain oral bacterial species can contribute to carcinogenesis, in particular, Fusobacterium nucleatum a
223 uPV1 vaccination were protected against skin carcinogenesis induced by chemicals or by ultraviolet ra
224 ted with human diseases groups, particularly carcinogenesis, inflammation, and infectious diseases.
225 es contribute to cellular transformation and carcinogenesis involving the deregulation of various mol
226 The contribution of the microenvironment to carcinogenesis is a key area of research, offering new p
233 To improve the understanding of keratinocyte carcinogenesis, it is critical to understand epigenetic
235 gnaling pathway and targeted therapy in skin carcinogenesis may helpful for the discovery of addition
236 microenvironment are active participants in carcinogenesis mediating both tumor initiation and progr
237 demonstrated an important role for ERBB3 in carcinogenesis, metastasis, and acquired drug resistance
238 ory gene expression patterns associated with carcinogenesis might be tested as chemopreventive agents
239 ish whether 4-nitroquinoline N-oxide-induced carcinogenesis mirrors the heterogeneity of human oral s
244 en oxidative stress, low-grade inflammation, carcinogenesis, obesity and physical activity are poorly
245 " We asked whether reflux-induced esophageal carcinogenesis occurred via minority MOMP and whether co
248 These observations provide insights into the carcinogenesis of POLE-driven tumors and valuable inform
249 isk human papillomavirus 16 (HPV16)-mediated carcinogenesis of the cervical epithelium than for other
251 cial; however, a deeper understanding of the carcinogenesis pathway supports a potential window of op
252 Combined, these data suggest that during carcinogenesis pERK initially facilitates and later anta
253 lop from duct-like cells through a multistep carcinogenesis process, from low-grade dysplastic lesion
255 sing a chemotherapy followed by the two-step carcinogenesis protocol potentiated the conversion of be
264 derstanding the largely uncharted biology of carcinogenesis requires deciphering molecular processes
265 t, dynamic models of HPV infection, cervical carcinogenesis, screening, and precancer and invasive ca
269 e pioneer factors exert effects that promote carcinogenesis, some of their functions may inhibit cert
271 's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, trauma
272 m solar UV irradiation, and a long-term skin carcinogenesis study showed that deletion of TRAF1 in mi
274 dical perspective as well as a new theory of carcinogenesis that is compatible with evolutionary theo
275 s and mechanisms of action of HDAC10 in lung carcinogenesis that will inform the rationale for target
276 ncer risk in order to identify mechanisms of carcinogenesis that will lead to the prevention of this
277 s, that have acquired DNA methylation during carcinogenesis, they induce the expression of thousands
278 ssion by hypermethylation may promote kidney carcinogenesis through exacerbating the functional decli
279 ow genetic risk variants might contribute to carcinogenesis through the regulation of susceptibility
280 o the attenuation of chemically induced skin carcinogenesis through the synergistic regulation of STA
281 cture as an enabling characteristic in early carcinogenesis to facilitate malignant transformation, w
282 tor linking chronic inflammation and gastric carcinogenesis using gastritis-prone SAMP1/YitFc (SAMP)
283 ce of Mst1r kinase to Kras driven pancreatic carcinogenesis using genetically engineered mouse models
284 of possible aetiological drivers of ovarian carcinogenesis using germline genetic variants to proxy
285 gated the preventive effects of KJT on colon carcinogenesis using the azoxymethane (AOM)-induced prec
287 progesterone control breast development and carcinogenesis via their cognate receptors expressed in
290 investigate the role of inflammation in lung carcinogenesis, we evaluated associations between proinf
291 ntify molecular events associated with HPV16 carcinogenesis, we evaluated viral variation, the integr
292 fic biospecimen for investigations of breast carcinogenesis, we measured genome-wide DNA methylation
293 tion between MTG16 and Kaiso in inflammatory carcinogenesis, we subjected single and double knockout
294 tinocyte stem cells in beta-HPV-induced skin carcinogenesis, we utilized a transgenic mouse model in
295 e temporal order of somatic mutations during carcinogenesis, which contributes to better understandin
296 oral molecular and cellular "atlas" of field carcinogenesis, will further delineate preneoplastic ini
297 s whereby these factors may influence breast carcinogenesis, with a focus on effects on progenitor ce
298 c inflammation is a risk factor for prostate carcinogenesis, with diet, chemical injury and an altere
299 in show a strong cooperative action in liver carcinogenesis, with Yap and Taz serving as mediators of
300 show that ATM loss accelerates Kras-induced carcinogenesis without conferring a specific phenotype t