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1 ased numbers of tumors during two-stage skin carcinogenesis.
2 specific transcription factors (TFs) in lung carcinogenesis.
3 sm by which p53 is activated to suppress BCC carcinogenesis.
4 mandatory for development of hepatocellular carcinogenesis.
5 by human liver tumors and its role in liver carcinogenesis.
6 n of nonmelanoma skin tumors during chemical carcinogenesis.
7 eady-to-use routes of dissemination in early carcinogenesis.
8 sidered to play a minor role in solid tumour carcinogenesis.
9 cesses ranging from embryonic development to carcinogenesis.
10 m can contribute to disease pathogenesis and carcinogenesis.
11 ) play important roles in drug responses and carcinogenesis.
12 ich represent important initiating events in carcinogenesis.
13 ical and clinically actionable insights into carcinogenesis.
14 ylphorbol-13-acetate (DMBA/TPA)-induced skin carcinogenesis.
15 MCV sT, which may contribute to Merkel cell carcinogenesis.
16 grity that might etiologically contribute to carcinogenesis.
17 mmatory and immune functions associated with carcinogenesis.
18 oprotein CagA into epithelial cells to drive carcinogenesis.
19 BPA to later-life predisposition to prostate carcinogenesis.
20 m development of pharmacotherapies to reduce carcinogenesis.
21 ession and thereby modulate inflammation and carcinogenesis.
22 complex relationships between aneuploidy and carcinogenesis.
23 manner, suggesting colibactin is a driver of carcinogenesis.
24 hole-genome duplication events in early lung carcinogenesis.
25 e viral infections have an important role in carcinogenesis.
26 f many years, promoting oncogenic traits and carcinogenesis.
27 nflammation and fully protected KO mice from carcinogenesis.
28 Obesity confers an independent risk for carcinogenesis.
29 rning how vascular morphology evolves during carcinogenesis.
30 athways and their potential roles in thyroid carcinogenesis.
31 the CBS/H2S axis plays a role in colorectal carcinogenesis.
32 essor genes and, therefore, is important for carcinogenesis.
33 and migration-favouring microenvironment for carcinogenesis.
34 the role of the parasite in the induction of carcinogenesis.
35 egies against HBV infection and HBV-mediated carcinogenesis.
36 expression of HIF target genes drives renal carcinogenesis.
37 cently potentially associated with digestive carcinogenesis.
38 ght is the major effector for skin aging and carcinogenesis.
39 s, which could be involved in hepatocellular carcinogenesis.
40 cer hallmark mechanisms that serve to enable carcinogenesis.
41 cer, but HPV infection is not sufficient for carcinogenesis.
42 as an essential mechanism to increase colon carcinogenesis.
43 iocellular proliferation/differentiation and carcinogenesis.
44 low-grade gut inflammation can promote colon carcinogenesis.
45 metastases, implying their stability during carcinogenesis.
46 d ras(Ha)/ROCK2/NF-kappaB signalling in skin carcinogenesis.
47 perturbs this equilibrium during intestinal carcinogenesis.
48 ma development at early stages of colorectal carcinogenesis.
49 promotion-malignant-conversion hypothesis of carcinogenesis.
50 re highly aggressive HCC induced by chemical carcinogenesis.
51 hot of DNA injuries at the earliest stage of carcinogenesis.
52 in is the fundamental contributor to in vivo carcinogenesis.
53 eration of tumor initiating cells (TICs) and carcinogenesis.
54 nduced lymphomagenesis and susceptibility to carcinogenesis.
55 netic dysregulation, which may favor gastric carcinogenesis.
56 TRAF1 is required for solar UV-induced skin carcinogenesis.
57 ng glycolysis, mediates circadian control of carcinogenesis.
58 echanisms underlying PCB- and dioxin-related carcinogenesis.
59 catenin MCC is needed for mucosal repair and carcinogenesis.
60 nity in regulating EC tissue homeostasis and carcinogenesis.
61 C), which activates CXCR2, during pancreatic carcinogenesis.
62 route in Kras(G12D)-driven mouse pancreatic carcinogenesis.
63 sents a new mechanism of miRNA regulation in carcinogenesis.
64 normal tissue is an important step in breast carcinogenesis.
65 UV, ROS and signal transduction during skin carcinogenesis.
66 a basis for organizing data on mechanisms of carcinogenesis.
67 cal role in oncogenic Kras-driven pancreatic carcinogenesis.
68 nfection-induced inflammation and associated carcinogenesis.
69 these receptors in early steps of esophageal carcinogenesis.
70 pared with low-risk determinants of cervical carcinogenesis.
71 namics are altered at the earliest stages of carcinogenesis.
72 t be addressed using in vivo models of colon carcinogenesis.
73 esity, all of which may increase the risk of carcinogenesis.
74 ogical and pathological processes, including carcinogenesis.
75 d about the implications of these lesions in carcinogenesis.
76 the possible role of periodontal disease in carcinogenesis.
77 rancies of which have all been implicated in carcinogenesis.
78 ecapitulates the sequential stages of breast carcinogenesis.
79 ypes are likely to be important for squamous carcinogenesis.
80 latter is due to its viral or UV-associated carcinogenesis.
81 irus (HPV) plays a major role in HPV-induced carcinogenesis.
82 plays an important role in arsenic -induced carcinogenesis.
83 d to elucidate their mechanisms of action in carcinogenesis.
84 and suggest that DLX3 is a modulator of skin carcinogenesis.
85 eregulation plays an important role in liver carcinogenesis.
86 uced DNA damage and repair and ultimately UV carcinogenesis.
87 n) of azoxymethane (AOM)-induced early colon carcinogenesis.
88 ther microbial effectors also have a role in carcinogenesis.
89 the epidemiology of cancer and mechanisms of carcinogenesis.
90 ), senescent cells can paradoxically promote carcinogenesis.
91 for highly penetrant male-restricted hepatic carcinogenesis.
92 ecular initiating event in genotoxin-induced carcinogenesis.
93 berrant metabolic function can contribute to carcinogenesis.
94 RNAs (lncRNAs) are important players in lung carcinogenesis.
95 on, cellular response to hypoxic stress, and carcinogenesis.
96 NA methylation alterations may contribute to carcinogenesis.
97 would further our understanding of aging and carcinogenesis.
98 ants, macroH2A1.1 and macroH2A1.2, and liver carcinogenesis.
99 hemselves, contributes to suppression of BCC carcinogenesis.
100 ergence between TGFbeta and MEK/ERK in early carcinogenesis.
101 or the CX3CR1 receptor may affect colorectal carcinogenesis.
102 signaling is a known mediator of colorectal carcinogenesis.
103 Papillomavirus (HPV) infection and cervical carcinogenesis.
104 ode long non-coding RNAs implicated in human carcinogenesis.
105 lyps in chemical and genetic models of colon carcinogenesis.
106 and p53 loss markedly accelerates murine BCC carcinogenesis.
107 ) has been implicated during development and carcinogenesis.
108 known about HH and WNT interactions in human carcinogenesis.
109 ons more reliably, and uncover mechanisms of carcinogenesis.
110 g profiles constitute pivotal mechanisms for carcinogenesis.
111 l proliferation during liver development and carcinogenesis.
112 atenin/TCF-LEF pathway in transformation and carcinogenesis.
113 duced regulatory elements implicated in lung carcinogenesis.
114 as key molecular characteristics during the carcinogenesis.
115 gulate gene-environment interaction in human carcinogenesis.
116 ful chemopreventive agent against colorectal carcinogenesis.
117 arcinomas, but this is insufficient to drive carcinogenesis.
118 t hepatocyte transformation and enhanced DEN-carcinogenesis.
119 ceptibility for specific patterns of mammary carcinogenesis.
120 e co-inherited with CDKN2A and may influence carcinogenesis.
121 Inflammation has been implicated in ovarian carcinogenesis.
122 testosterone plus estradiol (T+E) to promote carcinogenesis.
123 s a vital mechanism that contributes to skin carcinogenesis.
124 cRCC, and provides a better understanding of carcinogenesis.
125 gesting that GalNAc-T6 plays a role in colon carcinogenesis.
126 suppressor gene that modulates environmental carcinogenesis.
127 R accelerates ionizing radiation-induced BCC carcinogenesis.
128 biota are linked to chronic inflammation and carcinogenesis.
129 of GDP-fucose synthesis contributes to colon carcinogenesis.
130 al actions of retinol, including its role in carcinogenesis.
131 ctivation of the CBS/H2S axis promotes colon carcinogenesis.
132 , with length and diameter increasing during carcinogenesis.
133 receptors, which function as key inducers of carcinogenesis.
134 g the importance of cilia dysfunction in the carcinogenesis.
135 iating interactions between inflammation and carcinogenesis.
136 thelium expanded enteric nerves and promoted carcinogenesis.
137 cals produce effects in concert that lead to carcinogenesis?
139 in pancreatic development, pancreatitis, and carcinogenesis, although the biological role that these
142 ication of histone is extensively studied in carcinogenesis and cancer cell's response to chemotherap
144 DAR2 functions as an oncogene in endometrial carcinogenesis and could be a potential target for impro
146 injections of carbon tetrachloride to induce carcinogenesis and fibrosis and found that HCA and HCC n
147 genetic mechanisms contributing to pulmonary carcinogenesis and highlight ASXL3 as a novel candidate
148 a mechanism by which microbiota drive colon carcinogenesis and highlight atRA metabolism as a therap
150 ne/12-O-tetradecanoylphorbol 13-acetate skin carcinogenesis and identify Rho signaling dependent on R
152 with IgA(+) cell generation attenuates liver carcinogenesis and induces cytotoxic T-lymphocyte-mediat
154 microbiota at different stages of Barrett's carcinogenesis and investigate the Cytosponge as a minim
155 virus (HPV) plays a central role in cervical carcinogenesis and its oncogene E7 is essential in this
157 standing of common biology underlying breast carcinogenesis and may contribute to biomarker developme
158 evidence that betaPV is associated with cSCC carcinogenesis and may present a target for future preve
159 ole for hormone-related exposures in ovarian carcinogenesis and risk factor differences by histologic
161 ide a mechanistic insight into SWCNT-induced carcinogenesis and the role of SOX9 in CSC regulation an
164 ption factors are known to play key roles in carcinogenesis and therefore, are gaining popularity as
165 induce tumor infiltration by SC during early carcinogenesis and to attenuate pain, possibly resulting
166 s to delineate the mutations' involvement in carcinogenesis and to develop therapeutics, which we rev
167 n factor STAT3 has been implicated in breast carcinogenesis and tumor immunosuppression in advanced d
168 uppression of Plk3 expression contributes to carcinogenesis and tumor progression induced by nickel c
169 result, we conclude that the role of MTH1 in carcinogenesis and utility of its inhibition is yet to b
170 ck protein levels are often elevated in both carcinogenesis and viral infection and are associated wi
172 omeres, which are involved in cell division, carcinogenesis, and aging and constitute important thera
173 Steroid sex hormones can induce prostate carcinogenesis, and are thought to contribute to the dev
175 s performed on Sprague-Dawley rats to induce carcinogenesis, and LY3023414 was cyclically administere
176 y contribute to sex-based disparity in liver carcinogenesis, and suggest new possibilities for preven
177 phisms as quantitative trait loci in mammary carcinogenesis, and they implicate distinct interactions
178 asured the contribution of each signature to carcinogenesis, and used hierarchical clustering to subt
179 biota (GM) structure and function, and colon carcinogenesis are only beginning to be elucidated.
180 -Barr virus (EBV) latency and its associated carcinogenesis are regulated by dynamic changes in DNA m
181 l roles of Rad18 in DNA damage tolerance and carcinogenesis are unknown and were investigated here.
183 ociations between DEMs and TAA-induced liver carcinogenesis at an earlier stage than histopathologica
184 onses; evaluate biological events leading to carcinogenesis both spatially and temporally; examine th
185 e of 25-hydroxyvitamin D [25(OH)D] in breast carcinogenesis, but epidemiologic evidence is inconsiste
186 e is a highly susceptible period for mammary carcinogenesis, but few prospective studies have examine
187 ther light into the complexity of colorectal carcinogenesis, but it also puts forward a potential nov
188 c alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy co
189 thought to influence tissue homeostasis and carcinogenesis by acting as disrupters of endocrine func
191 whether AhR controls liver regeneration and carcinogenesis by restricting the expansion of stem-like
192 ling, is essential to promote hepatocellular carcinogenesis by two mechanisms: First, it prevents DNA
194 damage ranges from photoaging and cutaneous carcinogenesis caused by UV exposure, to treatment-limit
195 hat vitamin D and calcium inhibit colorectal carcinogenesis, daily supplementation with these nutrien
197 stion of which early molecular changes drive carcinogenesis during the long latency period of mesothe
198 and "SASP-like" inflammation in driving skin carcinogenesis, emphasizing how further understanding of
199 he earliest molecular events associated with carcinogenesis, enabling novel strategies to intercept t
201 ing of vasculature in the earliest stages of carcinogenesis from which one can extract robust endpoin
202 ashes NK-cell-mediated resistance to hepatic carcinogenesis, haematogenous liver and lung metastasis,
203 etiological role of the local microbiome and carcinogenesis has been mounting, no information exists
205 microenvironment is a critical modulator of carcinogenesis; however, in many tumor types, the influe
206 N AND The theoretical merits of the low-dose carcinogenesis hypothesis are well founded with clear bi
211 e results indicate that mutagenesis and skin carcinogenesis in IGF-1-deficient geriatric skin may be
213 e lowest BPA dose initiated maximal hormonal carcinogenesis in lateral prostates despite undetectable
214 tion-treated Ptch1(+/-) mice accelerates BCC carcinogenesis in male mice, in which UVR does not produ
215 endent mechanism, have been shown to promote carcinogenesis in many systems, including microbe-driven
224 skin differentiation and enhances epidermal carcinogenesis in vivo Phosphorylation of PKP1's N-termi
226 transformation (in vitro) and environmental carcinogenesis (in vivo), including investigations of th
227 a model population biomarker associated with carcinogenesis including breast, renal and gastric cance
228 fied multiple alterations likely involved in carcinogenesis, including a novel, functionally active t
229 nable to generate histamine did not suppress carcinogenesis, indicating a significant role of the com
232 ways previously linked to oncogene-initiated carcinogenesis instruct a long-lived granuloma-resident
234 ORTANCE Epstein-Barr virus (EBV) latency and carcinogenesis involve the selective epigenetic modifica
238 esponse) suggesting that the process of lung carcinogenesis is linked to chromatin remodeling, inflam
239 most commonly initiating event of intestinal carcinogenesis is mutation of the adenomatous polyposis
240 However, the mechanism by which E7 induces carcinogenesis is not fully understood; specific anti-HP
242 ng the contribution of missense mutations in carcinogenesis is to identify genes mutated with statist
248 microenvironment are active participants in carcinogenesis mediating both tumor initiation and progr
250 l of a dualistic model of epithelial ovarian carcinogenesis more than a decade ago, a large number of
255 Combined, these data suggest that during carcinogenesis pERK initially facilitates and later anta
256 isms by which H pylori might promote gastric carcinogenesis (persisting despite constant inflammation
257 disrupts Rb function, is critical for HPV16 carcinogenesis, presenting a highly specific target for
258 ects ubiquitination of other proteins in the carcinogenesis process, including proteins involved in i
259 on of in vivo stress using the DMBA/TPA skin carcinogenesis protocol revealed that combined inactivat
264 cells in opposing and promoting solid organ carcinogenesis, respectively, is viewed as a shifting ba
265 oteins, which promote cell proliferation and carcinogenesis resulting elevated levels of host antibod
266 t times, opposing roles of the microbiota in carcinogenesis serve to illustrate the complex and somet
267 wnstream targets of miR-451a and involved in carcinogenesis (shown in TCGA) were increased in NRs (qP
268 thesize that UVR has opposing effects on BCC carcinogenesis-stimulatory via mutagenesis and inhibitor
269 's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, trauma
270 m solar UV irradiation, and a long-term skin carcinogenesis study showed that deletion of TRAF1 in mi
271 ammatory response that is linked to asbestos carcinogenesis, thereby increasing the risk of developin
272 iates IL-17's function in promoting prostate carcinogenesis through induction of EMT, indicating IL-1
273 cleatum appears to play a role in colorectal carcinogenesis through suppression of the hosts' immune
274 ontributions of mutagenesis and selection in carcinogenesis, thus elucidating the site-specific drivi
275 does produce D3, UVR fails to accelerate BCC carcinogenesis, thus mirroring the plateauing in humans.
277 highly susceptible to upper digestive tract carcinogenesis upon initiation with 4-nitroquinoline 1-o
278 c link between microbiota and hepatocellular carcinogenesis using a streptozotocin-high fat diet (STZ
279 gated the preventive effects of KJT on colon carcinogenesis using the azoxymethane (AOM)-induced prec
281 encoded by Ptpn2, in chemically-induced skin carcinogenesis via the negative regulation of STAT3 and
283 echanism of calcipotriol action against skin carcinogenesis was examined in genetically engineered mo
285 investigate the role of inflammation in lung carcinogenesis, we evaluated associations between proinf
286 a (SqCC) and to identify new drivers of lung carcinogenesis, we examined the exome sequences and copy
287 ributions of TGFbeta signaling to pancreatic carcinogenesis, we generated mouse models of pancreatic
288 n patterns are regulated during iAs-mediated carcinogenesis, we show that iAs probably targets CTCF b
289 pathways in the onset and progression of EC carcinogenesis, we used high resolution mass spectrometr
290 tinocyte stem cells in beta-HPV-induced skin carcinogenesis, we utilized a transgenic mouse model in
291 s occur in the lower oesophagus in Barrett's carcinogenesis, which can be detected at the pre-invasiv
292 helial skin tumor formation in chemical skin carcinogenesis, which highlights an unexpected tumor-sup
293 helial skin tumor formation in chemical skin carcinogenesis, which highlights an unexpected tumor-sup
294 ding of how genomic variations contribute to carcinogenesis, which would impact the treatment of EBV-
295 mor formation and azoxymethane-induced colon carcinogenesis with no apparent evidence of tissue toxic
296 This article reviews the mechanisms of viral carcinogenesis, with an emphasis on the viral evasion of
297 light is a major etiological factor in skin carcinogenesis, with solar UV-stimulated signal transduc
298 show that ATM loss accelerates Kras-induced carcinogenesis without conferring a specific phenotype t
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