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1 itment as an essential mechanism to increase colon carcinogenesis.
2 y, suggesting that GalNAc-T6 plays a role in colon carcinogenesis.
3 C betaII (PKCbetaII) is induced early during colon carcinogenesis.
4 esults suggest a pivotal function for HuR in colon carcinogenesis.
5 ) expression, all presumed to participate in colon carcinogenesis.
6 genase (COX)-2 levels become elevated during colon carcinogenesis.
7 ression) of azoxymethane (AOM)-induced early colon carcinogenesis.
8 aII in the colon of transgenic mice enhances colon carcinogenesis.
9 e in human colonocytes, the target tissue of colon carcinogenesis.
10 protein kinase C betaII (PKCbetaII) promotes colon carcinogenesis.
11 (PKC beta II) is an early promotive event in colon carcinogenesis.
12 vitamin D are thought to be able to inhibit colon carcinogenesis.
13 flammatory agents such as Celecoxib suppress colon carcinogenesis.
14 ve agent thus far tested in the experimental colon carcinogenesis.
15 indicate that it is a critical early step in colon carcinogenesis.
16 activity, and apoptosis during experimental colon carcinogenesis.
17 to that recorded during the early stages of colon carcinogenesis.
18 c acid metabolism plays an important role in colon carcinogenesis.
19 administered during the progression stage of colon carcinogenesis.
20 ids (such as those in Western diets) promote colon carcinogenesis.
21 stitutive overexpression plays a key role in colon carcinogenesis.
22 ather than COX-1, as the isoform involved in colon carcinogenesis.
23 stitutive overexpression plays a key role in colon carcinogenesis.
24 CSE1L is involved in colon carcinogenesis.
25 many cancers and is a rate-limiting step in colon carcinogenesis.
26 ase (starting late in premalignant stage) of colon carcinogenesis.
27 ction in inflammation and is a key factor in colon carcinogenesis.
28 urs, is thought to play an important role in colon carcinogenesis.
29 sses strong chemopreventive activity against colon carcinogenesis.
30 ween a high-fiber diet and the prevention of colon carcinogenesis.
31 ance of alterations in this enzyme system in colon carcinogenesis.
32 sal, implicates hyperinsulinemic exposure in colon carcinogenesis.
33 between a high-fiber diet and the arrest of colon carcinogenesis.
34 wdered enteral formula would influence early colon carcinogenesis.
35 of ras-p21 during azoxymethane (AOM)-induced colon carcinogenesis.
36 or an important role of folate metabolism in colon carcinogenesis.
37 and PGE2 levels in the azoxymethane model of colon carcinogenesis.
38 rillyl alcohol on azoxymethane (AOM)-induced colon carcinogenesis.
39 HITC blocked the process of apoptosis during colon carcinogenesis.
40 ventive activity of perillyl alcohol against colon carcinogenesis.
41 NA levels play a direct pathogenetic role in colon carcinogenesis.
42 %, P < 0.003), which are early indicators of colon carcinogenesis.
43 an early event during multistage process of colon carcinogenesis.
44 ic role of the acetylator genotype (NAT2) in colon carcinogenesis.
45 malignant tumors as well as early markers of colon carcinogenesis.
46 r possesses chemopreventive activity against colon carcinogenesis.
47 osal colonization that is expected to impact colon carcinogenesis.
48 the amount and types of dietary fat modulate colon carcinogenesis.
49 exquisitely sensitive to chemically induced colon carcinogenesis.
50 the potential contribution of ETBF to human colon carcinogenesis.
51 established two-stage model of inflammatory colon carcinogenesis.
52 e (AOM)/dextran sulfate sodium (DSS)-induced colon carcinogenesis.
53 ous polyps in chemical and genetic models of colon carcinogenesis.
54 l Wnt signaling is thought to play a role in colon carcinogenesis.
55 latter recapitulating key features of human colon carcinogenesis.
56 was a critical event in HIF-2alpha-mediated colon carcinogenesis.
57 rotect against chronic inflammation-mediated colon carcinogenesis.
58 specific transcriptional program to promote colon carcinogenesis.
59 loss of GDP-fucose synthesis contributes to colon carcinogenesis.
60 ling support for the role of inflammation in colon carcinogenesis.
61 s as an oncogene or tumor suppressor gene in colon carcinogenesis.
62 ortant step in promoting EMT programs during colon carcinogenesis.
63 lpha protects mice from azoxymethane-induced colon carcinogenesis.
64 providing new mechanistic insight into human colon carcinogenesis.
65 that activation of the CBS/H2S axis promotes colon carcinogenesis.
66 catenin signaling plays an essential role in colon carcinogenesis.
67 ial growth factor, three genes implicated in colon carcinogenesis.
68 serve distinct, nonoverlapping functions in colon carcinogenesis.
69 eta-selective inhibitor, in a mouse model of colon carcinogenesis.
70 ha expression, and elevated NO production in colon carcinogenesis.
71 de, a major inflammatory pathway involved in colon carcinogenesis.
72 ammation is important for protection against colon carcinogenesis.
73 al role in normal intestinal homeostasis and colon carcinogenesis.
74 -deficient mice were protected markedly from colon carcinogenesis.
75 cause low-grade gut inflammation can promote colon carcinogenesis.
76 osis are likely to play an important role in colon carcinogenesis.
77 ylglutaryl CoA reductase inhibitors) inhibit colon carcinogenesis.
78 le of processing intermediates of gastrin in colon carcinogenesis.
79 ryl CoA reductase (HMGR) inhibitors] inhibit colon carcinogenesis.
80 and activation of this receptor will inhibit colon carcinogenesis.
81 ARbeta/delta) ligands potentiate or suppress colon carcinogenesis.
82 at must be addressed using in vivo models of colon carcinogenesis.
83 ly suggest that SST and TAC1 are involved in colon carcinogenesis.
84 yte cell proliferation, gene expression, and colon carcinogenesis.
85 -2), a well-established pathogenic factor in colon carcinogenesis.
86 ppm in either diet significantly suppressed colon carcinogenesis.
87 ed tool for detecting the earliest stages of colon carcinogenesis.
88 Protein kinase C betaII (PKCbetaII) promotes colon carcinogenesis.
89 ion, here we show that PPAR-delta attenuates colon carcinogenesis.
90 the azoxymethane (AOM)-treated rat model of colon carcinogenesis.
91 ice) exhibit hyperproliferation and enhanced colon carcinogenesis.
92 nesis restores susceptibility to AOM-induced colon carcinogenesis.
93 usible mechanism by which PKCbetaII promotes colon carcinogenesis.
94 are effective chemopreventive agents against colon carcinogenesis, administration of high doses of th
95 ny of the specific mutations responsible for colon carcinogenesis allows an understanding of the phen
97 reveal a mechanism by which microbiota drive colon carcinogenesis and highlight atRA metabolism as a
98 known if nonamidated gastrins play a role in colon carcinogenesis and if the effects are similar to t
99 malignant transformation in animal models of colon carcinogenesis and in human patients with ulcerati
100 tion protein, claudin-1, is increased during colon carcinogenesis and particularly metastatic colorec
101 or, celecoxib, approved for the treatment of colon carcinogenesis and rheumatoid arthritis, affects C
102 se this knowledge could provide insight into colon carcinogenesis and suggest ways to suppress Cox-2
103 ce that the SphK1/S1P pathway contributes to colon carcinogenesis and that inhibition of this pathway
104 ndomly damages genes known to participate in colon carcinogenesis and that it affects multiple target
105 on of PPARbeta attenuates chemically induced colon carcinogenesis and that PPARbeta-dependent inducti
106 t of genistein on azoxymethane (AOM)-induced colon carcinogenesis and to study its modulatory role on
107 II mice exhibit hyperproliferation, enhanced colon carcinogenesis, and marked repression of TGFbetaRI
108 hanism whereby dietary sphingolipids inhibit colon carcinogenesis, and might have implications for di
109 nzyme cyclooxygenase-2 plays a major role in colon carcinogenesis, and that nonsteroidal anti-inflamm
110 t that the FACL4 pathway may be important in colon carcinogenesis, and that the development of select
111 anisms whereby fat or red meat may influence colon carcinogenesis are discussed, although none appear
113 microbiota (GM) structure and function, and colon carcinogenesis are only beginning to be elucidated
115 ation in the Pirc rats- the genetic model of colon carcinogenesis, both in the uninvolved colonic muc
116 ARgamma can suppress beta-catenin levels and colon carcinogenesis but only before damage to the APC/b
117 donic acid metabolism has been implicated in colon carcinogenesis, but the role of hematopoietic 5-li
119 oncogenes and tumor promoters, occurs during colon carcinogenesis by examining its level in colon tum
121 k of colon cancer and that the inhibition of colon carcinogenesis by NSAIDs is mediated through the m
123 the possibility that lymphocytes may inhibit colon carcinogenesis by reducing bacterially driven infl
125 dy demonstrates that inflammation-associated colon carcinogenesis can be initiated and promoted solel
126 PA), which inhibits PKC beta II activity and colon carcinogenesis, causes inhibition of Cox-2 protein
127 iation stage might either enhance or inhibit colon carcinogenesis, depending on whether AOM or MAMAc
128 es suggest that the effect of dietary fat in colon carcinogenesis depends not only on the amount but
129 DAG kinase, and PKC that may play a role in colon carcinogenesis depends on the types and amount of
130 roliferation and increased susceptibility to colon carcinogenesis due, at least in part, to repressio
131 notype (Loeb) with the concepts of multistep colon carcinogenesis (Fearon and Vogelstein) and clonal
132 rize the effects of dietary sphingolipids on colon carcinogenesis, female CF1 mice were administered
133 trans-differentiation, crypt regeneration or colon carcinogenesis following bacterial infection.
135 ed during the promotion/progression stage of colon carcinogenesis, ie., continuous celecoxib administ
136 plays a requisite role in the initiation of colon carcinogenesis in a preclinical mouse model by pro
137 lipids, or phytic acid differentially affect colon carcinogenesis in a well-established colon cancer
138 ) by which the lipid fraction of WB inhibits colon carcinogenesis in addition to alteration of iNOS a
139 s well as for suppression of early events in colon carcinogenesis in CFI mice treated with 1,2-dimeth
141 ed during the promotion/progression stage of colon carcinogenesis in comparison to the effect during
144 ports the present findings of an increase in colon carcinogenesis in GAS-KO mice lacking normal physi
145 rotein kinase C (PKC) has been implicated in colon carcinogenesis in humans and in rodent models.
151 ion inhibits chronic inflammation-associated colon carcinogenesis in mice, likely as a result of incr
155 tent cancer chemopreventive efficacy against colon carcinogenesis in rat model; however, the mechanis
156 shown to inhibit azoxymethane (AOM)-induced colon carcinogenesis in rats when administered continuou
160 y significantly reduce the increased risk of colon carcinogenesis in response to PG.Oncogene advance
161 ted that colonic PKCbetaII is induced during colon carcinogenesis in rodents and humans, and that ele
162 ient to confer susceptibility to AOM-induced colon carcinogenesis in transgenic mice, 2) PKCbetaII re
163 mportance of PKCbetaII and PKCiota/lambda in colon carcinogenesis in two complimentary models of colo
164 d for oncogenic Ras- and carcinogen-mediated colon carcinogenesis in vivo and define a procarcinogeni
167 K1/S1P pathway may play an important role in colon carcinogenesis, in part, by regulating COX-2 expre
168 en during the promotion/progression stage of colon carcinogenesis, indicating that the chemopreventiv
169 des that, knockout of AIB1 in mice inhibited colon carcinogenesis induced by azoxymethane/dextran sod
172 k of colon cancer and that the inhibition of colon carcinogenesis is mediated through modulation of p
173 nonsteroidal antiinflammatory agents inhibit colon carcinogenesis is through the inhibition of prosta
174 f this agent in the postinitiation period of colon carcinogenesis, male F344 rats 6 weeks of age were
175 echanisms by which high dietary fat enhances colon carcinogenesis may be through the modulation of co
176 ch the high fat content of the diet promotes colon carcinogenesis may include the production of secon
177 ses of these agents in combination inhibited colon carcinogenesis more effectively than when they wer
180 in colonic epithelial cell proliferation and colon carcinogenesis, possibly through activation of the
181 , Hur(IKO) mice subjected to an inflammatory colon carcinogenesis protocol [azoxymethane and dextran
182 ation and its uniform dysregulation early in colon carcinogenesis, reflecting loss of ligand expressi
183 led celebrex), approved for the treatment of colon carcinogenesis, rheumatoid arthritis, and other in
185 ltaT17 cell-derived IL17 in bacteria-induced colon carcinogenesis, stressing the importance of therap
187 fingerprinting, to show that in experimental colon carcinogenesis the predysplastic epithelial microv
190 nvestigated the preventive effects of KJT on colon carcinogenesis using the azoxymethane (AOM)-induce
191 deletion on chronic inflammation-associated colon carcinogenesis using the azoxymethane/dextran sodi
193 ffect of folate transporter gene ablation on colon carcinogenesis was evaluated 8 and 38 weeks post-a
194 ments with cell lines and an animal model of colon carcinogenesis we show that increase in the degree
195 To examine further the role of gastrins in colon carcinogenesis, we generated gastrin gene knockout
196 ly evident preneoplastic lesions in chemical colon carcinogenesis, were measured in rapid and slow ac
197 in the diet and at wide pH ranges, inhibits colon carcinogenesis when administered during the postin
198 are highly susceptible to carcinogen-induced colon carcinogenesis, whereas mice expressing kinase-def
199 protective role of amidated gastrins against colon carcinogenesis, which supports the present finding
200 on with host molecular processes involved in colon carcinogenesis will be key to defining preventive
201 ous tumor formation and azoxymethane-induced colon carcinogenesis with no apparent evidence of tissue
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