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1 SPO1 might be developed for the treatment of intestinal adenomas.
2 and transgenic mice developing autochthonous intestinal adenomas.
3 lin-dependent kinase 4 (Cdk4) in Min/+ mouse intestinal adenomas.
4 6) background, mice develop large numbers of intestinal adenomas.
5 s, such as sulindac, undergo a regression of intestinal adenomas.
6 ility of Apc-mutant cells to expand and form intestinal adenomas.
7 ) intestinal stem cells and their progeny in intestinal adenomas.
8 or both progression and maintenance of small intestinal adenomas.
9 exhibit a fivefold increase in the number of intestinal adenomas.
10 -) mice had a 96% reduction in the number of intestinal adenomas.
11 oietic PGD synthase tended to have 80% fewer intestinal adenomas.
12 redominantly macrophages) in human and mouse intestinal adenomas.
13 ntion of the angiogenic switch and growth in intestinal adenomas.
14 use is a model for CRC and develops numerous intestinal adenomas.
15 utations in their germ line (ApcMin) develop intestinal adenomas.
16 ion in both the normal intestinal mucosa and intestinal adenomas.
17 iferation, as guanylin expression is lost in intestinal adenomas.
18 ed in the tumor cells of greater than 80% of intestinal adenomas.
19 The treated p27-/- mice also developed intestinal adenomas.
20 n their 129/Sv epithelium and also developed intestinal adenomas.
21 cyclin D1 and Cdk4 expression in Min/+ mouse intestinal adenomas.
23 rols, and some IFN-gamma(-/-) mice developed intestinal adenomas after colonization with C. albicans.
24 case-control study included 77 CRC cases, 72 intestinal adenoma and 76 healthy controls (for a total
26 nt tumour susceptibilities, most notably, to intestinal adenomas and adenocarcinomas, and different m
28 complex; its expression was higher in human intestinal adenomas and carcinomas than in healthy intes
29 ncreased in human colonic and Apc+/min mouse intestinal adenomas and correlated with increased COX-2
30 pproximately three times the number of small intestinal adenomas and four times the number of colon a
31 erexpression of cyclin D1 and Cdk4 occurs in intestinal adenomas and is associated with increased cel
32 at Dnmt1(N/+) retards the net growth rate of intestinal adenomas and reduces tumor multiplicity by ap
33 bserved similar effects on the prevention of intestinal adenomas and reduction of xenograft tumor vol
34 program is conserved and functional in mouse intestinal adenomas and results in silencing of active i
35 al mediator of TGF-beta-induced apoptosis in intestinal adenomas and show that the common progression
36 e expression of TGF-beta RII in premalignant intestinal adenomas and the relationship with cell cycle
38 PC (Min) offspring mice were largely free of intestinal adenoma, and several chromosome substitution
40 e to treatment, cells from T-cell lymphomas, intestinal adenomas, and mammary tumors rapidly induced
42 of the secretome of cultured primary benign intestinal adenomas (ApcMin/+) and highly expressed by a
44 ly reduced both the number and size of small intestinal adenomas arising in this model, and it acted
45 Cdk) 4 may be involved in the development of intestinal adenomas associated with familial adenomatous
46 yndrome by interbreeding caused formation of intestinal adenomas at a significantly reduced incidence
47 background, ApcMin/+ acquires multiple small intestinal adenoma before becoming moribund with anemia.
48 phenotype was discordant, with reduced small intestinal adenoma burden yet development of large non-m
49 4, protein and mRNA levels were increased in intestinal adenomas but not in normal intestinal epithel
50 n significantly inhibited the development of intestinal adenomas by 48% (P=0.002), 50% (P=0.001), and
52 develop more than three times the number of intestinal adenomas compared to Min/+ Mlh1+/+ or +/- mic
55 hibition of cyclooxygenase (COX)-2 abrogates intestinal adenoma development at early stages of colore
56 mines chemopreventive effects of CP-31398 on intestinal adenoma development in an animal model of fam
58 , Mgmt deficiency did not affect spontaneous intestinal adenoma development in Apc(Min/+) mice, sugge
61 endocrine cell differentiation induced small-intestinal adenomas expressing serotonin, a feature not
62 Although PPARdelta has been shown to promote intestinal adenoma formation and growth, the molecular m
64 that miR-26a expression potently suppressed intestinal adenoma formation in Apc(min/+) mice, a model
65 r-initiating activity of beta-catenin during intestinal adenoma formation in Apc(Min/+) mice, and red
72 normal intestinal crypts are monoclonal, but intestinal adenomas frequently have a polyclonal structu
74 els of cyclin D1 and Cdk4 in the majority of intestinal adenomas from human FAP patients in compariso
76 senger RNA and its targets were increased in intestinal adenomas from patients and mice compared with
78 acrophage Cox-2 in colorectal (but not small intestinal) adenomas from cLys-Cox-2 x Apc (Min/+) mice
79 trating that deletion of PPARdelta decreases intestinal adenoma growth in Apc(Min/+) mice and inhibit
80 l that loss or inhibition of CB1 accelerated intestinal adenoma growth in Apc(Min/+) mice whereas act
81 s support NAG-1 as an important regulator of intestinal adenoma growth in vivo and suggest that NAG-1
82 conclude that IGF-II supply is a modifier of intestinal adenoma growth, and we provide genetic eviden
84 on of Apc(APC(Delta1638/+)), Smad4-deficient intestinal adenomas had increased levels of beta-catenin
85 trating the polyclonal structure of familial intestinal adenomas, high tumor multiplicity made it dif
86 inal-specific Bmi1 deletion suppressed small intestinal adenomas in a manner that was indistinguishab
90 n has implicated Cox-2 in the development of intestinal adenomas in experimental animals and in adeno
91 oral MTDIA as an anti-cancer therapeutic for intestinal adenomas in immunocompetent APC(Min/+) mice,
93 portant role in promoting the development of intestinal adenomas in the presence of Apc(Min) mutation
95 e index, net growth rate and multiplicity of intestinal adenomas in two distinct models of familial c
98 gf2r tumour suppressor function, we utilised intestinal adenoma models known to be Igf2 dependent.
99 es mammary carcinoma in females and enhances intestinal adenoma multiplicity by a tumor necrosis fact
101 cam and difluoromethylornithine each reduced intestinal adenoma multiplicity in the absence of p53 fu
102 pcMin/+ leads to a 3-fold reduction in small intestinal adenoma number (P<0.0001) compared to ApcMin/
103 ols, vilVEGF1-Min mice developed 6-fold more intestinal adenomas of all sizes, with more advanced his
106 gnificant number of mice totally free of any intestinal adenomas (P < 0.001), in contrast to the 100%
108 ApcMin mouse model, which forms spontaneous intestinal adenomas, reductions in Gpr182 led to more ad
110 (Min/+) mice developed, on average, 59% more intestinal adenomas than Apc(Min/+) mice (P < 0.0001).
111 )Nos2(-/-) mice developed significantly more intestinal adenomas than Apc(Min/+)Nos2(+/+) littermates
112 n the tumor-prone Min/+ background exhibited intestinal adenomas that strongly expressed endogenous s
113 f transgenic pancreatic islet carcinomas and intestinal adenomas was also slower in Bmx(-/-) mice.
115 tor p27(kip1) developed both small and large intestinal adenomas when fed a control AIN-76A diet.
116 ukocyte populations were also found in human intestinal adenomas, which suggests that CXCR2 antagonis
117 hich designated Apc (R850X/+) (Min), develop intestinal adenomas, while the bulk of the disease is in