ライフサイエンスコーパス: intestinal adenoma

1 redominantly macrophages) in human and mouse intestinal adenomas.

2 ) intestinal stem cells and their progeny in intestinal adenomas.

3 6) background, mice develop large numbers of intestinal adenomas.

4 s, such as sulindac, undergo a regression of intestinal adenomas.

5 or both progression and maintenance of small intestinal adenomas.

6 exhibit a fivefold increase in the number of intestinal adenomas.

7 -) mice had a 96% reduction in the number of intestinal adenomas.

8 and transgenic mice developing autochthonous intestinal adenomas.

9 oietic PGD synthase tended to have 80% fewer intestinal adenomas.

10 ntion of the angiogenic switch and growth in intestinal adenomas.

11 use is a model for CRC and develops numerous intestinal adenomas.

12 utations in their germ line (ApcMin) develop intestinal adenomas.

13 ion in both the normal intestinal mucosa and intestinal adenomas.

14 iferation, as guanylin expression is lost in intestinal adenomas.

15 ed in the tumor cells of greater than 80% of intestinal adenomas.

16 The treated p27-/- mice also developed intestinal adenomas.

17 n their 129/Sv epithelium and also developed intestinal adenomas.

18 cyclin D1 and Cdk4 expression in Min/+ mouse intestinal adenomas.

19 lin-dependent kinase 4 (Cdk4) in Min/+ mouse intestinal adenomas.

20 at results in the spontaneous development of intestinal adenomas (100% incidence).

21 rols, and some IFN-gamma(-/-) mice developed intestinal adenomas after colonization with C. albicans.

22 After only 6 weeks of treatment, intestinal adenomas and aberrant crypt foci were counted

23 nt tumour susceptibilities, most notably, to intestinal adenomas and adenocarcinomas, and different m

24 complex; its expression was higher in human intestinal adenomas and carcinomas than in healthy intes

25 ncreased in human colonic and Apc+/min mouse intestinal adenomas and correlated with increased COX-2

26 pproximately three times the number of small intestinal adenomas and four times the number of colon a

27 erexpression of cyclin D1 and Cdk4 occurs in intestinal adenomas and is associated with increased cel

28 at Dnmt1(N/+) retards the net growth rate of intestinal adenomas and reduces tumor multiplicity by ap

29 bserved similar effects on the prevention of intestinal adenomas and reduction of xenograft tumor vol

30 program is conserved and functional in mouse intestinal adenomas and results in silencing of active i

31 al mediator of TGF-beta-induced apoptosis in intestinal adenomas and show that the common progression

32 e expression of TGF-beta RII in premalignant intestinal adenomas and the relationship with cell cycle

33 Overexpression of Id1 causes intestinal adenomas and thymic lymphomas in mice, sugges

34 Loss of Apc in Lrig1(+) cells leads to intestinal adenomas, and genetic ablation of Lrig1 resul

35 e to treatment, cells from T-cell lymphomas, intestinal adenomas, and mammary tumors rapidly induced

36 of the secretome of cultured primary benign intestinal adenomas (ApcMin/+) and highly expressed by a

37 ly reduced both the number and size of small intestinal adenomas arising in this model, and it acted

38 Cdk) 4 may be involved in the development of intestinal adenomas associated with familial adenomatous

39 yndrome by interbreeding caused formation of intestinal adenomas at a significantly reduced incidence

40 background, ApcMin/+ acquires multiple small intestinal adenoma before becoming moribund with anemia.

41 4, protein and mRNA levels were increased in intestinal adenomas but not in normal intestinal epithel

42 n significantly inhibited the development of intestinal adenomas by 48% (P=0.002), 50% (P=0.001), and

43 For the Mom1 modifier of intestinal adenomas caused by ApcMin, these tests are us

44 develop more than three times the number of intestinal adenomas compared to Min/+ Mlh1+/+ or +/- mic

45 pc(Min/+) mice led to approximately 50% more intestinal adenomas compared with controls.

46 We show that APC(-/-)-driven intestinal adenomas compete with and kill surrounding ce

47 hibition of cyclooxygenase (COX)-2 abrogates intestinal adenoma development at early stages of colore

48 mines chemopreventive effects of CP-31398 on intestinal adenoma development in an animal model of fam

49 Intestinal adenoma development in Apc(Min) mice is influ

50 , Mgmt deficiency did not affect spontaneous intestinal adenoma development in Apc(Min/+) mice, sugge

51 im levels and sensitivity to TGF-beta during intestinal adenoma development.

52 f the canonical Wnt pathway and critical for intestinal adenoma development.

53 endocrine cell differentiation induced small-intestinal adenomas expressing serotonin, a feature not

54 liferation plays a role in susceptibility to intestinal adenoma formation and/or progression.

55 that miR-26a expression potently suppressed intestinal adenoma formation in Apc(min/+) mice, a model

56 r-initiating activity of beta-catenin during intestinal adenoma formation in Apc(Min/+) mice, and red

57 A), was evaluated for its ability to prevent intestinal adenoma formation in ApcMin mice.

58 Cox-2 overexpression accompanies intestinal adenoma formation in both humans and mice.

59 Here, we show that small intestinal adenoma formation is dramatically reduced in

60 To determine whether KLF5 contributes to intestinal adenoma formation, we examined tumor burdens

61 ting a dominant genetic restriction point in intestinal adenoma formation.

62 widely used as a model recapitulating early intestinal adenoma formation.

63 normal intestinal crypts are monoclonal, but intestinal adenomas frequently have a polyclonal structu

64 Intestinal adenomas from compound Apc(min/+) apobec-1(-/

65 els of cyclin D1 and Cdk4 in the majority of intestinal adenomas from human FAP patients in compariso

66 imary human colon and breast cancers, and in intestinal adenomas from Min (Apc(min/+)) mice.

67 senger RNA and its targets were increased in intestinal adenomas from patients and mice compared with

68 iniscent of those reported for tubulovillous intestinal adenomas from patients.

69 acrophage Cox-2 in colorectal (but not small intestinal) adenomas from cLys-Cox-2 x Apc (Min/+) mice

70 trating that deletion of PPARdelta decreases intestinal adenoma growth in Apc(Min/+) mice and inhibit

71 l that loss or inhibition of CB1 accelerated intestinal adenoma growth in Apc(Min/+) mice whereas act

72 s support NAG-1 as an important regulator of intestinal adenoma growth in vivo and suggest that NAG-1

73 conclude that IGF-II supply is a modifier of intestinal adenoma growth, and we provide genetic eviden

74 ts implicate PPAR-delta in the regulation of intestinal adenoma growth.

75 on of Apc(APC(Delta1638/+)), Smad4-deficient intestinal adenomas had increased levels of beta-catenin

76 trating the polyclonal structure of familial intestinal adenomas, high tumor multiplicity made it dif

77 inal-specific Bmi1 deletion suppressed small intestinal adenomas in a manner that was indistinguishab

78 colorectal adenomas and against spontaneous intestinal adenomas in Apc(Min) mice.

79 rypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in APC(Min+/-) (Min) mice.

80 eric bacteria are necessary for formation of intestinal adenomas in C57BL/6-ApcMin/+ mouse.

81 n has implicated Cox-2 in the development of intestinal adenomas in experimental animals and in adeno

82 After ovariectomy, intestinal adenomas in Min/+ mice increased by 77% (P =

83 portant role in promoting the development of intestinal adenomas in the presence of Apc(Min) mutation

84 18)9Lub (Rb9) suppresses the multiplicity of intestinal adenomas in this mouse model.

85 e index, net growth rate and multiplicity of intestinal adenomas in two distinct models of familial c

86 In a mouse intestinal adenoma model, TIGAR deficiency decreased tum

87 d confers a long-term survival benefit in an intestinal adenoma model.

88 es mammary carcinoma in females and enhances intestinal adenoma multiplicity by a tumor necrosis fact

89 e was previously identified as a modifier of intestinal adenoma multiplicity in Apc Min/+ mice.

90 cam and difluoromethylornithine each reduced intestinal adenoma multiplicity in the absence of p53 fu

91 pcMin/+ leads to a 3-fold reduction in small intestinal adenoma number (P<0.0001) compared to ApcMin/

92 ols, vilVEGF1-Min mice developed 6-fold more intestinal adenomas of all sizes, with more advanced his

93 The multiplicity and invasiveness of intestinal adenomas of Apc(Min/+) (Min) mice was enhance

94 gnificant number of mice totally free of any intestinal adenomas (P < 0.001), in contrast to the 100%

95 ApcMin mouse model, which forms spontaneous intestinal adenomas, reductions in Gpr182 led to more ad

96 In both mice, intestinal adenomas showed copy-neutral loss of heterozy

97 (Min/+) mice developed, on average, 59% more intestinal adenomas than Apc(Min/+) mice (P < 0.0001).

98 )Nos2(-/-) mice developed significantly more intestinal adenomas than Apc(Min/+)Nos2(+/+) littermates

99 n the tumor-prone Min/+ background exhibited intestinal adenomas that strongly expressed endogenous s

100 f transgenic pancreatic islet carcinomas and intestinal adenomas was also slower in Bmx(-/-) mice.

101 Only very occasional intestinal adenomas were observed in beta-naphthoflavone

102 tor p27(kip1) developed both small and large intestinal adenomas when fed a control AIN-76A diet.

103 ukocyte populations were also found in human intestinal adenomas, which suggests that CXCR2 antagonis

104 hich designated Apc (R850X/+) (Min), develop intestinal adenomas, while the bulk of the disease is in