ライフサイエンスコーパス: intestinal tumor

1 on of alpha 4 beta 7 integrin similar to the intestinal tumor.

2 lls from p21(-/-) mice, which do not develop intestinal tumors.

3 ly decreased in both human colonic and mouse intestinal tumors.

4 GD synthase controls an inhibitory effect on intestinal tumors.

5 inactivation of JNK1 spontaneously developed intestinal tumors.

6 ignal-regulated kinase 1/2 (ERK1/2) in small intestinal tumors.

7 and destabilization of KLF5 protein occur in intestinal tumors.

8 d a dose-dependent decrease in the number of intestinal tumors.

9 erexpressing NUP88 are cancer prone and form intestinal tumors.

10 esis, while hypomethylation protects against intestinal tumors.

11 ackgrounds for susceptibility to mammary and intestinal tumors.

12 mutation could preferentially occur in small intestinal tumors.

13 umor spectra; only Mlh1(-/-) animals develop intestinal tumors.

14 in mice with an inherited predisposition to intestinal tumors.

15 d within the cell lineage that gives rise to intestinal tumors.

16 es are correlated with PHGDH levels in human intestinal tumors.

17 TAT3 in the adenoma-to-carcinoma sequence of intestinal tumors.

18 RH-1 was shown to contribute to formation of intestinal tumors.

19 umor model that normally only develops small intestinal tumors.

20 py, highlighting the aspects unique to small intestinal tumors.

21 helial expressed IL-33 during development of intestinal tumors.

22 results: Some indicate an increased risk for intestinal tumors.

23 an increase in the occurrence of hepatic and intestinal tumors, a subset of which exhibited strong tr

24 nflammation, Ikkbeta(EE)(IEC) mice developed intestinal tumors after a long latency.

25 n our studies of a mouse model that develops intestinal tumors after low dietary folate, we found red

26 Neuroendocrine tumors, particularly small intestinal tumors, also grouped as 'carcinoids', are def

27 Comparative expression levels of UGT1A1 in intestinal tumors and normal surrounding tissue are dram

28 These hybrids developed few intestinal tumors and often lived longer than 1 year.

29 (b) a significant reduction in the number of intestinal tumors, and (c) improved overall survival.

30 tal cancer, Usp28 deletion resulted in fewer intestinal tumors, and importantly, in established tumor

31 reduced lifespan and increased incidence of intestinal tumors, Apc(Min/+)Fbxw7(DeltaG) mice may be u

32 Nutritional and genetic risk factors for intestinal tumors are additive on mouse tumor phenotype,

33 The majority of these intestinal tumors are associated with the accumulation o

34 Large intestinal tumors are predominantly adenomas, whereas th

35 by primary IECs and selectively activated in intestinal tumors as a result of impaired stratification

36 in/+);Tgfbr1(+/-) mice develop twice as many intestinal tumors as Apc(Min/+);Tgfbr1(+/+) mice, as wel

37 Mice with LOI developed twice as many intestinal tumors as did control littermates.

38 Wnt/beta-catenin pathway is specific to the intestinal tumors, as genomic instability but not activa

39 and 1638N in multiplicity and regionality of intestinal tumors, as well as in incidence of extracolon

40 cells restored GUCY2C signaling, eliminating intestinal tumors associated with a high calorie diet.

41 638N) mice because of a high multiplicity of intestinal tumors at a younger age.

42 of V33 with Apc (Min/+) mice, had increased intestinal tumor burden compared with littermate Apc (Mi

43 Surprisingly, the small intestinal tumor burden was actually lower in -/- animal

44 in/+);Tgfbr1(+/+) and Apc(Min/+);Tgfbr1(+/-) intestinal tumors, but cyclin D1 expression and cellular

45 , dietary CP-31398 suppressed development of intestinal tumors by 36% (P < 0.001) and 75% (P < 0.0001

46 e, de Sousa e Melo et al. (2017) reveal that intestinal tumors can contain dynamic pools of functiona

47 bed for juvenile polyposis syndrome, a human intestinal tumor caused by mutations in BMP signaling pa

48 secretin release from murine neuroendocrine intestinal tumor cell line STC-1 and secretin cells enri

49 suggest that Sphk1 plays a critical role in intestinal tumor cell proliferation and that inhibitors

50 Sphk1 is expressed and is required for small intestinal tumor cell proliferation in Apc Min/+ mice.

51 A greater number of intestinal tumor cells from VEGFR2(DeltaIEC) mice were i

52 Treatment of WNT-activated intestinal tumor cells with SMC2 siRNA significantly red

53 ation of STAT3 and expression of survivin in intestinal tumor cells.

54 In vivo, both intestinal tumors derived from mice transgenic for villi

55 ort that MYC-nick is abundant in colonic and intestinal tumors derived from mouse models with mutatio

56 KLF5 expression was examined in intestinal tumors derived from transgenic mice expressin

57 Thus, although intestinal tumors develop in Apc(1638N/+) mice on focal

58 The mammary and intestinal tumor development as well as the increase in

59 ct the role of p21 in sulindac inhibition of intestinal tumor development in Apc1638+/- mice, we quan

60 The involvement of Arrb2 in intestinal tumor development via the regulation of the W

61 de novo DNA methyltransferase 3a (Dnmt3a) in intestinal tumor development, we analyzed the expression

62 fore investigated the role of calcineurin in intestinal tumor development.

63 ved from the commensal microbiota to promote intestinal tumor development.

64 on of Dnmt3a inhibits the earliest stages of intestinal tumor development.

65 and promote chronic inflammation, promoting intestinal tumor development.

66 In Mir34a-deficient mice, colitis-associated intestinal tumors displayed upregulation of p-STAT3, IL-

67 s essential for the initiation and growth of intestinal tumors displaying elevated Wnt pathway activi

68 he growth-related functions of KLF5 and that intestinal tumors down-regulate KLF5 expression by multi

69 tion promotes the spontaneous development of intestinal tumors driven by mutations in the adenomatous

70 nq1 mutant mice developed significantly more intestinal tumors, especially in the proximal small inte

71 n of pancreaticobiliary tumors compared with intestinal tumors expressed MUC-1 [86.4% (95% CI 75.1%-9

72 beled bone marrow-derived cells to mice with intestinal tumors, finding that fusion between circulati

73 It also reduces intestinal tumor formation after administration of chemi

74 2 (Tgfbr2(IEKO)) alone is not sufficient for intestinal tumor formation and lack of Pten (Pten(IEKO))

75 Apc-associated intestinal tumor formation appears to require functional

76 drinking fluid significantly decreased small intestinal tumor formation by 37% or 47%, respectively,

77 mice, targeted inactivation of p21 increased intestinal tumor formation in a gene-dose-dependent mann

78 g sulindac was still effective in inhibiting intestinal tumor formation in Apc(+/-),p27(+/-) or Apc(+

79 ockout of PKClambda significantly suppresses intestinal tumor formation in Apc(min/+) mice.

80 We have demonstrated previously that intestinal tumor formation in B6 Min/+ mice is always ac

81 inactivation of p27(kip1) was sufficient for intestinal tumor formation in mice, but this was strictl

82 We also examined bFGF in intestinal tumor formation of APC(Min/+) mice with and w

83 The aggressive intestinal tumor formation of APC(Min/+); Fbw7(DeltaIEC)

84 e of miR-34a/b/c function for suppression of intestinal tumor formation, we generated Apc(Min/+) mice

85 ecific Sirt1 heterozygous mice have enhanced intestinal tumor formation, whereas intestine-specific S

86 while having no discernable effect on small intestinal tumor formation.

87 n, which is considered the earliest stage of intestinal tumor formation.

88 ntive agents in a mouse model of spontaneous intestinal tumor formation.

89 ollowed by dextran sodium sulfate, to assess intestinal tumor formation.

90 ng, with Apc(min/+) mice, which are prone to intestinal tumor formation.

91 We found that Ikkepsilon was activated in intestinal tumors forming upon loss of the tumor suppres

92 Relative to controls and gamma-ray, intestinal tumor frequency and grade was significantly h

93 Therefore, intestinal tumor frequency, size, cluster, and grade wer

94 lon tumors from human clinical specimens and intestinal tumors from Apc(Min/+) mice compared with nor

95 airs (n = 19, p < 0.0002) and in a cohort of intestinal tumors from Apc-deficient Min/+ mice.

96 Almost 90% of the intestinal tumors from both Msh6(-/-)Apc1638N and Msh3(-

97 ate that Apc expression is suppressed in all intestinal tumors from both untreated and treated AKR Mi

98 Intestinal tumors from CD4-TLR4-APC(Min/+) mice displaye

99 K-ras-activating mutations were detected in intestinal tumors from either untreated or ENU-treated M

100 Intestinal tumors from mice and humans can have a polycl

101 We analyzed matrilysin expression in benign intestinal tumors from mice heterozygous for the ApcMin

102 colon cancer, diminished the number of small intestinal tumors generated.

103 Oral intake of Sb reduced intestinal tumor growth and dysplasia in C57BL/6J Min/+

104 +) mice whereas activation of CB1 attenuated intestinal tumor growth by inducing cell death via down-

105 murf2 degrades wild-type Smurf2 and controls intestinal tumor growth in mice by up-regulating TGF-bet

106 we show that altered IGF-II supply modifies intestinal tumor growth.

107 nding/degradation repeats (20AARs); very few intestinal tumors have proteins with no 20AARs.

108 r deficiency alone caused the development of intestinal tumors in >60% of mice.

109 irs the progression and maintenance of small intestinal tumors in a cell autonomous and highly Arf-de

110 blocking its binding to BCL9, and attenuates intestinal tumors in Apc(Min) mice.

111 P-S also prevents the growth of intestinal tumors in Apc/Min mice.

112 F1/cip1) increases the frequency and size of intestinal tumors in Apc1638+/- mice that inherit a muta

113 COX-2 is expressed at high levels in intestinal tumors in humans and rodents.

114 of EGFR from epithelial cells of established intestinal tumors in mice given AOM and DSS did not redu

115 ndent manner and promotes the development of intestinal tumors in mice.

116 in human colorectal cancer cell lines and in intestinal tumors in mice.

117 tations also frequently occur in ENU-induced intestinal tumors in Min mice.

118 errupted long-term celecoxib administration, intestinal tumors in Min/+ mice initially regressed and

119 he normal intestinal mucosa, is increased in intestinal tumors in Mlh1(-/-) mice, and is reduced in t

120 c mutations implicated in the development of intestinal tumors in Mlh1-/- Apc1638N animals.

121 ficantly increased the frequency and size of intestinal tumors in Muc2 knockout mice and also led to

122 fr activity is required for establishment of intestinal tumors in the Apc(Min) model between initiati

123 ation resulted in almost complete absence of intestinal tumors in the ApcMin mouse model of colon can

124 ast, the incidence and growth of macroscopic intestinal tumors in the same animals was strongly suppr

125 correlated with activating KRAS mutations in intestinal tumors in vitro and in vivo.

126 mutation that leads to a markedly increased intestinal tumor incidence and mortality rate.

127 R) mutant mice developed significantly fewer intestinal tumors, indicating that Mlh1 missense mutatio

128 Pten (Pten(IEKO)) alone had a weak effect on intestinal tumor induction.

129 To study the role of E(2) in intestinal tumor inhibition, we separately crossed C57BL

130 longator complex, is required for Wnt-driven intestinal tumor initiation and radiation-induced regene

131 lpha activation, and (b) loss of PKCalpha in intestinal tumors is associated with increased levels of

132 previously reported that the multiplicity of intestinal tumors is increased dramatically by crossing

133 ike nontransformed epithelium lacking ERBB3, intestinal tumors lacking ERBB3 had reduced PI3K/AKT sig

134 e majority of somatic human APC mutations in intestinal tumors lead to APC truncation.

135 ogue of vitamin D can significantly decrease intestinal tumor load in Apc(min) mice without severe to

136 association between eicosanoid biosynthesis, intestinal tumor load, and the chemotherapeutic effect o

137 the CEA-based vaccine significantly reduced intestinal tumor load.

138 In murine intestinal tumors, matrilysin transcripts show striking

139 Whereas Pms2-deficient mice do not develop intestinal tumors, mice deficient in Pms2 and heterozygo

140 ted directly by crossing BAH KO mice with an intestinal tumor model, APCmin mice.

141 We tested this using the Apc(Min/+) mouse intestinal tumor model, in which effects on tumor initia

142 mented colon tumorigenesis in the Apc(min/+) intestinal tumor model.

143 Existing mouse intestinal tumor models display mainly small intestinal

144 8N mice showed no difference in survival and intestinal tumor multiplicity as compared with Apc1638N

145 ry administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%.

146 matous polyoposis coli (Apc) allele and that intestinal tumor multiplicity in B6 Min/+ mice can be si

147 The intestinal tumor multiplicity in mice heterozygous for A

148 5-aza-2'-deoxycytidine significantly reduces intestinal tumor multiplicity in the predisposed Min mou

149 FR tyrosine phosphorylation failed to affect intestinal tumor multiplicity or distribution but induce

150 reduced survival and a 6-7-fold increase in intestinal tumor multiplicity.

151 ir interaction on azoxymethane (AOM)-induced intestinal tumor number and size in mice.

152 6A diet at doses of 0.1 and 1% decreased the intestinal tumor number by 75 and 71%, respectively.

153 of ApcMin with cyclin D1-/- mice reduced the intestinal tumor number in animals genetically heterozyg

154 Small intestinal tumor numbers were unaffected.

155 Increased Jagged1 was also present in intestinal tumors of Apc(1638N/+) and Apc(Min/+) mice, b

156 ferative index in IEC resulting in increased intestinal tumors of larger size and grade due to prefer

157 urthermore, all matrilysin-expressing benign intestinal tumors of the Min mouse expressed a member of

158 In addition, increased rates of apoptosis in intestinal tumors (P < 0.01-0.0001) were observed in ani

159 typically develop three to five spontaneous intestinal tumors per animal.

160 noma, and STC-1 cells, derived from a murine intestinal tumor, process pro-CCK mainly to amidated CCK

161 anscription, providing a direct link between intestinal tumor progression and altered function of KLF

162 Collectively, these data indicate that intestinal tumor progression is associated with a change

163 to dysplastic growth in the early stages of intestinal tumor progression, independent of its effects

164 omponents and growth factors associated with intestinal tumor progression.

165 Bile acids are intestinal tumor promoters and their concentrations have

166 hormones for GCC are uniformly deficient in intestinal tumors, reactivation of dormant GCC signaling

167 ygenase-2 (COX-2) is aberrantly expressed in intestinal tumors resulting from APC mutation, and is al

168 Despite the absence of cyclin D1, intestinal tumors still developed.

169 -2 gene in Min mice reduced the incidence of intestinal tumors, suggesting that it is required for tu

170 cular mechanism underlying fbw7 mutations in intestinal tumor suppression is unclear.

171 Fbw7 exhibited haploinsufficiency for intestinal tumor suppression.

172 mportant new avenue by which Mule acts as an intestinal tumor suppressor by regulation of the intesti

173 None of these modifiers is associated with intestinal tumor susceptibility, which indicates that th

174 6LXRalpha mice also developed fewer, smaller intestinal tumors than APC(min/+)/iVP16 mice.

175 We analyzed intestinal tumors that arose in mice that express an onc

176 These mice develop multiple intestinal tumors that show loss of wild-type Apc protei

177 Formation of intestinal tumor was induced in C57BL/6J mice using azox

178 Susceptibility to intestinal tumors was independent of mammary tumor susce

179 sion of genetically and carcinogen-initiated intestinal tumors was significantly accelerated in Myo1a

180 Human and mouse intestinal tumors were also analyzed.

181 control and treated animals and DMH-induced intestinal tumors were assayed for JNK and ERK activity

182 Normal-seeming mucosa and intestinal tumors were harvested and assayed for apoptos

183 ations detected in mismatch repair-deficient intestinal tumors were located upstream of the third 20-

184 ukemia virus and develop twice the number of intestinal tumors when crossed with mice carrying a muta