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 results: Some indicate an increased risk for intestinal tumors.

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

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

5 GD synthase controls an inhibitory effect on intestinal tumors.

6 inactivation of JNK1 spontaneously developed intestinal tumors.

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

8 and destabilization of KLF5 protein occur in intestinal tumors.

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

10 esis, while hypomethylation protects against intestinal tumors.

11 utant mice, which are predisposed to develop intestinal tumors.

12 ackgrounds for susceptibility to mammary and intestinal tumors.

13 mutation could preferentially occur in small intestinal tumors.

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

15 in mice with an inherited predisposition to intestinal tumors.

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

17 SCs and their relevance to the beginnings of intestinal tumors.

18 ribution of CBCs and RSCs in mouse and human intestinal tumors.

19 f CD8(+) T cells that impaired the growth of intestinal tumors.

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

21 erexpressing NUP88 are cancer prone and form intestinal tumors.

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

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

24 g a potential utility for early diagnosis of intestinal tumors.

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

26 umor model that normally only develops small intestinal tumors.

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

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

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

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

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

32 Min/+) mice also developed fewer and smaller intestinal tumors and had significantly longer survival

33 esulting in development of fewer and smaller intestinal tumors and longer mouse survival.

34 The specific role of RIPK3 in intestinal tumors and MDSC function sheds light on a key

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

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

37 ependent feedback amplification loop between intestinal tumors and the microbiome.

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

39 upregulated in intestinal stem cells, mouse intestinal tumors, and human colorectal cancer (CRC) tis

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

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

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

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

44 Large intestinal tumors are predominantly adenomas, whereas th

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

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

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

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

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

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

51 n inflamed rectum at an early age and caused intestinal tumors at a late age, which were linked to in

52 638N) mice because of a high multiplicity of intestinal tumors at a younger age.

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

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

55 ased FSP-specific adaptive immunity, reduced intestinal tumor burden, and prolonged overall survival.

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

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

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

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

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

61 or cells, which can supply cells to multiple intestinal tumor cell lineages, whereas most lineage-tra

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

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

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

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

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

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

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

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

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

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

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

73 the regulation of tumorigenesis, the role in intestinal tumor development remains to be elucidated.

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

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

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

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

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

79 and promote chronic inflammation, promoting intestinal tumor development.

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

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

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

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

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

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

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

87 It also reduces intestinal tumor formation after administration of chemi

88 inactivation in a murine tumor model drives intestinal tumor formation and epithelial-mesenchymal tr

89 2 (Tgfbr2(IEKO)) alone is not sufficient for intestinal tumor formation and lack of Pten (Pten(IEKO))

90 Apc-associated intestinal tumor formation appears to require functional

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

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

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

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

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

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

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

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

99 IF-1 is a pivotal pro-tumorigenic factor for intestinal tumor formation, controlling key oncogenic pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Intestinal tumors from mice and humans can have a polycl

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

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

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

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

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

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

123 duction, which in turn significantly reduces intestinal tumor growth.

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

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

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

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

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

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

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

131 ations that stabilize beta-catenin and cause intestinal tumors in mice and humans.

132 mutations that stabilize B-catenin and cause intestinal tumors in mice and humans.

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

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

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

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

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

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

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

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

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

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

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

144 ed that RIPK3-mediated inflammation promoted intestinal tumors in two intestinal tumor models, Apc(Mi

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

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

147 r generations affected by a wide spectrum of intestinal tumors, including hyperplastic polyps, adenom

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

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

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

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

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

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

154 Although its role in driving intestinal tumors is well characterized, WNT's role in g

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

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

157 er inducer Snail in primary adult Drosophila intestinal tumors leads to the dissemination of tumor ce

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

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

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

161 In murine intestinal tumors, matrilysin transcripts show striking

162 RNase-A@AuNCs could successfully examine intestinal tumor mice from healthy mice, indicating a po

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

164 diate MDSC subset (I-MDSC) is expanded in an intestinal tumor model (Apc(Min/+) mice), but the import

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

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

167 genesis on the microbiome using a Drosophila intestinal tumor model.

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

169 Existing mouse intestinal tumor models display mainly small intestinal

170 flammation promoted intestinal tumors in two intestinal tumor models, Apc(Min/+) mice and an MC38 tra

171 Intestinal tumor multifocality was confirmed by histolog

172 8N mice showed no difference in survival and intestinal tumor multiplicity as compared with Apc1638N

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

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

175 The intestinal tumor multiplicity in mice heterozygous for A

176 5-aza-2'-deoxycytidine significantly reduces intestinal tumor multiplicity in the predisposed Min mou

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

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

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

180 6A diet at doses of 0.1 and 1% decreased the intestinal tumor number by 75 and 71%, respectively.

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

182 Small intestinal tumor numbers were unaffected.

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

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

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

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

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

188 ocus (7q31.2) perfectly segregating with the intestinal tumor predisposition in the family.

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

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

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

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

193 omponents and growth factors associated with intestinal tumor progression.

194 Bile acids are intestinal tumor promoters and their concentrations have

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

196 n, Paneth cell-specific Apc mutations led to intestinal tumors reminiscent not only of those arising

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

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

199 Two loci are overrepresented among cases of intestinal tumor subtype.

200 -2 gene in Min mice reduced the incidence of intestinal tumors, suggesting that it is required for tu

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

202 Fbw7 exhibited haploinsufficiency for intestinal tumor suppression.

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

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

205 6LXRalpha mice also developed fewer, smaller intestinal tumors than APC(min/+)/iVP16 mice.

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

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

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

209 Susceptibility to intestinal tumors was independent of mammary tumor susce

210 roughout the lifespan, and the occurrence of intestinal tumors was larger in SXRKO mice chronically e

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

212 Human and mouse intestinal tumors were also analyzed.

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

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

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

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

217 ncers, primarily lymphomas, lung cancer, and intestinal tumors, whereas Pold1 mutant mice also develo

218 1 year of age, Mcl1(DeltaIEC) mice developed intestinal tumors with morphologic and genetic features