ライフサイエンスコーパス: adenomatous

1 identify endoscopic features associated with adenomatous and hyperplastic histology.

2 of dietary PUFA intake on risk of colorectal adenomatous and hyperplastic polyps.

3 ven MINT loci in primary CRC with contiguous adenomatous and normal tissues of 79 patients.

4 2, 3, 12, 17, 25, and 31 in sets of normal, adenomatous, and malignant tissues from 46 patients with

5 with fundic gland polyp (FGP) formation and adenomatous change, which are similar to those observed

6 use colon epithelium is sufficient to induce adenomatous changes and the generation of Paneth-like ce

7 ficantly lower expression of HMOX-1 in their adenomatous colon tissues.

8 = 0.02), and 0.39 for RASSF1A (p < 0.01) in adenomatous compared to normal parathyroid tissue.

9 Individual adenomatous crypts were clonal for mtDNA mutations and c

10 Methylation patterns of adenomatous crypts were determined by clonal bisulphite

11 Adenomatous crypts within human tumors contain actively

12 e APW and RPW tests, respectively, to detect adenomatous disease.

13 ly history of colorectal cancer, or interval adenomatous findings could explain only a minority of su

14 essed to two types of more advanced lesions, adenomatous gland forming lesion (Type 1) and atypical g

15 thyroid mass, especially co-existing with an adenomatous goiter, should prompt a work-up for thyroid

16 invasive precursor lesions known as atypical adenomatous hyperplasia (AAH) and bronchioloalveolar car

17 mocyte proliferations designated as atypical adenomatous hyperplasia (AAH).

18 Alveolar adenomatous hyperplasia and adenocarcinoma were signific

19 ced the development of premalignant atypical adenomatous hyperplasia lesions at 6 wk after urethane i

20 s(G12D) model displayed features of atypical adenomatous hyperplasia, adenocarcinoma in situ, and inv

21 inflammation promotes proliferation of early adenomatous lesions in a TLR-dependent manner.

22 ing on the progression of Kras-induced early adenomatous lesions in the lung.

23 ly after parathyroidectomy, 100 to 300 mg of adenomatous or hyperplastic diseased parathyroid tissue

24 n-6 PUFAs were not associated with adenomatous or hyperplastic polyps in either men or wome

25 Using flow cytometric analysis of resected adenomatous parathyroid glands, we have isolated and cha

26 DA) model built to discriminate healthy from adenomatous parathyroid tissue was able to correctly cla

27 Age over 60 years old, adenomatous polyp and heavy alcohol consumption may affe

28 ate endoscopic prediction of hyperplastic or adenomatous polyp histology could reduce procedural time

29 of digital chromoendoscopy for prediction of adenomatous polyp histology was 90.1 %.

30 The Adenomatous Polyp Prevention on Vioxx (APPROVe) study as

31 ssion analysis, age over 60 years old, male, adenomatous polyp, current smoking and heavy alcohol con

32 types in a murine model of colon cancer, the adenomatous polyposis (APC) mutant (Apc (716/+)) model.

33 ications of MMVTx for patients with familial adenomatous polyposis (FAP) and the technical feasibilit

34 Patients with familial adenomatous polyposis (FAP) are at markedly increased ri

35 amatically altered for the worse in familial adenomatous polyposis (FAP) because these patients harbo

36 We studied patients with Familial Adenomatous Polyposis (FAP) because they are virtually c

37 identified as a candidate gene for familial adenomatous polyposis (FAP) but further study identified

38 tumors often occur in patients with familial adenomatous polyposis (FAP) coli who have germ line muta

39 rative colitis (UC) in 37 patients, familial adenomatous polyposis (FAP) in 12 patients, and colonic

40 of thyroid cancer in patients with Familial adenomatous polyposis (FAP) in a prospective study of th

41 Familial adenomatous polyposis (FAP) is a human cancer syndrome c

42 Familial Adenomatous Polyposis (FAP) is characterized by marked u

43 ial cancer predispositions known as familial adenomatous polyposis (FAP) or Gardner syndrome.

44 rliest colonic tissue alteration in familial adenomatous polyposis (FAP) patients, we present the hyp

45 s after 4-6 months of treatment for familial adenomatous polyposis (FAP) patients.

46 atous polyposis coli (APC) underlie familial adenomatous polyposis (FAP), an inherited cancer syndrom

47 ive colitis, indeterminate colitis, familial adenomatous polyposis (FAP), and a select group of patie

48 atorial chemoprevention efficacy in familial adenomatous polyposis (FAP), signal of benefit from imag

49 type 2 (MEN2), Cowden syndrome, and familial adenomatous polyposis (FAP).

50 colorectal polyps in children with familial adenomatous polyposis (FAP).

51 gous to those responsible for human familial adenomatous polyposis (FAP).

52 oter 1B occur in rare families with familial adenomatous polyposis (FAP).

53 ccur in up to 21 % of patients with Familial Adenomatous Polyposis (FAP).

54 to iPSCs derived from patients with familial adenomatous polyposis (FAP-iPSCs) harboring germline mut

55 testinal tissues from patients with familial adenomatous polyposis (n = 18) or sessile serrated adeno

56 Patients with familial adenomatous polyposis after pouch surgery (n = 9), indiv

57 edisposes to a new subtype of BER-associated adenomatous polyposis and CRC.

58 in animals and in patients with the familial adenomatous polyposis by downregulating beta-catenin sig

59 The adenomatous polyposis cell (APC) tumor suppressor is a m

60 e conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine

61 n on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where red

62 The tumor suppressor Adenomatous polyposis coli (APC) affects the function of

63 induced by the rare inheritance of a mutant adenomatous polyposis coli (Apc) allele.

64 ministering LPA to mice heterozygous for the adenomatous polyposis coli (Apc) allele.

65 contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathoge

66 ested that specific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response

67 onal and transcriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are

68 expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oli

69 Finally, CBC stem cells deficient in adenomatous polyposis coli (Apc) and Math1 were able to

70 ther, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose poly

71 nce microscopy to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 du

72 firmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional

73 First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stom

74 polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP

75 Here we find that the tumor suppressor adenomatous polyposis coli (APC) controls microtubule ta

76 C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenom

77 Mutations in adenomatous polyposis coli (APC) disrupt regulation of W

78 As Adenomatous Polyposis Coli (APC) functions in many of th

79 mice bearing a heterozygote mutation in the adenomatous polyposis coli (APC) gene (Apc(Min/+) mice).

80 ted gene-targeted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are ort

81 of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent

82 ased in human cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimu

83 We show that a deficiency in the adenomatous polyposis coli (APC) gene and subsequent act

84 Patients with mutations in the Adenomatous Polyposis Coli (APC) gene are at increased r

85 Somatic mutations of the adenomatous polyposis coli (APC) gene are initiating eve

86 The adenomatous polyposis coli (APC) gene encodes APC tumour

87 Since the Adenomatous Polyposis Coli (APC) gene is mutated in the

88 The Adenomatous Polyposis Coli (APC) gene is mutated in the

89 Although beta-catenin and adenomatous polyposis coli (APC) gene mutations are well

90 Adenomatous polyposis coli (APC) gene mutations have bee

91 Mutations in the adenomatous polyposis coli (APC) gene occur in the vast

92 The adenomatous polyposis coli (APC) gene product is mutated

93 letion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal

94 ssf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate inte

95 n the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult b

96 intestinal carcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to ac

97 requently bear inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is

98 velop through loss of normal function of the Adenomatous polyposis coli (APC) gene.

99 g, in particular, tumor suppressors TP53 and adenomatous polyposis coli (APC) gene.

100 imiting mutations in human CRC occurs in the adenomatous polyposis coli (APC) gene.

101 omas had somatic truncation mutations to the adenomatous polyposis coli (Apc) gene.

102 Wnt/beta-catenin pathway signaling following adenomatous polyposis coli (APC) inactivation.

103 Mutations in the tumor suppressor adenomatous polyposis coli (APC) initiate most colon can

104 The tumor suppressor adenomatous polyposis coli (APC) is a crucial regulator

105 Adenomatous polyposis coli (APC) is a large multidomain

106 Adenomatous polyposis coli (APC) is a microtubule plus-e

107 The tumor suppressor Adenomatous polyposis coli (APC) is a negative regulator

108 Mutational inactivation of adenomatous polyposis coli (APC) is an early event in co

109 The tumor suppressor adenomatous polyposis coli (APC) is an essential negativ

110 The tumor suppressor adenomatous polyposis coli (APC) is an essential negativ

111 ASE of adenomatous polyposis coli (APC) is associated with path

112 Adenomatous polyposis coli (APC) is best known for its c

113 Mutation of the tumor suppressor adenomatous polyposis coli (APC) is considered an initia

114 The tumor suppressor adenomatous polyposis coli (APC) is implicated in regula

115 The tumor suppressor protein adenomatous polyposis coli (APC) is multifunctional - it

116 Adenomatous polyposis coli (APC) is one such MAP with a

117 Loss of tumor suppressor adenomatous polyposis coli (APC) is thought to initiate

118 aling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate

119 Today, the tumor suppressor adenomatous polyposis coli (APC) may have the same compl

120 Here, we show that adenomatous polyposis coli (APC) modulates microtubule (

121 esis that initiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by

122 Adenomatous polyposis coli (APC) mutation is the most co

123 Adenomatous polyposis coli (APC) mutations are linked to

124 In this study, we show that adenomatous polyposis coli (APC) mutations found in huma

125 nt/beta-catenin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in app

126 The tumor suppressor Adenomatous polyposis coli (APC) negatively regulates Wn

127 (CRCs), an initiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, a

128 n that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activat

129 d glycogen synthase kinase 3beta (GSK-3beta)/adenomatous polyposis coli (APC) pathways.

130 The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in reg

131 nestin expressing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligode

132 ibition of GSK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus end

133 The adenomatous polyposis coli (APC) protein functions as a

134 CtBP interacts with adenomatous polyposis coli (APC) protein, and is stabili

135 Fap1 also interacts with the adenomatous polyposis coli (Apc) protein, but the functi

136 inked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflamm

137 The tumor suppressor protein adenomatous polyposis coli (APC) regulates cell protrusi

138 Adenomatous polyposis coli (APC) regulates the activity

139 is functionally important for cell migration.Adenomatous polyposis coli (APC) regulates the localizat

140 gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential fun

141 ne such pathway the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell pr

142 ting factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cyt

143 Binding of adenomatous polyposis coli (APC) to the microtubule plus

144 In turn, KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a s

145 The adenomatous polyposis coli (APC) tumor suppressor forms

146 Acquired or inherited mutations in the adenomatous polyposis coli (APC) tumor suppressor gene a

147 The adenomatous polyposis coli (APC) tumor suppressor gene e

148 The Adenomatous Polyposis Coli (APC) tumor suppressor gene i

149 Inactivation of the adenomatous polyposis coli (APC) tumor suppressor is fre

150 The adenomatous polyposis coli (Apc) tumor suppressor is inv

151 ce with IEC-specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus,

152 atase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protei

153 Mutation of the adenomatous polyposis coli (APC) tumor suppressor stabil

154 rcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a neg

155 in signaling is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which

156 calculating the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene i

157 ollows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and a

158 RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and t

159 Mutations in the adenomatous polyposis coli (APC) tumour suppressor are t

160 Mutations in Adenomatous polyposis coli (APC) underlie familial adeno

161 In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be importa

162 We found that the tumor suppressor adenomatous polyposis coli (APC) was required for microt

163 These mice were crossed with adenomatous polyposis coli (Apc)(min/+) mice, or given a

164 ne the genetic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor

165 Inactivating mutations within adenomatous polyposis coli (APC), a negative regulator o

166 approaches suggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt sig

167 Adenomatous polyposis coli (APC), a tumor suppressor com

168 Adenomatous polyposis coli (Apc), a tumor suppressor gen

169 Adenomatous polyposis coli (APC), a tumor suppressor gen

170 Specific site of CpG islands of adenomatous polyposis coli (APC), a well studied tumor s

171 The tumor suppressor adenomatous polyposis coli (APC), an essential negative

172 atenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also

173 forms a complex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (

174 Together with its direct binding partner adenomatous polyposis coli (APC), EB1 can stabilize micr

175 Mutations in known driver genes [e.g., adenomatous polyposis coli (APC), KRAS, or PIK3CA] found

176 Individual crypt adenomatous polyposis coli (APC), p53, K-RAS, and 17p lo

177 in acromegaly patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH

178 e designed against beta-catenin (Ctnnb1) and adenomatous polyposis coli (Apc), two commonly mutated g

179 ical Wnt signaling by targeting the gene for Adenomatous Polyposis Coli (Apc), which controls Wnt sig

180 e, we show that the tumor suppressor protein adenomatous polyposis coli (APC), which is a known MT-as

181 o develop colitis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the i

182 to the inactivation of the tumor suppressor adenomatous polyposis coli (APC).

183 by aberrant function of the tumor suppressor Adenomatous polyposis coli (Apc).

184 P), Skp1, transducin beta-like 1 (TBL1), and adenomatous polyposis coli (APC).

185 runcating mutations in the tumor suppressor, adenomatous polyposis coli (APC).

186 glycogen synthase kinase-3beta, axin-1, and adenomatous polyposis coli (APC).

187 ation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinas

188 We analyzed adenomatous polyposis coli (Apc)min/+/Sigirr-/- mice for

189 Arm is targeted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3

190 V integration site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been

191 In addition we identified adenomatous polyposis coli 1 (APC1) as an interaction pa

192 Germline specific overexpression of Adenomatous Polyposis Coli 2 (APC2) rescued GSC loss in

193 sly in germ cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-G

194 vilVEGF1 mice were bred to Min mice (adenomatous polyposis coli [APC] +/-).

195 ation of the centrosomal proteins Ninein and adenomatous polyposis coli abolished this bias.

196 G-protein signaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby

197 atenin and the destruction complex component adenomatous polyposis coli at a similar SLS motif to the

198 as associated with reduced expression of the adenomatous polyposis coli gene (APC).

199 iation domain family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in his

200 Mice carrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which desi

201 eficient mice carrying the Min allele of the adenomatous polyposis coli gene.

202 and compared to control mice carry wildtype Adenomatous polyposis coli gene.

203 t is caused by inactivating mutations in the Adenomatous polyposis coli gene.

204 Crossing Tfam(+/-) mice to the adenomatous polyposis coli multiple intestinal neoplasia

205 Here, we demonstrate that adenomatous polyposis coli mutant APC(Min/+) mice, which

206 RC) harboring functional mutations in either adenomatous polyposis coli or beta-catenin.

207 ling induced by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncov

208 Most information about the roles of the adenomatous polyposis coli protein (APC) and its binding

209 We recently identified adenomatous polyposis coli protein (APC) as a key regula

210 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc

211 We propose that adenomatous polyposis coli protein (APC) is a key coordi

212 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas

213 W480 cells stably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin

214 syndrome caused by germline mutations in the adenomatous polyposis coli tumor suppressor gene.

215 he microtubule motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC

216 However, little is known about adenomatous polyposis coli's (APC's) role in the mammali

217 member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g.

218 In the context of APC (adenomatous polyposis coli) deficiency (Apc(Min/+) mice)

219 g in T cell lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T ce

220 mutation of the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant

221 that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of bet

222 We had shown that the APC (adenomatous polyposis coli) protein controls localizatio

223 Disruption of Apc (adenomatous polyposis coli) within hepatocytes activates

224 ectly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wing

225 aditionally attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead t

226 I, IGF2; tumor suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1;

227 a-catenin pathway mutations, such as loss of adenomatous polyposis coli, are insensitive to this nove

228 Because mutations in adenomatous polyposis coli, beta-catenin and other compo

229 -catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-caten

230 Inactivation of the tumor suppressor adenomatous polyposis coli, with the resultant activatio

231 e glycogen synthase kinase 3beta (GSK3beta)- adenomatous polyposis coli-axin-mediated degradation pat

232 otubule organization and capture dynamics in adenomatous polyposis coli-deficient radial progenitors.

233 ted signaling and glycogen synthase kinase-3/adenomatous polyposis coli-mediated beta-catenin activat

234 ence in normal intestinal homeostasis and in adenomatous polyposis coli-mediated tumorigenesis.

235 intestinal tumors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and acti

236 f cell lines even harboring mutations in the adenomatous polyposis coli/beta-catenin pathway.

237 ble in cell lines harboring mutations in the adenomatous polyposis coli/beta-catenin pathway.

238 erived WNT2 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon

239 ive colitis in 73% of the cases and familial adenomatous polyposis in 17%.

240 Familial adenomatous polyposis is an inherited genetic disease, w

241 and multiple POFLs associated with familial adenomatous polyposis is reviewed.

242 families showed recessive inheritance of the adenomatous polyposis phenotype and progression to CRC i

243 In this study, using a human familial adenomatous polyposis syndrome susceptible mouse model,

244 polyposis coli (APC) gene reduces intestinal adenomatous polyposis via Axin/beta-catenin axis and the

245 es of hereditary syndromes, such as familial adenomatous polyposis, a cancer predisposition syndrome

246 , germline mutation of which causes familial adenomatous polyposis, an autosomal intestinal cancer sy

247 rosis, Duchenne Muscular Dystrophy, Familial Adenomatous Polyposis, Hereditary Non-polyposis Colorect

248 yndromes, including Lynch syndrome, familial adenomatous polyposis, MUTYH-associated polyposis, and c

249 ately 30% of families affected by colorectal adenomatous polyposis, no germline mutations have been i

250 A diagnosis of Lynch syndrome, familial adenomatous polyposis, or another genetic syndrome can i

251 In murine models of familial adenomatous polyposis, specifically the multiple intesti

252 Studies of tumors from human familial adenomatous polyposis, sporadic colon cancer, and mouse

253 on-negative Lynch syndrome, 16 with familial adenomatous polyposis, two with constitutional mismatch

254 opic expression of APC, but not its familial adenomatous polyposis-related truncation mutant, promine

255 ch are similar to those observed in familial adenomatous polyposis.

256 is associated with pathogenesis of familial adenomatous polyposis.

257 ng causes of death in patients with familial adenomatous polyposis.

258 t with Apc, are important models of familial adenomatous polyposis.

259 a development in an animal model of familial adenomatous polyposis.

260 n additional recessive subtype of colorectal adenomatous polyposis.

261 m 102 unrelated individuals with unexplained adenomatous polyposis.

262 equently remains unresolved in patients with adenomatous polyposis.

263 sies from IPAA patients with UC and familial adenomatous polyposis.

264 pathogenic variants associated with familial adenomatous polyposis.

265 diseases, three females (1.6 %) had familial adenomatous polyposis; three patients (1 male and two fe

266 The primary outcome measure was advanced adenomatous polyps (AAPs).

267 persons who have first-degree relatives with adenomatous polyps (adenomas).

268 inations, but not for patients with low-risk adenomatous polyps (OR = 1.8; 95% CI, 0.9-3.7).

269 io [OR] = 3.1; 95% CI, 1.7-5.5) or high-risk adenomatous polyps (OR = 3.0; 95% CI, 1.2-8.0), compared

270 7; 95% confidence interval [CI], 1.64-6.47), adenomatous polyps (RR, 2.18; 95% CI, 1.18-4.61) and hea

271 op consensus guidelines for the detection of adenomatous polyps and CRC in asymptomatic average-risk

272 ion of CBS in human biopsies of precancerous adenomatous polyps and show that forced upregulation of

273 Adenomatous polyps are precursors to colorectal cancer (

274 y layers of the intestinal wall, cancer, and adenomatous polyps based on the REIMS fingerprint of eac

275 in 7 (6%), hyperplastic polyps in 4 (3.5%), adenomatous polyps in 2(2%), history of ulcerative colit

276 ction of IL10 and have increased colitis and adenomatous polyps in chemical and genetic models of col

277 n-3 PUFAs are associated with lower risk of adenomatous polyps in women, and the association may be

278 urveillance colonoscopy for individuals with adenomatous polyps is based on adenoma histology, size,

279 Treg cells that expand in adenomatous polyps no longer produce IL-10 and instead s

280 classified as having no evidence of disease, adenomatous polyps of less than 10 mm, of 10 mm or more,

281 In 2003-2005, cases with adenomatous polyps only (n = 639), hyperplastic polyps o

282 (95% confidence interval (CI): 1.4, 2.5) for adenomatous polyps only, 5.0 (95% CI: 3.3, 7.3) for hype

283 the hypothesis that colonoscopic removal of adenomatous polyps prevents death from colorectal cancer

284 Similar values were found when only adenomatous polyps were considered.

285 r high grade dysplasia or size > 1 cm or > 3 adenomatous polyps) were found in 98 cases (7 %), low ri

286 characteristics of these tests for detecting adenomatous polyps, advanced adenomas based on size, or

287 be prevented by the detection and removal of adenomatous polyps, and survival is significantly better

288 s of human colorectal carcinoma (CRC) and in adenomatous polyps, indicating its suppression occurs ea

289 can detect cancer early and also can detect adenomatous polyps, thus providing a greater potential f

290 orectal cancer (CRC) patients with normal or adenomatous polyps, we found that both the adenoma and c

291 ed apoptosis, and suppressed angiogenesis in adenomatous polyps, which reduced both tumor number and

292 olonoscopies that identified hyperplastic or adenomatous polyps.

293 cer was prevented by colonoscopic removal of adenomatous polyps.

294 system for differentiating hyperplastic from adenomatous polyps.

295 cially in the context of hyperplastic and/or adenomatous polyps.

296 APC gene and individual risk of metachronous adenomatous polyps.

297 scopic findings, and of these, 256 cases had adenomatous polyps.

298 and two-fold (P = .02), respectively, during adenomatous transformation in normal rectal epithelium.

299 ACF, once postulated as the ACF destined for adenomatous transformation, have been rarely identified

300 273 colorectal glands (126 hyperplastic, 147 adenomatous) were isolated via laser capture microdissec