ライフサイエンスコーパス: adenomatous

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

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

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

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

5 y three phenotypes: (1) CRC, (2) one or more adenomatous colon polyps, and (3) control participants o

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

7 = 0.02), and 0.39 for RASSF1A (p < 0.01) in adenomatous compared to normal parathyroid tissue.

8 Individual adenomatous crypts were clonal for mtDNA mutations and c

9 Methylation patterns of adenomatous crypts were determined by clonal bisulphite

10 Adenomatous crypts within human tumors contain actively

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

12 pic imaging, it is possible to differentiate adenomatous from hyperplastic diminutive (1-5 mm) polyps

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

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

15 les, many of which are preneoplasia atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (A

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

17 ere classified as pre-invasive (P1, atypical adenomatous hyperplasia and adenocarcinoma in situ), min

18 Alveolar adenomatous hyperplasia and adenocarcinoma were signific

19 g adenocarcinomas were included: 31 atypical adenomatous hyperplasia and adenocarcinomas in situ (cla

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

21 pecimens, including 89 premalignant atypical adenomatous hyperplasia lesions, 15 adenocarcinomas in s

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

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

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

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

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

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

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

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

30 Positive adenomatous polyp detection rate in patient's age > 40 y

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 and normal pouch from patient with familial adenomatous polyposis (n = 6).

54 ative colitis (UC) versus controls (familial adenomatous polyposis [FAP]).

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

56 tions affecting NTHL1 predispose carriers to adenomatous polyposis and colorectal cancer, but the com

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

58 isease progression in patients with familial adenomatous polyposis are unknown.

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

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

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

62 al crypt, augmenting CRC tumorigenesis in an adenomatous polyposis coli (APC(Delta14/+)) mouse model.

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

64 as a binding partner of the tumor suppressor adenomatous polyposis coli (APC) [1]; however, the signi

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

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

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

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

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

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

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

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

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

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

75 As in mammals, loss of adenomatous polyposis coli (APC) causes Drosophila intes

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

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 The adenomatous polyposis coli (APC) gene encodes APC tumour

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

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

87 The adenomatous polyposis coli (APC) gene is mutated within

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

89 Adenomatous polyposis coli (APC) gene mutations have bee

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

91 The adenomatous polyposis coli (APC) gene plays, among other

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

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

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

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

96 cancer cases due to somatic mutations in the adenomatous polyposis coli (APC) gene.

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

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

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

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

101 criptional and epigenetic changes induced by adenomatous polyposis coli (Apc) inactivation in intesti

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

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

104 Adenomatous polyposis coli (APC) is a large multidomain

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

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

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

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

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

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

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

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

113 The tumor suppressor adenomatous polyposis coli (APC) is frequently mutated i

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

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

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

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

118 te that intestinal epithelial suppression of adenomatous polyposis coli (Apc) mitigates RIGS lethalit

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

120 ects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are

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

122 gastric cancer cells even in the presence of adenomatous polyposis coli (Apc) mutation.

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

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

125 Depletion of the tumor suppressors adenomatous polyposis coli (APC) or Axin dramatically in

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

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

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

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

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

131 ver beta-catenin/E-cadherin and beta-catenin/adenomatous polyposis coli (APC) PPIs.

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

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

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

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

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

137 Adenomatous polyposis coli (APC) regulates the activity

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

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

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

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

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

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

144 The adenomatous polyposis coli (APC) tumor suppressor forms

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

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

147 cells lines with truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor gene t

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

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

150 The adenomatous polyposis coli (APC) tumor suppressor protei

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

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

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

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

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

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

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

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

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

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

161 Adenomatous polyposis coli (APC), a protein with both tu

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

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

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

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

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

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

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

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

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

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

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

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

174 ulation and epithelial over-proliferation in Adenomatous polyposis coli (APC)-mutated intestine.

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

176 iously disclosed the discovery of truncating adenomatous polyposis coli (APC)-selective inhibitor 1 (

177 RC) through mutation of the tumor suppressor Adenomatous Polyposis Coli (APC).

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

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

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

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

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

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

184 py, FRAP, live cell imaging, and a mutant of Adenomatous polyposis coli (APC-m4) defective in actin n

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

186 alignancies due to inactivating mutations of adenomatous polyposis coli (in colorectal cancer) or act

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

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

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

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

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

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

193 Mutations in the adenomatous polyposis coli gene (Apc) are a major driver

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

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

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

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

198 olocalizes with the tumor suppressor protein adenomatous polyposis coli in the TJs of epithelial cell

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

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

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

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

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

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

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

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

207 have bi-allelic mutations in APC2, encoding adenomatous polyposis coli protein 2.

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

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

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

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

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

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

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

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

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

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

218 her beta-catenin activation or loss of APC - adenomatous polyposis coli) upon expression of CRE recom

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

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

221 adenoma growth in the context of mutant Apc (adenomatous polyposis coli).

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

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

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

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

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

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

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

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

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

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

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

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

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

235 Familial adenomatous polyposis is an inherited genetic disease, w

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

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

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

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

240 and inherited conditions (Lynch and familial adenomatous polyposis), by changing only 2 tissue-specif

241 associated with thyroid cancer (eg, familial adenomatous polyposis), or one or more first-degree rela

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

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

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

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

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

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

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

249 this trial involving patients with familial adenomatous polyposis, the incidence of disease progress

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

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

252 h either drug alone, in adults with familial adenomatous polyposis.

253 m 102 unrelated individuals with unexplained adenomatous polyposis.

254 equently remains unresolved in patients with adenomatous polyposis.

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

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

257 is associated with pathogenesis of familial adenomatous polyposis.

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

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

260 pathogenic variants associated with familial adenomatous polyposis.

261 n additional recessive subtype of colorectal adenomatous polyposis.

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

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

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

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

266 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

267 7; 95% confidence interval [CI], 1.64-6.47), adenomatous polyps (RR, 2.18; 95% CI, 1.18-4.61) and hea

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

269 Adenomatous polyps are precursors to colorectal cancer (

270 Detection rates of adenomatous polyps at initial colonoscopy was higher in

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

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

273 nic milieu as reflected by the high rates of adenomatous polyps in AN participants.

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

275 asurement test for the diagnosis of CRCs and adenomatous polyps in plasma and stool samples in an Ira

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

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

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

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

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

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

282 Adenomatous polyps were detected in 16 of 32 AN particip

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

284 o underwent colonoscopy, 34.6% had 1 or more adenomatous polyps, 4.7% had 1 or more advanced adenomat

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

286 nomatous polyps, 4.7% had 1 or more advanced adenomatous polyps, and 5.7% had 1 or more serrated poly

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

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

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

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

291 olonoscopies that identified hyperplastic or adenomatous polyps.

292 cer was prevented by colonoscopic removal of adenomatous polyps.

293 system for differentiating hyperplastic from adenomatous polyps.

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

295 as a non-invasive assay to diagnose CRC and adenomatous polyps.

296 ignificantly altered in AN participants with adenomatous polyps.

297 nd the extent of immune cell infiltration in adenomatous premalignancy and associated lung adenocarci

298 l landscape and adaptive immune responses in adenomatous premalignancy.See related commentary by Merr

299 GS-Wnt mice developed adenomatous tooth-like gastric cancer.

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