ライフサイエンスコーパス: adenoma

1 t the time of colonoscopy than those without adenoma.

2 eded the formation of aberrant crypt foci or adenoma.

3 for the two main tissue types of healthy and adenoma.

4 enefits most patients with intermediate-risk adenomas.

5 the 18 patients with 21 to approximately 100 adenomas.

6 etection of 2483 cancers and 12,030 advanced adenomas.

7 ND1 regulatory genes in sporadic parathyroid adenomas.

8 as/polyps (SSA/Ps), and traditional serrated adenomas.

9 compared with corresponding benign precursor adenomas.

10 promising new approaches to treat pituitary adenomas.

11 y macrophages) in human and mouse intestinal adenomas.

12 tivation of an oncogene in established colon adenomas.

13 SAs, and 2.3% for patients with conventional adenomas.

14 e primary outcome was prevalence of advanced adenomas.

15 nic mice developing autochthonous intestinal adenomas.

16 d 0.98 (0.96-1.0) between CRC and colorectal adenomas.

17 gher than that of patients with conventional adenomas.

18 Most patients (59.9 %) had adenomas.

19 nondiminutive serrated lesions and advanced adenomas.

20 d the prevalence of any adenomas or advanced adenomas.

21 ase regulator, is upregulated in parathyroid adenomas.

22 ent hemoglobin in detecting CRC and advanced adenomas.

23 rapid progression of some polyps to advanced adenomas.

24 d inactivation of these genes in parathyroid adenomas.

25 ions such as aseptic meningitis or pituitary adenomas.

26 2 adenomas at the index examination (RR vs 1 adenoma, 1.47; 95% CI, 1.27-1.71), more than 3 serrated

27 l, 3340 participants (20.4%) had nonadvanced adenomas, 1643 participants (10.0%) had advanced adenoma

28 portions of subjects found to have 1 or more adenomas (38.8% vs 41.7% respectively; P = .27), advance

29 CI: 2.02-19.53; P = .001) and all colorectal adenomas (39.0% vs 19.0% in unexposed; mOR = 3.29; 95% C

30 P < .001), as was the prevalence of villous adenomas (5.5% vs 1.3% in unexposed; mOR = 6.28; 95% CI:

31 rate (5.0%) and positive predictive values (adenoma, 51.5%; CRC, 3.4%) were highest in round 1.

32 with Lynch syndrome--78 low-grade dysplastic adenomas, 57 high-grade dysplastic adenomas, and 31 colo

33 person sensitivity and specificity to detect adenomas 6 mm and larger comparable with colonoscopy (se

34 8% vs 41.7% respectively; P = .27), advanced adenomas (7.7% vs 8.2%; P = .73) or clinically significa

35 g allowed correct localization of nine of 10 adenomas (90% sensitivity), without any false-positive r

36 757 cases vs 1698 controls with conventional adenomas (95% CI, 2.25-2.80), and 1.30 in the 55 cases v

37 Additionally, follicular adenoma, a benign subtype of thyroid neoplasm, was also

38 ells' associations with synchronous advanced adenoma (AA) and colorectal carcinoma (CRC) is currently

39 cellular vesicle samples of 6 adrenocortical adenomas (ACA) and 6 histologically verified adrenocorti

40 Clinically nonfunctioning adenomas account for 15% to 54% of adenomas and present

41 tent CRC model that recapitulates the entire adenoma-adenocarcinoma-metastasis axis in vivo.

42 e chips on normal human colonic mucosa (NR), adenomas (ADs), and colorectal carcinoma (CRC).

43 r proportions of participants have 1 or more adenomas, advanced adenomas, or serrated polyps.

44 xpressed by intestinal stem cells [ISCs] and adenomas) affects intestinal homeostasis, regeneration,

45 y drug sulindac decreases size and number of adenomas after 4-6 months of treatment for familial aden

46 iminate chief cell adenoma from oxyphil cell adenoma allowed us to correctly classify >99% of the spe

47 g in both types of adenomas, with Apc-mutant adenomas also exhibiting unique changes in pathways rela

48 each group: 1.3% [95% CI, -0.1% to 2.8%] for adenoma and 0.7% [95% CI, -0.2% to 1.6%] for advanced ne

49 each group: 9.0% [95% CI, 7.3% to 10.7%] for adenoma and 2.4% [95% CI, 1.3% to 3.3%] for advanced neo

50 ach group: 10.3% [95% CI, 9.5% to 12.1%] for adenoma and 3.1% [95% CI, 2.0% to 4.1%] for advanced neo

51 usual care, the between-group differences in adenoma and advanced neoplasia detection rates were high

52 novel driver mutations that developed during adenoma and cancer evolution, particularly in OR1B1 (GPC

53 In addition, the adenoma and cancer further developed intratumor heteroge

54 r adenomatous polyps, we found that both the adenoma and cancer were of monoclonal origin, and both s

55 ummary, we demonstrated that both colorectal adenoma and CRC are monoclonal in origin, and the CRCs f

56 emoglobin/g), positive predictive values for adenoma and CRC, and FIT sensitivity for detecting CRC o

57 Moreover, mixed tumors with hepatocellular adenoma and hepatoblastoma (HB) were also frequently obs

58 apping fashion in parathyroid chief cells in adenoma and hyperplastic glands, and also in normal para

59 In the parotid space, pleomorphic adenoma and in the prestyloid parapharyngeal space, squa

60 ility criteria included a recently diagnosed adenoma and no remaining colorectal polyps after complet

61 Microsimulation using the ASCCA (Adenoma and Serrated pathway to Colorectal CAncer) model

62 New Hampshire since 2004, including rates of adenoma and SP detection.

63 TH)-secreting tumors account for 2% to 6% of adenomas and are associated with obesity, hypertension,

64 Large polyps, advanced neoplasia (advanced adenomas and cancer), and invasive cancer were seen in 3

65 rmance of CTC in the detection of colorectal adenomas and cancers using endoscopy as the reference st

66 rence of parathyroid tumours, often atypical adenomas and carcinomas, ossifying jaw fibromas, renal t

67 hematologic malignancies and hepatocellular adenomas and carcinomas.

68 tis, cirrhosis, and the formation of hepatic adenomas and carcinomas.

69 as in the siblings of patients with advanced adenomas and compared it with that of siblings of indivi

70 l adenomas, reductions in Gpr182 led to more adenomas and decreased survival.

71 Adenomas and derived tumoroids of ApcMin/+ mice with dis

72 clinically relevant parameters on pituitary adenomas and may represent a valuable therapeutic tool.

73 thyroid cancers (n = 128) and compared with adenomas and normal thyroid tissues (n = 62).

74 ge-related cells are often dispersed in lung adenomas and PanINs, contrasting with more contiguous gr

75 Prolactinomas account for 32% to 66% of adenomas and present with amenorrhea, loss of libido, ga

76 nctioning adenomas account for 15% to 54% of adenomas and present with mass effects; surgery is gener

77 Human sessile serrated adenomas and right-sided colorectal tumors with epigenet

78 used to reduce the recurrence of colorectal adenomas and the incidence of colorectal cancer.

79 Overexpression of Id1 causes intestinal adenomas and thymic lymphomas in mice, suggesting that I

80 identified by OC, and 15.6% had conventional adenomas and/or serrated polyps >/=6 mm.

81 ontralateral side of the neck, missed double adenoma, and absence of any abnormal lesion detected on

82 ells from patients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but not in patients with

83 noma, colonic carcinoid, parotid pleomorphic adenoma, and teratoma.

84 es of 14 patients with CRC, 16 with advanced adenomas, and 18 with nonadvanced adenomas, as well as 2

85 omas, 1643 participants (10.0%) had advanced adenomas, and 189 participants (1.2%) had colorectal can

86 as/polyps, 70 sporadic high-grade dysplastic adenomas, and 19 hyperplastic polyps--and tissue derived

87 ysplastic adenomas, 57 high-grade dysplastic adenomas, and 31 colon cancer samples.

88 es of 81 patients with CRC, 40 with advanced adenomas, and 43 with nonadvanced adenomas, as well as 1

89 ced adenomas, the total number of colorectal adenomas, and adenoma size and features.

90 and serrated or hyperplastic, and polyps or adenomas, and colorectal (or synonymous terms), publishe

91 Bcl-2 is upregulated in adenomas, and its loss or inhibition impairs outgrowth o

92 mortality, test accuracy in detecting CRC or adenomas, and serious adverse events.

93 and its main subtypes, aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), r

94 ng may be important in aldosterone-producing adenoma (APA).

95 Aldosterone-producing adenomas (APAs) are benign tumors of the adrenal gland t

96 Aldosterone-producing adenomas (APAs) vary in phenotype and genotype.

97 If no adenomas are found, the screening interval can gradually

98 Small and flat adenomas are known to carry a high miss-rate during stan

99 this study, SSA/Ps and traditional serrated adenomas are referred to collectively as STSAs.

100 h advanced adenomas, and 43 with nonadvanced adenomas, as well as 129 persons without colorectal neop

101 h advanced adenomas, and 18 with nonadvanced adenomas, as well as 24 persons without colorectal neopl

102 ite, 1.7; 95% CI, 1.22-2.43), detection of 2 adenomas at the index examination (RR vs 1 adenoma, 1.47

103 Autonomous thyroid adenomas (ATAs) are a frequent cause of hyperthyroidism.

104 ce of Paneth cells in colorectal adenomas to adenoma burden and male gender.

105 that HuR activation is an early event in FAP-adenoma but is not present in IBD-dysplasia.

106 ct of vitamin D3 supplementation on advanced adenomas, but not on adenoma risk overall, significantly

107 orectal cancer (CRC) and colorectal advanced adenoma (CAA)] frequently develop in individuals at ages

108 nosed at >/=60 years with CRC or an advanced adenoma can be offered average-risk screening options be

109 known genes involved in early phases of the adenoma-carcinoma sequence (such as, APC).

110 Here, we dissect this adenoma-carcinoma sequence in vivo by using an orthotopi

111 In the adenoma-carcinoma sequence, it is proposed that intestin

112 Upregulation of EREG during the adenoma-carcinoma transition was associated with demethy

113 pt cells, differentiated surface epithelium, adenomas, carcinomas and metastases, and used gene expre

114 ur persons comprised colorectal and duodenal adenomas, colorectal cancer, gastric cancer, and an earl

115 noma had a 6-fold increased odds of advanced adenoma compared with subjects who had a sibling with a

116 (R990H) identified in aldosterone-producing adenomas conducts omega-currents in resting state, but n

117 ecorded Paneth cell status in the colorectal adenomas consecutively collected between February 2014 a

118 in hypercortisolemia with cortisol-producing adenoma (CPA), and to investigate a possible relationshi

119 oid expansion stimulated by HGF or EGF using adenomas derived from Lgr5(Creert2)/Met(fl/fl)/Apc(fl/fl

120 Participants in the trial had at least 1 adenoma, detected at their index colonoscopy, and were r

121 ists' colonoscopy performance is measured by adenoma detection rate (ADR).

122 oscopist a wide-field red-flag technique for adenoma detection.

123 cyclooxygenase (COX)-2 abrogates intestinal adenoma development at early stages of colorectal carcin

124 ted in gastric metaplasia, inflammation, and adenoma development, characterized by excessive STAT3 ac

125 nificance: These findings suggest that colon adenomas driven by APC mutations are distinct from those

126 ple who are diagnosed with intermediate-risk adenomas during screening.

127 r, including colorectal cancer (and advanced adenomas), endometrial cancers, and breast cancer.

128 occurrence of 1 or more adenomas or advanced adenomas (estimated diameter, >/=1 cm; or with villous h

129 ularly in OR1B1 (GPCR signaling pathway) for adenoma evolution, and LAMA1 (PI3K-Akt signaling pathway

130 rs, restores host tissue growth and contains adenoma expansion, indicating that cell competition is e

131 gh the dysregulated mucosal barrier in colon adenomas, facilitates the adenoma to adenocarcinomas tra

132 analysis was performed for sessile serrated adenomas for 2007-2012.

133 cating the importance of screening 2 or more adenomas for genetic variants.

134 ion results in lung hyperplasia, followed by adenoma formation and later adenocarcinoma development.

135 ts intestinal homeostasis, regeneration, and adenoma formation in mini-gut organoids and mice.

136 short-term O(6)-methylguanine and long-term adenoma formation in the lung tissues in A/J mice.

137 proliferative zone observed in crypts before adenoma formation, also found in irradiated crypts.

138 f ETBF clearance profoundly influences colon adenoma formation, defining a period during which the co

139 ration, particularly during regeneration and adenoma formation.

140 nal homeostasis and regeneration, as well as adenoma formation.

141 , cells explanted from miR-34a/b/c-deficient adenomas formed tumor organoids at an increased rate.

142 were considered cases, and those found to be adenoma-free were considered controls.

143 n healthy parathyroid tissue and parathyroid adenoma from 18 patients.

144 hemoglobin in discriminating CRC or advanced adenoma from control samples.

145 inations that differentiated CRC or advanced adenoma from control samples.

146 LS-DA model built to discriminate chief cell adenoma from oxyphil cell adenoma allowed us to correctl

147 Adenomas from 219 APA patients (95 men; 44.2%; aged 50.5

148 We identified mosaic variants in APC in adenomas from 9 of the 18 patients with 21 to approximat

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

150 ession, consistent with atypical parathyroid adenomas, from 9 months of age.

151 Deficiency in pleomorphic adenoma gene 1 (PLAG1) leads to reduced fertility in mal

152 upregulated upon detachment via pleomorphic adenoma gene 1 (PLAG1), provides anti-anoikis and pro-me

153 regulation of the proto-oncogene pleomorphic adenoma gene 1 (PLAG1), suggesting that HMGA2 promotes t

154 ent) and placebo (cervix carcinoma and colon adenoma) groups.

155 -mediated signalling from macrophages drives adenoma growth and progression in vivo in the Apc (Min/+

156 Importantly, fission is reactivated to drive adenoma growth.

157 her than absolute, Hippo activity determines adenoma growth.

158 A/P), traditional serrated adenomas, tubular adenomas >/=10 mm or with high-grade dysplasia, and conv

159 /=6 mm was 90.7% (95% CI, 86.7-94.5) and for adenomas >/=10 mm the negative predictive value was 98.6

160 The prevalence of adenomas >/=10 mm was higher among exposed than unexpose

161 The negative predictive value of CTC for adenomas >/=6 mm was 90.7% (95% CI, 86.7-94.5) and for a

162 y, proximal polyps, or a high-grade or large adenoma (>/=20 mm) at baseline (8865 [74%] patients) was

163 ings of individuals with at least 1 advanced adenoma had a 6-fold increased odds of advanced adenoma

164 , premalignant potential of sessile serrated adenomas has been described and screening utilization of

165 stasis and long-term risks of hepatocellular adenoma (HCA) and carcinoma (HCC).

166 events in hepatocellular carcinoma (HCC) and adenoma (HCA), particularly associated with a risk of ma

167 nction, and long-term risk of hepatocellular adenoma (HCA).

168 Hepatocellular adenomas (HCAs) also often express biliary/progenitor ma

169 Hepatocellular adenomas (HCAs) are benign liver tumors that can be assi

170 BACKGROUND & AIMS: Hepatocellular adenomas (HCAs) are benign liver tumors that can be assi

171 Hepatocellular adenomas (HCAs) are rare benign tumors divided into thre

172 d the prevalence of any adenomas or advanced adenomas [highest compared with lowest: red meat, PR: 1.

173 ified patients who has aldosterone producing adenoma (HR = 0.50, p = 0.005) also confirmed adrenalect

174 s effects of index SPs (n = 1016), high-risk adenomas (HRA, n = 817), low-risk adenomas (n = 1418), a

175 cells, normal mouse intestinal epithelia and adenomas, human cancer cell lines with or without drug t

176 lonoscopy examinations at 3 or 5 years after adenoma identification, as recommended by the endoscopis

177 in Apc-mutant and Ctnnb1-mutant mouse colon adenomas identified candidate genes for subsequent evalu

178 ctomy for iris melanoma in 15 cases and iris adenoma in 1 case underwent prosthetic iris device impla

179 lyps) were found in 98 cases (7 %), low risk adenoma in 158 cases (11.3 %), and hyperplastic polyps i

180 mily history of CRC or a documented advanced adenoma in a first-degree relative age <60 years or 2 fi

181 ntly reduce the risk of recurrent colorectal adenomas in a recent randomized clinical trial.

182 We also quantified adenomas in Ah(Cre)/Met(fl/fl)/Apc(fl/+) mice compared w

183 ed to participate in the formation of benign adenomas in autophagy-deficient livers, its role in HCC

184 TAT3 to the spontaneously developing gastric adenomas in gp130(F/F) mice, which carry a knockin mutat

185 s in all AhR-/- mice but mostly premalignant adenomas in less than half of AhR+/+ mice.

186 id metabolism genes and development of liver adenomas in males.

187 been shown to be associated with colorectal adenomas in many, but not all, studies, and the associat

188 A) showed significantly decreased binding to adenomas in the mouse tissue and in sections of human co

189 mor formation in the cecum but did not yield adenomas in the proximal colon.

190 ence, a >/=90% negative predictive value for adenomas in the rectosigmoid and a >/=90% agreement in s

191 y associated with the prevalence of advanced adenomas in the rectum only (multiple times per day comp

192 y associated with the prevalence of advanced adenomas in the rectum, but prospective cohort studies a

193 We determined the prevalence of advanced adenomas in the siblings of patients with advanced adeno

194 ve case-control study using 1,900 colorectal adenomas including 785 from females, and 1,115 from male

195 For tubular adenomas, increased expression was primarily noted in st

196 saic c.4666dupA APC variant in only 10 of 16 adenomas, indicating the importance of screening 2 or mo

197 For all other pituitary adenomas, initial therapy is generally transsphenoidal s

198 gous, was able to convert the benign tubular adenomas into more proliferative tumors.

199 sms among siblings of patients with advanced adenomas is not clear.

200 of segments with BBPS scores of 1 had missed adenomas larger than 5 mm (15.9%) than segments with BBP

201 quate bowel preparation for the detection of adenomas larger than 5 mm and should return for screenin

202 me was the proportion of colon segments with adenomas larger than 5 mm that were missed in the first

203 d show that forced upregulation of CBS in an adenoma-like colonic epithelial cell line is sufficient

204 mice initially formed hyperplastic and early adenoma-like lesions that later completely regressed, th

205 and progression of Apc (Min/+) mouse colonic adenomas, linked to increased epithelial cell beta-caten

206 idelines to survey individuals with low-risk adenomas (LRAs; 1-2 small tubular adenomas, < 1 cm) ever

207 h low-risk adenomas (LRAs; 1-2 small tubular adenomas, < 1 cm) every 5-10 years for colorectal cancer

208 Pituitary adenomas may hypersecrete hormones or cause mass effects

209 on for the prevention of advanced colorectal adenomas may vary according to vitamin D receptor genoty

210 ctomy, were diagnosed with intermediate-risk adenomas mostly (>99%) between Jan 1, 1990, and Dec 31,

211 high-risk adenomas (HRA, n = 817), low-risk adenomas (n = 1418), and no adenomas (n = 3198) on subse

212 = 817), low-risk adenomas (n = 1418), and no adenomas (n = 3198) on subsequent HRA or large SPs (>1 c

213 Villous adenomas (n = 545; 3.6 %), dysplasia (n = 49; 0.4 %), an

214 , cell viability and apoptosis) in pituitary adenomas (n = 74), and to compare with the responses of

215 ma with high grade dysplasia, n = 3; villous adenoma, n = 3), and 20 cases with newly diagnosed prima

216 lonic lesions diagnosed in 56 cases (tubular adenoma, n = 36; tubulovillous adenoma with low grade dy

217 ow grade dysplasia, n = 27; sessile serrated adenoma, n = 4; tubulovillous adenoma with high grade dy

218 Non-functioning pituitary adenomas (NFPAs) are the most frequent pituitary tumors.

219 ed in an approximate 50% reduction in (micro)adenoma numbers.

220 Paneth cell presence in the adenomas of distal colorectum may be a negative indicato

221 pe CaV 1.3 channels in aldosterone-producing adenomas of patients with primary hyperaldosteronism.

222 discordance, including incorrectly localized adenoma on the contralateral side of the neck, missed do

223 ons was uncommon when compared with advanced adenomas (one of 372 lesions vs 22 of 395 lesions, respe

224 Secondary outcomes included detection of any adenoma or advanced neoplasia (including CRC) and screen

225 ociation according to the type of colorectal adenoma or the location in the colorectum is unclear.We

226 elicited for their etiology, including being adenomas or adenocarcinomas [4, 5], virally transformed

227 es assessed were the occurrence of 1 or more adenomas or advanced adenomas (estimated diameter, >/=1

228 d meat consumption and the prevalence of any adenomas or advanced adenomas [highest compared with low

229 cessed meat intake and the prevalence of any adenomas or advanced adenomas.

230 deep sequence analysis of APC in at least 2 adenomas or carcinomas per patient.

231 at were ultimately resected were neoplastic (adenomas or serrated lesions), of which 43% (nine of 21)

232 RA compared to the reference group (no index adenomas or SPs).

233 ost common cause in adulthood is a pituitary adenoma, or treatment with pituitary surgery or radiothe

234 rticipants have 1 or more adenomas, advanced adenomas, or serrated polyps.

235 We investigated adenoma organoid expansion stimulated by HGF or EGF usin

236 MET-deficient adenoma organoids did not respond to HGF stimulation, bu

237 Similarly, HGF-mediated expansion of adenoma organoids required CD44v4-10.

238 Adenoma organoids stimulated with EGF or HGF expanded to

239 ate did not prevent recurrence of colorectal adenomas over a 3-year period.

240 Pituitary adenoma (PA) is one of the most common intracranial neop

241 ver, the potential role of LDHA in pituitary adenoma (PA) remains unknown.

242 imH mutation patterns of fecal isolates from adenoma patients (n= 59), colorectal cancer patients (n=

243 recursor lesions (including sessile serrated adenoma/polyps (SSA/P), traditional serrated adenomas, t

244 mprise hyperplastic polyps, sessile serrated adenomas/polyps (SSA/Ps), and traditional serrated adeno

245 n expression, especially in sessile serrated adenomas/polyps and Lynch syndrome.

246 , tended to be stronger for sessile serrated adenomas/polyps than hyperplastic polyps.

247 lorectal tissue samples--48 sessile serrated adenomas/polyps, 70 sporadic high-grade dysplastic adeno

248 The same mice were evaluated for adenoma prevalence and size.

249 Observations: Prevalence of pituitary adenomas ranges from 1 in 865 adults to 1 in 2688 adults

250 The primary outcome was adenoma recurrence assessed by colonoscopy after 3 years

251 D3 or calcium supplementation on colorectal adenoma recurrence.

252 Removal of adenomas reduces colorectal cancer incidence and mortali

253 se model, which forms spontaneous intestinal adenomas, reductions in Gpr182 led to more adenomas and

254 oral contraceptive pill (OCP) and associated adenoma regression.

255 ely 65% of the cases of hypercortisolism) is adenoma resection and medical therapies including ketoco

256 (n = 15), 47% (n = 14), and 90% (n = 27) of adenomas respectively.

257 f 80% and 45% for detecting CRC and advanced adenomas, respectively, at 95% specificity, which was hi

258 lementation on advanced adenomas, but not on adenoma risk overall, significantly varied according to

259 cluded 1107 patients with 1 or more sporadic adenoma(s) removed from the colon or rectum at centers i

260 Patients with pituitary adenomas should be identified at an early stage so that

261 miR-34a/b/c-deficient adenomas showed elevated proliferation and decreased apo

262 the total number of colorectal adenomas, and adenoma size and features.

263 ma numbers and significantly reduced average adenoma size.

264 Sessile serrated adenomas (SSAs) and traditional serrated adenomas (TSAs)

265 nsion of organoids generated from crypts and adenomas, stimulated by HGF or EGF, that were derived fr

266 Moreover, the parathyroid adenoma subtypes (chief cells and oxyphil cells) were ch

267 of inflammation related to multiple hepatic adenomas that completely resolved after cessation of the

268 ere the proportion of patients with advanced adenomas, the total number of colorectal adenomas, and a

269 P model recapitulates tumor progression from adenoma through metastases.

270 n of ODC in normal intestinal epithelial and adenoma tissue, and therefore PA reduction might be a po

271 N2B and RASSF1A) was analysed in parathyroid adenoma tissues (n = 30).

272 l barrier in colon adenomas, facilitates the adenoma to adenocarcinomas transition.

273 ked appearance of Paneth cells in colorectal adenomas to adenoma burden and male gender.

274 o predict the ultimate response of pituitary adenomas to BIM-23A760.

275 ted adenomas (SSAs) and traditional serrated adenomas (TSAs) constituted 36.8% (137 of 372) and 4.3%

276 adenoma/polyps (SSA/P), traditional serrated adenomas, tubular adenomas >/=10 mm or with high-grade d

277 RC) surveillance tests for intermediate-risk adenomas, using a hypothetical scenario.

278 High risk adenomas (villous or tubulovillous or high grade dysplas

279 The prevalence of advanced adenoma was 11.5% among the exposed subjects and 2.5% am

280 revalence of colorectal cancer and high-risk adenoma was found in the Thai population aged 50-65 year

281 s was a pheochromocytoma, a cortical adrenal adenoma was histologically proven.

282 The pleomorphic adenoma was the most common benign tumour and was also t

283 SUVmax of the nine preoperatively identified adenomas was 4.9 (interquartile range, 2.45-7.35), which

284 In a mouse lung model of KRas(G12D)-driven adenomas, we find that co-activation of Myc drives the i

285 Persons found to have colorectal adenoma were considered cases, and those found to be ade

286 Persons with adenoma were more likely to have unfavorable cholesterol

287 pression of CYP11B2 and gonadal receptors in adenomas were also explored.

288 Apc-mutant adenomas were characterized by increased expression of t

289 ified, of whom 11 944 with intermediate-risk adenomas were included in this analysis.

290 Single and multiple adenomas were more common in men than women (57.7 % vs 4

291 of Apc, Kras, p53, and Smad4 Importantly, no adenomas were observed in the small intestine.

292 ed precancerous colon polyps and soft tissue adenomas, whereas short-stature humans harboring an inac

293 ease (hypercortisolism due to ACTH-producing adenomas, which is the cause in approximately 65% of the

294 ated Apc (R850X/+) (Min), develop intestinal adenomas, while the bulk of the disease is in the small

295 ssile serrated adenoma, n = 4; tubulovillous adenoma with high grade dysplasia, n = 3; villous adenom

296 ases (tubular adenoma, n = 36; tubulovillous adenoma with low grade dysplasia, n = 27; sessile serrat

297 n FCH PET/MR imaging allowed localization of adenomas with high accuracy when conventional imaging re

298 ysis, only 7 participants (26.9%) identified adenomas with sufficient sensitivity such that further a

299 with high-grade dysplasia, and conventional adenomas with villous histology) were seen in 4.3% of pa

300 ted canonical Wnt signaling in both types of adenomas, with Apc-mutant adenomas also exhibiting uniqu