ライフサイエンスコーパス: adenoma

1 pared to non-CRC samples (Normal or advanced adenoma).

2 es disease, toxic multinodular goiter, toxic adenoma).

3 ced neoplasms (colorectal cancer or advanced adenoma).

4 h pattern, grade of dysplasia, and number of adenomas).

5 antly associated with recurrence of advanced adenoma.

6 t SSPs are relatively uncommon compared with adenoma.

7 s no-adenoma, low-risk adenoma, or high-risk adenoma.

8 H. pylori and the progression of colorectal adenoma.

9 in 15 patients with a dysplastic colorectal adenoma.

10 ocedure and imaging protocol for parathyroid adenoma.

11 h factor I (IGF1), most often by a pituitary adenoma.

12 th the independent development of colorectal adenoma.

13 predictive value (PPV) for CRC and advanced adenoma.

14 tial circulating mRNA markers for colorectal adenoma.

15 with benign cytology, to identify follicular adenoma.

16 C and 216 participants (10.1%) with advanced adenoma.

17 nterval development of preneoplastic colonic adenoma.

18 e in the preoperative imaging of parathyroid adenoma.

19 nsplantation for hepatocellular carcinoma or adenoma.

20 nuclear localization in both mouse and human adenomas.

21 . performed a whole-exome study of pituitary adenomas.

22 n) mice with increased numbers of high-grade adenomas.

23 rveillance guidelines for high- and low-risk adenomas.

24 um, or both for the prevention of colorectal adenomas.

25 s upregulated in AIP-mutation-positive human adenomas.

26 Ts) for colorectal cancer (CRC) and advanced adenomas.

27 ers is correlated with the number of colonic adenomas.

28 PV of FIT for detection of CRCs and advanced adenomas.

29 can differentiate metastases from lipid-poor adenomas.

30 be developed for the treatment of intestinal adenomas.

31 adenomas removed at screening; 82.2% had no adenomas.

32 hormone-secreting (GH-secreting) somatotroph adenomas.

33 g risk of colorectal cancer in patients with adenomas.

34 0-5.5 and HR for distal SPs with synchronous adenomas 2.4; 95% CI, 1.7-3.4).

35 person-years) vs 309 in individuals without adenomas (22.2 per 100,000 person-years).

36 astases had higher T2-weighted SI ratio than adenomas (3.6 +/- 1.7 [95% confidence interval {CI}: 0.2

37 leted a follow-up colonoscopy: 57.8% had any adenoma, 33.6% had an advanced adenoma (adenoma with adv

38 or CRC (HR for proximal SPs with synchronous adenomas 4.0; 95% CI, 3.0-5.5 and HR for distal SPs with

39 Adenomas 5 mm or smaller were detected in a significantl

40 9), carcinoids 0.59 (95% CI, 0.16-2.10), and adenomas 5.73 (95% CI, 3.70-8.88).

41 rigeminal neuralgia (565 [11.5%]), pituitary adenomas (641 [13.1%]), haemangioblastoma (29 [0.6%]), a

42 ses Drosophila intestinal stem cells to form adenomas [9].

43 Compared with adenomas, a higher proportion of SSPs were solitary (69.

44 atients with adenomas would develop advanced adenomas, a surrogate for CRC.

45 %), followed by those with baseline advanced adenoma (AA) (21.9%; 95% CI 15.7-28.1).

46 comprising colorectal cancer (CRC), advanced adenoma (AA), or inflammatory bowel disease (IBD), is un

47 ow sensitivity for the detection of advanced adenomas (AAs).

48 body epithelial and neuroepithelial tumors (adenoma, adenocarcinoma, and medulloepithelioma) showed

49 isease severity is notable for enrichment of adenoma/adenocarcinoma and innate immune genes.

50 RPE adenoma/adenocarcinoma can simulate choroidal melanoma.

51 57.8% had any adenoma, 33.6% had an advanced adenoma (adenoma with advanced histology or polyp >=10 m

52 Compared with individuals without adenomas, adenomas >=20 mm in diameter and high-grade dy

53 However, detecting adenomas against the backdrop of an inflamed mucosa (e.g

54 Rates of metachronous adenoma and advanced adenoma at follow-up were 58% and 2

55 lytic cohort simulation model for colorectal adenoma and cancer with a lifelong time horizon was deve

56 not allow differentiation between follicular adenoma and carcinoma on Bethesda type IV lesions.

57 lori infection is associated with colorectal adenoma and confers a 1.3- to 2.26-fold increased risk.

58 ssociated variants in MMR genes and risks of adenoma and CRC and somatic mutations in APC and CTNNB1

59 ositive nuclear staining in normal, advanced adenoma and CRC was 0, 24 and 41%, respectively (P < 0.0

60 In our study, advanced adenoma and CRC were associated with activation of beta-

61 athogenic variants in MMR genes with risk of adenoma and CRC, and somatic mutations in APC and CTNNB1

62 murine lung tissue confirmed a diagnosis of adenoma and early adenocarcinoma, a pathologic subtype o

63 mens from 2010 to 2012 (46 CRCs, 74 advanced adenomas and 32 normal colon tissues).

64 th morphologic and genetic features of human adenomas and carcinomas.

65 Ccne1(T) mice developed more hepatocellular adenomas and HCCs than control mice.

66 edications may reduce development of colonic adenomas and may contribute to CRC prevention.

67 colonoscopy, included both patients free of adenomas and patients bearing adenomas whose risk status

68 Traditional serrated adenomas and SSLs are precursors to colorectal cancer.

69 mutation is a hallmark of hormone-secreting adenomas and that SCNAs correlate with adenoma phenotype

70 h the development of precancerous colorectal adenomas and their progression to tumors, as well as the

71 Is among cases (556 hyperplastic polyp, 1753 adenoma, and 208 SSL) and controls (3804) in the large c

72 fspring mice were largely free of intestinal adenoma, and several chromosome substitution (consomic)

73 fter removal of high-risk adenomas, low-risk adenomas, and after negative colonoscopy for all colonos

74 ratios (HRs) for small bowel adenocarcinoma, adenomas, and carcinoids.

75 wannomas, WHO grade 1 meningiomas, pituitary adenomas, and haemangioblastoma.

76 well as detected number of cancers, advanced adenomas, and positive test results at positivity thresh

77 r sigmoidoscopy if any polyp of >=10 mm, >=3 adenomas, any advanced adenomas, or CRC was found or, su

78 cell proliferation and aldosterone producing adenoma (APA) development.

79 lelic Igf2r expression suppressed intestinal adenoma (Apc(Min)).

80 Growth, survival and intestinal adenoma appear dependent on IGF2R-domain-11 IGF2 binding

81 signals in the serum of patients carrying an adenoma as small as 6-9 mm in maximum linear dimension.

82 The risk of recurrent colonic adenoma associated with high-grade dysplasia (HGD) colon

83 Rates of metachronous adenoma and advanced adenoma at follow-up were 58% and 20%, respectively.

84 Recurrence of colonic adenoma at time of follow-up colonoscopy is common in pa

85 (mean age, 60 years +/- 15) with lipid-poor adenomas at 1.5- and 3-T MRI between June 2016 and March

86 t 14 and 20 weeks of age and increased liver adenomas at 45 weeks of age in male offspring.

87 ntly increased in veterans with 1 or 2 small adenomas at baseline (odds ratio 0.96; 95% CI 0.67-1.41)

88 Individuals with only 1 or 2 small adenomas at baseline have a low risk of advanced neoplas

89 that analyzed detection of CRC and advanced adenomas at different FIT positivity thresholds, we foun

90 new lesions occurred only in hepatocellular adenomas at risk of progression.

91 Endoscopically invisible micro-adenomas at the margins of the EMR site might contribute

92 ear factor 1alpha-inactivated hepatocellular adenomas being the most common subtype showing progressi

93 ver, risks of small bowel adenocarcinoma and adenomas (but not carcinoids) are significantly increase

94 ndations consider characteristics of removed adenomas, but not colonoscopist performance.

95 tion rates (DR) for right-sided conventional adenomas (cAD) and serrated polyps (SP) compared to ceca

96 in APC, KRAS, SMAD4, and TP53, known as the adenoma-carcinoma sequence (ACS).

97 The colorectal adenoma-carcinoma sequence has provided a paradigmatic f

98 r (CRC) originating through the conventional adenoma-carcinoma sequence have provided insight into th

99 ign nonfunctioning adrenal tumors (NFATs) or adenomas causing mild autonomous cortisol excess (MACE),

100 d reduces proliferation and Wnt signaling in adenoma cells, resulting in development of fewer and sma

101 tween colorectal cancer risk and patient and adenoma characteristics (diameter, growth pattern, grade

102 39-1.41), whereas for individuals with other adenoma characteristics the risk was lower (SIR 0.35; 95

103 For individuals with high-risk adenomas, colorectal cancer incidence was 1.14% (95% CI

104 3), which is consistent with the traditional adenoma-colorectal cancer pathway.

105 higher in those with hyperplastic polyps and adenomas compared to those with no polyps.

106 ) [P = 0.010; OR 3.09(1.32-7.25 95% CI)] and adenoma count >= 3 [P = 0.002; OR 3.08(1.52-6.24 95% CI)

107 ogistic regression analysis revealed that an adenoma count of >= 3 at baseline colonoscopy was strong

108 RC and surveillance benefits were higher for adenomas detected at FIT screening and lower for older p

109 Adenomas detected per colonoscopy were significantly hig

110 colonoscopy significantly increases ADR and adenomas detected per colonoscopy without increasing wit

111 Secondary outcomes were adenomas detected per colonoscopy, non-neoplastic resect

112 flexure were associated with lower chance of adenoma detection (eg, 0.77, 0.66-0.91; p=0.0015 for pro

113 d to quantify the change in CRC and advanced adenoma detection and number of positive test results at

114 opists with low vs high performance quality (adenoma detection rate <20% vs >=20%) in the Polish scre

115 opic withdrawal time > 12 min, and quarterly Adenoma Detection Rate (ADR) ranging from 50 to 70% for

116 CIR) is associated with significant improved adenoma detection rate (ADR), however, self-reported CIR

117 predictors of failure, and its impact on the adenoma detection rate (ADR).

118 ing centres to examine factors affecting the adenoma detection rate (ADR).

119 The primary outcome was adenoma detection rate (ADR, the percentage of patients

120 ion of patients with 1 adenoma or carcinoma (adenoma detection rate [ADR]).

121 of infused water during insertion increased adenoma detection rate but the impact on AMR had not bee

122 eparation, performed by endoscopists with an adenoma detection rate of 20% or greater.

123 Advanced adenoma detection rate was lower in the first FIT round

124 We conducted a retrospective analysis of adenoma detection rates (ADR) in initial screening colon

125 Adenoma detection rates (defined as the proportion of pa

126 rvals (CIs) and no significant difference in adenoma detection rates by pancolonic chromoendoscopy (3

127 ltivariate analysis, factors associated with adenoma detection were male sex (relative risk 1.69, 95%

128 further investigate the role of diabetes in adenoma detection.

129 have a pathophysiological role in colorectal adenoma development and, after successful eradication of

130 y that supports intestinal tissue repair and adenoma development.

131 jor surgery, endoscopic excision of advanced adenomas, diagnosis of high-grade dysplasia in the rectu

132 Most families with a history of CRC and/or adenomas do not carry genetic variants associated with c

133 ge 3 (NHE3) and Cl-HCO(3) [down-regulated in adenoma (DRA) or putative anion transporter 1 (PAT1)] ex

134 The down-regulated in adenoma (DRA) protein, encoded by SLC26A3, a key intesti

135 sed risk of advanced and multiple colorectal adenomas during a surveillance colonoscopy interval star

136 tients who undergo polypectomy for HGD colon adenomas during baseline colonoscopy.

137 RC and related death by baseline colonoscopy adenoma findings.

138 ARdelta has been shown to promote intestinal adenoma formation and growth, the molecular mechanisms u

139 In these mice, we observe adenoma formation over a time frame of three to six mont

140 sitive cell type in the lung is sensitive to adenoma formation when expressing a mutant Kras(G12D) al

141 0021861) were the main processes involved in adenoma formation.

142 s; however, no differences were noted in the adenoma frequency.

143 t. The TGFBR inhibitor restored apoptosis in adenomas from Apc(Min/+) mice expressing RSPO1-Fc back t

144 ng RSPO1-Fc back to the same level as in the adenomas from mice given the control vector.

145 o to shift gene expression within Apc-mutant adenomas from stem cell-like to differentiation along No

146 ular signatures of normal, benign follicular adenoma (FTA), and malignant follicular carcinoma (FTC)

147 Pleomorphic adenoma gene 1 (PLAG1) is a transcription factor involve

148 tin receptor ligand that targets somatotroph adenoma GH secretion in patients with acromegaly, inhibi

149 .94; 95% CI 1.90-6.56), whereas the low-risk adenoma group (10,978 patients) did not have a significa

150 Compared with the no-adenoma group (45,881 patients), the high-risk adenoma g

151 enoma group (45,881 patients), the high-risk adenoma group (7563 patients) had a higher risk of CRC (

152 isk adenoma groups were compared with the no-adenoma group using Cox regression adjusting for confoun

153 related deaths among the high- and low-risk adenoma groups were compared with the no-adenoma group u

154 Drivers of sporadic benign pituitary adenoma growth are largely unknown.

155 ntestinal cancer, we show that Tgifs promote adenoma growth in the context of mutant Apc (adenomatous

156 year risk for advanced neoplasia (defined as adenomas >=10mm, adenomas with villous histology or high

157 gher or comparable only for individuals with adenomas >=20 mm in diameter (standardized incidence rat

158 Compared with individuals without adenomas, adenomas >=20 mm in diameter and high-grade dysplasia we

159 follow-up showed that 78% of hepatocellular adenomas had long-term stability or regression.

160 Surveillance of patients with colorectal adenomas has limited long-term evidence to support curre

161 , particularly SSLs and traditional serrated adenomas, have an increased risk of synchronous and meta

162 Background Hepatocellular adenomas (HCAs) are rare benign liver tumors.

163 (LRAs) (1 to 2 small adenomas) or high-risk adenomas (HRAs) (3 to 10 small adenomas or >=1 large ade

164 Risk of advanced adenoma in 10 years was 17.8% in patients with pathogeni

165 d non-users (P = .006), The PPV for advanced adenoma in aspirin users was 27.2% vs 32.6% for matched

166 The PPV for advanced adenoma in DOAC users was 20.5% vs 32.4% in matched non-

167 ficant difference in PPV for CRC or advanced adenoma in warfarin users compared to non-users.

168 s were found in 234 individuals and advanced adenomas in 1305 individuals.

169 pancolonic chromoendoscopy for detection of adenomas in patients with Lynch syndrome.

170 ce was shown to result in the development of adenomas in small intestine and colon.

171 F accumulation, AEC and BEC hyperplasia, and adenomas in the lung, leading to early lethality correla

172 eting of Fzd inhibited the growth of gastric adenomas in vivo.

173 Potential new targets in corticotroph adenomas include the epidermal growth factor receptor, c

174 alues, sensitivity for detection of advanced adenomas increased from 21% (95% CI, 18%-25%) to 31% (95

175 The presence of synchronous adenomas increased the risk for CRC (HR for proximal SPs

176 For low-risk adenoma individuals, colorectal cancer incidence was 0.5

177 Addition of RSPO1 to organoids derived from adenomas inhibits their growth and promotes proliferatio

178 ome 5, suggesting that PWD variants restrict adenoma initiation by controlling stem cell homeostasis.

179 Risk of further developing advanced adenomas is associated with gender and the number of col

180 is important as the detection rate of these adenomas is expected to further increase with the introd

181 Sensitivity of 1-time testing for advanced adenomas is low, regardless of the threshold.

182 arbonate exchanger SLC26A3 (downregulated in adenoma) is expressed mainly in colonic epithelium, wher

183 One cohort included patients bearing adenomas known to be growing on the basis of longitudina

184 hrough 2010; findings were categorized as no-adenoma, low-risk adenoma, or high-risk adenoma.

185 ectal cancer risk after removal of high-risk adenomas, low-risk adenomas, and after negative colonosc

186 ients aged 50, 60, or 70 years with low-risk adenomas (LRAs) (1 to 2 small adenomas) or high-risk ade

187 The proportion of patients with adenomas <=5 mm was higher in the MB-MMX group (180 of 4

188 (95% CI 2.7%-5.4%) for baseline 1 to 2 small adenomas (<1cm, and without villous histology or high-gr

189 ess of prospective microbiome monitoring for adenomas may be limited but supports the potential causa

190 Ten patients developed adenomas (median age, 18 years), and another 8 developed

191 Reports showed adenoma miss rates (AMRs) of 22.5-27% in the right colon

192 suppressor function, we utilised intestinal adenoma models known to be Igf2 dependent.

193 c polyps (n = 34; 32%), traditional serrated adenomas (n = 3; 3%), sessile serrated adenomas/polyps (

194 After resection of solitary hepatocellular adenomas, new lesions occurred only in hepatocellular ad

195 the B6 genetic background displayed reduced adenoma numbers.

196 12 human colorectal tumors (11 carcinomas, 1 adenoma) obtained through saturation microdissection of

197 was associated with similar odds of tubular adenoma (Odds ratio (OR) 1.07, 95% CI 0.69-1.66) or vill

198 We described a rare case of pleomorphic adenoma of the lacrimal gland (PALG) causing hyperopic s

199 y and histopathology confirmed a pleomorphic adenoma of the orbit.

200 26.5%; RR, 1.26; 95% CI, 1.01-1.52), as were adenomas of 6 to 9 mm (detected in 10.6% of subjects in

201 Adenomas of Apc(Min/+) mice injected with the RSPO1-Fc v

202 proliferation, and less crypt branching than adenomas of mice given the control vector.

203 ded 615 adults with no history of colorectal adenoma or cancer at baseline who participated in a repe

204 dpoint was the proportion of patients with 1 adenoma or carcinoma (adenoma detection rate [ADR]).

205 tients with at least 1 histologically proven adenoma or carcinoma).

206 stopathological results of either follicular adenoma or carcinoma.

207 teatohepatitis and a risk for hepatocellular adenoma or carcinoma.

208 with pathologic confirmation of parathyroid adenoma or hyperplasia.

209 r small (6-9 mm) nonadvanced adenomas, or an adenoma or sessile serrated lesion >=10 mm.

210 or high-risk adenomas (HRAs) (3 to 10 small adenomas or >=1 large adenoma) removed after screening w

211 rrent high-risk classification cutoff of >=3 adenomas or any adenoma with villous growth pattern, hig

212 risk factors, including a history of colonic adenomas or caffeine usage.

213 median time of 7.8 years for development of adenomas or CRC.

214 ven when most of the specimens correspond to adenomas or even other benign lesions.

215 histopathology did not uncover any pituitary adenomas or somatotroph hyperplasia in either group.

216 atio (OR) 1.07, 95% CI 0.69-1.66) or villous adenoma (OR 1.26, 95% CI 0.17-9.42).

217 ancer (OR 0.83, 95% CI 0.20-3.39) or tubular adenoma (OR 1.49 95% CI 0.83-2.67).

218 with low-risk adenomas (LRAs) (1 to 2 small adenomas) or high-risk adenomas (HRAs) (3 to 10 small ad

219 ngs were categorized as no-adenoma, low-risk adenoma, or high-risk adenoma.

220 ore diminutive or small (6-9 mm) nonadvanced adenomas, or an adenoma or sessile serrated lesion >=10

221 polyp of >=10 mm, >=3 adenomas, any advanced adenomas, or CRC was found or, subsequent to, FIT >15 mu

222 Addition of RSPO1 reduced the number of adenoma organoids derived from Apc(Min/+) mice and suppr

223 orld regions, alternative polyp definitions, adenoma), outcomes (prevalence, clinical features), and

224 index did not differ between metastases and adenomas (P = .748).

225 Papillary adenoma (PA) is a small benign lesion morphologically si

226 Pituitary adenomas (PAs) are benign growths arising from epithelia

227 These results elucidating somatotroph adenoma pathophysiology identify pathways for targeted t

228 a targeted mRNA sequencing for 40 colorectal adenoma patients and 39 colonoscopy-proven normal contro

229 83 and 5569 faecal-based miRNA tests in CRC, adenoma patients and healthy individuals, respectively.

230 n the detection of plasma mRNA in colorectal adenoma patients and normal healthy subjects.

231 d RHOA (0.35-fold with adjusted P < 0.01) in adenoma patients was significantly lower than those in n

232 eting adenomas and that SCNAs correlate with adenoma phenotype.

233 Constitutive Wnt activation upon loss of Adenoma polyposis coli (APC) acts as main driver of colo

234 rated adenomas (n = 3; 3%), sessile serrated adenomas/polyps (SSA/Ps) (n = 70; 66%), unspecified SPs

235 uded conventional adenomas, sessile serrated adenomas/polyps (SSA/Ps), or colorectal cancer, and RRs

236 sociated with gender and the number of colon adenomas present.

237 Adenoma prevalence was 4.3% (3/70) in IBD patients and 3

238 follow-up, the incidence rates of colorectal adenoma progression in participants with persistent H. p

239 p)) resulted in worse survival and increased adenoma proliferation.

240 r any adenoma (range, 56.7%-70.7%), advanced adenoma (range, 20.0%-33.6%), and CRC (range, 0%-7.1%) w

241 The test yields for any adenoma (range, 56.7%-70.7%), advanced adenoma (range, 2

242 ful eradication of H. pylori, the colorectal adenoma ratio might decrease.

243 The colorectal adenoma ratio of patients uninfected with H. pylori was

244 recurrence, proximal recurrence, and distal adenoma recurrence with odds ratios of 4.32 (2.06-9.04 9

245 ALY gained in most alternative scenarios for adenoma recurrence, CRC incidence, longevity, quality of

246 margins of the EMR site might contribute to adenoma recurrence, which occurs in 15% to 30% of patien

247 cancer (CRC) and CRC-related death following adenoma removal are uncertain.

248 Colonoscopy surveillance after adenoma removal is an increasing burden in many countrie

249 tal cancer incidence and mortality following adenoma removal.

250 performance on colorectal cancer risk after adenoma removal.

251 on risk of colorectal cancer and death after adenoma removal.

252 30 colorectal cancers in individuals who had adenomas removed at screening (46.5 per 100,000 person-y

253 ividuals had low-risk and 6.6% had high-risk adenomas removed at screening; 82.2% had no adenomas.

254 (HRAs) (3 to 10 small adenomas or >=1 large adenoma) removed after screening with colonoscopy or fec

255 reen colonoscopy to assess recurrent colonic adenoma risk factors.

256 g risk of colorectal cancer in patients with adenomas (risk difference per 100,000 person-years, 5.6;

257 For advanced adenomas, sensitivity was 0.40 (CI, 0.33 to 0.47) and th

258 Study endpoints included conventional adenomas, sessile serrated adenomas/polyps (SSA/Ps), or

259 cing of 159 prospectively resected pituitary adenomas showed that somatic copy number alteration (SCN

260 eveloped a high-risk classification based on adenoma size >=20 mm or high-grade dysplasia (instead of

261 process of progression from sessile serrated adenoma (SSA) to dysplasia and carcinoma has not been el

262 ultinodular goiter (TMNG), and toxic thyroid adenoma (TA).

263 etes medications were more likely to have an adenoma than those taking medication (OR = 2.38, 95% CI:

264 mice to determine Hnf1b+ cells give rise to adenomas that express SPC and TTF1.

265 se model (CPC;Apc) that develops spontaneous adenomas that overexpress cMet was used to demonstrate f

266 human colon tumors, with adjacent normal and adenoma tissues, were analyzed by immunohistochemistry f

267 In addition to the adenoma to carcinoma sequence, colorectal carcinogenesis

268 g (Lgr5(+)) cancer stem cells and promote an adenoma-to-adenocarcinoma progression.

269 ntake, and low-grade dysplasia while colonic adenomas trended towards significance.

270 ater binding to tubular and sessile serrated adenomas versus hyperplastic polyps and normal mucosa.

271 not significantly correlated with the total adenoma volume.

272 als, and 48 patients received a diagnosis of adenomas vs 50 reference individuals.

273 However, failure to recognize adenomas (vs hyperplastic polyps), or discarding a polyp

274 In conclusion, more adenoma was found in nodules >=4-cm, including those wit

275 Adenoma was higher (30% vs 14%) and malignancy lower in

276 (number of procedures in which at least one adenoma was removed or biopsied, divided by total number

277 e, aneuploidy, and senescence in somatotroph adenomas, we studied links between cAMP signaling and DN

278 Age greater than 65 and diagnosis of cancer/adenoma were associated with less opioid use.

279 Organoids and adenomas were analyzed by quantitative reverse-transcrip

280 With up to 14 years of follow-up, high-risk adenomas were associated with an increased risk of CRC a

281 Three more ampullary adenomas were detected using CAE compared to FVE.

282 ipation was higher and more CRC and advanced adenomas were detected with repeated FIT compared to sig

283 was found in 2 patients (0.2%), and advanced adenomas were found in 44 patients (5.4%).

284 Patients with multiple hepatocellular adenomas were more likely to show progressive disease, w

285 Low-risk adenomas were not associated with a significantly increa

286 ticipants recently diagnosed with colorectal adenomas were randomly assigned to 1 mg/d of folic acid

287 markers for normal stem/progenitor cells and adenomas were validated by immunohistochemistry and flow

288 s the proportion of patients with at least 1 adenoma) were compared between groups, with a noninferio

289 of age, recently diagnosed with a colorectal adenoma, were randomly assigned to 1000 IU/d of vitamin

290 t 2) were higher in metastases compared with adenomas when assessed by both radiologists.

291 epleted in stool corresponding with baseline adenomas, while Desulfovibrio was enriched both in stool

292 CRP levels were enhanced only with high-risk adenomas, while PI16 levels, not associated with growth,

293 tients free of adenomas and patients bearing adenomas whose risk status was judged by histopathology.

294 any adenoma, 33.6% had an advanced adenoma (adenoma with advanced histology or polyp >=10 mm), and 2

295 classification cutoff of >=3 adenomas or any adenoma with villous growth pattern, high-grade dysplasi

296 e and somatostatin receptors on corticotroph adenomas with cabergoline or pasireotide, or both, contr

297 nd to have incidental hyperplastic polyps or adenomas with low-grade dysplasia.

298 sufficient to inhibit the growth of gastric adenomas with or without mutations to Apc.

299 anced neoplasia (defined as adenomas >=10mm, adenomas with villous histology or high-grade dysplasia,

300 largely on the likelihood that patients with adenomas would develop advanced adenomas, a surrogate fo