ライフサイエンスコーパス: high-grade dysplasia

1 nite for dysplasia", low grade dysplasia, or high grade dysplasia).

2 (2 developed adenocarcinoma and 1 developed high-grade dysplasia).

3 patients with intramucosal adenocarcinoma or high grade dysplasia.

4 nts revealed low-grade, 105 moderate, and 52 high-grade dysplasia.

5 y of progression to cancer for patients with high-grade dysplasia.

6 s without dysplasia and 6% for patients with high-grade dysplasia.

7 ewis(x), were associated with risk of EAC or high-grade dysplasia.

8 cinomas of the gastric cardia, or esophageal high-grade dysplasia.

9 tients with BE most likely to develop EAC or high-grade dysplasia.

10 tection at the stage of mucosal carcinoma or high-grade dysplasia.

11 of superficial esophageal adenocarcinoma or high-grade dysplasia.

12 xyntic atrophy, metaplasia, hyperplasia, and high-grade dysplasia.

13 e RFA the intervention of choice in cases of high-grade dysplasia.

14 patients with intramucosal adenocarcinoma or high-grade dysplasia.

15 d 6.87 (95% CI: 2.61-18.07) for adenoma with high-grade dysplasia.

16 's and fundal biopsies from the patient with high-grade dysplasia.

17 dr1a-/- mice showed IBD with foci of low- to high-grade dysplasia.

18 es and risk factors for CRC and adenoma with high-grade dysplasia.

19 agnosed with invasive cancer or adenoma with high-grade dysplasia.

20 agnosed with invasive cancer or adenoma with high-grade dysplasia.

21 promise for those with superficial cancer or high-grade dysplasia.

22 iate strategy in a subgroup of patients with high-grade dysplasia.

23 nomas that were >1 cm in size or that showed high-grade dysplasia.

24 into the upper epithelial layers in cases of high-grade dysplasia.

25 d esophagus and is curative in patients with high-grade dysplasia.

26 e to the development of colorectal carcinoma/high-grade dysplasia.

27 endoscopic photodynamic therapy to eradicate high-grade dysplasia.

28 5) for LGD, and 0.43 (95% CI, 0.36-0.46) for high-grade dysplasia.

29 ith risk factors such has family history and high-grade dysplasia.

30 patients), 51 were non-dysplastic and 14 had high-grade dysplasia.

31 non-dysplastic cases and five patients with high-grade dysplasia.

32 intraductal papillary mucinous neoplasm had high-grade dysplasia.

33 mas and adenomas with a villous component or high-grade dysplasia.

34 either benign or high-grade atypia (HGA) [>/=high-grade dysplasia].

35 ee of dysplasia (RR for cancer, 0.45; RR for high-grade dysplasia, 0.52; RR for low-grade dysplasia,

36 17.7%), as well as low- (10.8% vs. 3.8%) and high-grade dysplasia (1.5% vs. 0%) were predominant in T

37 e compared with those in 12 patients (1 with high-grade dysplasia, 11 with adenocarcinoma) who had vi

38 adenomas, 15 patients with advanced adenomas/high-grade dysplasia, 12 patients with genetic mutation

39 Patients developed high-grade dysplasia 16, 28, and 37 months after PDT.

40 creases the risk of progression to cancer or high-grade dysplasia 2-fold among patients with BE, comp

41 colitic mucosa and low-grade dysplasia (57), high-grade dysplasia (2), or carcinoma (1) in polyps fro

42 Thirty-three patients with high-grade dysplasia (23 patients) or adenocarcinoma (10

43 Twenty-seven patients (30%) had high-grade dysplasia, 26 had low-grade dysplasia (29%),

44 , 2.1-4.9 vs. tubular), and in adenomas with high-grade dysplasia (32.0% vs. 13.6%; OR, 3.0; 95% CI,

45 rade dysplasia, whereas 125 (72%) had either high-grade dysplasia (33%) or invasive carcinoma (39%).

46 Barrett's esophagus (22%), to low- (45%) and high-grade dysplasia (43%) and adenocarcinoma (37%).

47 00 person-years among patients with baseline high-grade dysplasia (95% CI 4.2-12.5).

48 00 person-years among patients with baseline high-grade dysplasia (95% CI 8.8-20.7).

49 ients with high-risk adenomas (adenomas with high-grade dysplasia, a villous component, or a size >/=

50 sed and full-thickness, in the 23 cases with high-grade dysplasia adjacent to BAA and in carcinoma in

51 51 of 52 (98%); among subjects with initial high-grade dysplasia, all dysplasia was eradicated in 50

52 ression in plasma EV of the 11 patients with high-grade dysplasia alone, only 1 had high MUC5AC expre

53 ccurate tests to diagnose adenocarcinoma and high-grade dysplasia among mucinous pancreatic cysts are

54 etent) mice of the NU/J strain progressed to high grade dysplasia and to carcinoma in situ.

55 were 1.09 (95% CI, 0.85-1.33) for low-grade/high-grade dysplasia and 0.14 (95% CI, 0.06-0.22) for GC

56 and pathogenesis have shown that the risk of high-grade dysplasia and adenocarcinoma may be related t

57 taplasia disappeared in 14% of patients, and high-grade dysplasia and adenocarcinoma were prevented i

58 n receptor modulator, promoted regression of high-grade dysplasia and cancer that arose in the cervix

59 e (IBD) are at increased risk for developing high-grade dysplasia and colorectal cancer.

60 organ-sparing option for some patients with high-grade dysplasia and early adenocarcinoma.

61 gus is commonly practiced in order to detect high-grade dysplasia and early esophageal adenocarcinoma

62 ct which cases of BE will progress to EAC or high-grade dysplasia and identified those that can be me

63 The total malignancy rate including high-grade dysplasia and invasive carcinoma in IPMNs wit

64 negative BD-IPMNs, a malignancy rate of 18% (high-grade dysplasia and invasive carcinoma) was found.

65 iate-grade dysplasia: n = 48) and high-risk (high-grade dysplasia and invasive carcinoma: n = 30) gro

66 lasia as early as 3 months and progressed to high-grade dysplasia and invasive intramucosal carcinoma

67 ation therapy is the treatment of choice for high-grade dysplasia and is an option for low-grade dysp

68 ll prostatic lobes, which then progressed to high-grade dysplasia and microinvasive carcinoma by 24 w

69 over three years between the development of high-grade dysplasia and pancreatic cancer.

70 mor multiplicity and burden, protection from high-grade dysplasia and significantly reduced colitis.

71 ntraductal papillary mucinous neoplasms with high-grade dysplasia and some enlarged pancreatic intrae

72 Patients with low-grade and high-grade dysplasia and submucosal or more advanced can

73 teristics (>/=25% villous component), and/or high-grade dysplasia and/or diameter >/=10 mm.

74 r in 16% (10 indefinite, 23 low-grade, and 4 high-grade dysplasias and 5 cancers).

75 ed detection rate of 100% (8/8) in detecting high-grade dysplasias and carcinomas over white-light de

76 omas (<1cm, and without villous histology or high-grade dysplasia) and no neoplasia, respectively (lo

77 d by a region of precursor lesions (low- and high-grade dysplasia) and occasional "remote," nonadjace

78 colon neoplasias (cancers and adenomas with high-grade dysplasia), and also from a cohort of individ

79 agus, 19.0% in low grade dysplasia, 35.7% in high grade dysplasia, and 16.7% in esophageal adenocarci

80 ocytes in normal cervical epithelia, low and high grade dysplasias, and cervical carcinomas.

81 ts with adenocarcinoma, 2 of 2 patients with high-grade dysplasia, and 2 of 8 patients with low-grade

82 in 4.8% of normal cervix, 0% of HIV-negative high-grade dysplasia, and 40% of HIV-positive high-grade

83 as negative for dysplasia, 46% of those with high-grade dysplasia, and 40% of those with cancer but i

84 n 9.5% of normal cervix, 57% of HIV-negative high-grade dysplasia, and 50% of HIV-positive high-grade

85 easured <1.0 cm but had villous histology or high-grade dysplasia, and 9.9% (357/3609) had adenomas >

86 ic lesions that include low-grade dysplasia, high-grade dysplasia, and adenocarcinomas.

87 adenomas, tubular adenomas >/=10 mm or with high-grade dysplasia, and conventional adenomas with vil

88 er of BE progression to low-grade dysplasia, high-grade dysplasia, and EA using microdissected paraff

89 duals and patients with Barrett's esophagus, high-grade dysplasia, and esophageal adenocarcinoma by m

90 ith low-grade dysplasia, moderate dysplasia, high-grade dysplasia, and invasive cancer.

91 lasia into low/intermediate-grade dysplasia, high-grade dysplasia, and invasive carcinoma, respective

92 denoma, one 12-mm tubular adenoma with focal high-grade dysplasia, and no polyp but a previous tubula

93 stritis to hyperplasia, low-grade dysplasia, high-grade dysplasia, and ultimately malignant adenocarc

94 mucosae, 42% of low-grade dysplasias, 79% of high-grade dysplasias, and 75% of adenocarcinomas, respe

95 n size, any adenoma with villous features or high-grade dysplasia, any dysplastic serrated lesion, or

96 pecially in the presence of large polyps and high-grade dysplasia, appears to be effective in prevent

97 another form of esophageal tumor, and 6 had high-grade dysplasia associated with Barrett epithelia.

98 partially obstructive esophageal carcinoma, high-grade dysplasia associated with Barrett's esophagus

99 When patients with high-grade dysplasia at baseline were excluded, however,

100 ar trend was observed among patients without high-grade dysplasia at baseline.

101 est RII mutation detected was in a region of high-grade dysplasia but was absent from the surrounding

102 or 2 small (<1 cm) tubular adenomas with no high-grade dysplasia can have a follow-up evaluation in

103 arker candidates for malignant potential and high-grade dysplasia/cancer were identified by an explor

104 e with non-neoplastic disease and those with high-grade dysplasia/cancer with 72.1% of cases correctl

105 nd prostate stem-cell antigen could identify high-grade dysplasia/cancer with an accuracy of 96% (95%

106 , 28.6% in low-grade dysplasia, and 57.1% in high-grade dysplasia-carcinoma in situ and invasive carc

107 tic ducts, hyperplasia, low-grade dysplasia, high-grade dysplasia-carcinoma in situ, and carcinoma) f

108 High-risk disease was defined as high-grade dysplasia/carcinoma.

109 group comprised 27 non-dysplastic and eight high-grade dysplasia cases, whereas the high-risk group

110 The incidences of cervical carcinoma and of high-grade dysplasia (CIN 3) were consequently reduced b

111 compared with normal squamous mucosa, and in high-grade dysplasia compared with BE and low-grade dysp

112 Among patients with high-grade dysplasia, complete eradication occurred in 8

113 ected mice in both dietary cohorts exhibited high-grade dysplasia consistent with gastric intraepithe

114 ensa (P = 0.80); sensitivity for cancer plus high-grade dysplasia did not differ among tests.

115 ent in dysplasia after PDT but occurrence of high-grade dysplasia during follow-up was used.

116 patients in the surveillance group developed high-grade dysplasia during follow-up.

117 en patients were diagnosed with adenoma with high-grade dysplasia during follow-up.

118 cell metaplasia, Barrett esophagus, low- and high-grade dysplasia, esophageal adenocarcinoma, squamou

119 A patient with low- or high-grade dysplasia found in a discrete adenoma-like po

120 in an endoscopically nonresectable polyp and high-grade dysplasia found in flat mucosa are both stron

121 cence (DNF) index technique to differentiate high-grade dysplasia from either low-grade or nondysplas

122 ows: grade 1, adenoma; grade 2, adenoma with high-grade dysplasia; grade 3, well-differentiated adeno

123 Cases who progressed to EAC (n = 89) or high-grade dysplasia >/= 6 months after diagnosis with B

124 acteristics (>/= 1 cm, villous components or high-grade dysplasia, >/= 3 polyps, and >/= 1 proximal p

125 at had advanced histologic features (cancer, high-grade dysplasia, >=25% villous features), 3 or more

126 Intramucosal adenocarcinoma and high grade dysplasia have a low likelihood of lymphatic

127 gus (BE) patients are routinely screened for high grade dysplasia (HGD) and esophageal adenocarcinoma

128 istry on tissue microarrays, containing EAC, high grade dysplasia (HGD), low grade dysplasia (LGD), B

129 history of pancreatic cancer (P = 0.027) and high-grade dysplasia (HGD) (P = 0.003) were independent

130 There is an unclear risk of colonic high-grade dysplasia (HGD) and colorectal cancer (CRC) a

131 ents with regards to rates of progression to high-grade dysplasia (HGD) and esophageal adenocarcinoma

132 s with LGD, we investigated the incidence of high-grade dysplasia (HGD) and esophageal adenocarcinoma

133 with Barrett's esophagus for progression to high-grade dysplasia (HGD) and esophageal adenocarcinoma

134 th low-grade dysplasia (LGD) can progress to high-grade dysplasia (HGD) and esophageal adenocarcinoma

135 is to evaluate the role of esophagectomy for high-grade dysplasia (HGD) and intramucosal adenocarcino

136 of recurrent colonic adenoma associated with high-grade dysplasia (HGD) colon polyps at baseline colo

137 Patients with preoperative high-grade dysplasia (HGD) had cancer in 29% compared wi

138 The identification of any high-grade dysplasia (HGD) in Barrett's esophagus has be

139 Photodynamic therapy (PDT) for high-grade dysplasia (HGD) in Barrett's esophagus is a F

140 ty (HR 4.53, 95%CI 1.34-15.26; P = 0.02) and high-grade dysplasia (HGD) in the original resection (HR

141 nondysplastic epithelium of UC patients with high-grade dysplasia (HGD) or cancer (UC progressors).

142 egions containing low-grade dysplasia (LGD), high-grade dysplasia (HGD) or carcinoma (C), with 81% se

143 oidy is associated with later development of high-grade dysplasia (HGD) or colorectal cancer.

144 BE patients at high risk for progression to high-grade dysplasia (HGD) or EAC are needed to improve

145 Only high-grade dysplasia (HGD) or EAC were defined as progre

146 esophagus patients is recommended to detect high-grade dysplasia (HGD) or early cancer.

147 Patients with Barrett's esophagus (BE) and high-grade dysplasia (HGD) or early neoplasia increasing

148 ntify factors associated with progression to high-grade dysplasia (HGD) or esophageal adenocarcinoma

149 However, little is known about their risk of high-grade dysplasia (HGD) or esophageal adenocarcinoma

150 d 54 BE samples collected from patients with high-grade dysplasia (HGD) or esophageal adenocarcinoma

151 esection (ER) and ablation for patients with high-grade dysplasia (HGD) or intramucosal adenocarcinom

152 gress from low-grade dysplasia (LGD) through high-grade dysplasia (HGD) to invasive cancer.

153 ents with UC who developed carcinoma (CA) or high-grade dysplasia (HGD) was examined for changes in e

154 agus is frequently recommended for Barrett's high-grade dysplasia (HGD) without cancer.

155 es were 4 sites from 4 different patients as high-grade dysplasia (HGD), 8 sites from 5 different pat

156 with low-grade dysplasia (LGD), 26.7 % with high-grade dysplasia (HGD), 9.6 % serrated polyps and 11

157 tic BE, 10 with low-grade dysplasia, 13 with high-grade dysplasia (HGD), and 8 from patients with eso

158 patients with Barrett's esophagus (BE) with high-grade dysplasia (HGD), but its effects in patients

159 If detected as high-grade dysplasia (HGD), most esophageal cancers can

160 ge patients with BE and low-grade dysplasia, high-grade dysplasia (HGD), or early-stage EA.

161 for dysplasia, low-grade dysplasia (LGD), or high-grade dysplasia (HGD).

162 no dysplasia, low-grade dysplasia (LGD), or high-grade dysplasia (HGD).

163 patients with Barrett's esophagus (BE) with high-grade dysplasia (HGD).

164 the preferred treatment for BE patients with high-grade dysplasia (HGD).

165 for the treatment of Barrett esophagus with high-grade dysplasia (HGD).

166 hly methylated in dysplastic epithelium from high-grade dysplasia (HGD)/cancer patients with UC; meth

167 ARID1A mutations were detected in 15% (3/20) high-grade dysplasia (HGD)/EAC patients.

168 en shown to be effective in the treatment of high-grade dysplasia (HGD)/mucosal carcinoma in Barrett'

169 plastic Barrett's esophagus (NDBE; n=66) and high-grade dysplasia (HGD; n=43).

170 os, 5.8 and 50.3 for low-grade dysplasia and high-grade dysplasia [HGD] respectively) predicted EAC i

171 tion, and outcome of all cases of cancer and high-grade dysplasia identified are described and risks

172 lous adenoma in 7.9 percent, an adenoma with high-grade dysplasia in 1.6 percent, and invasive cancer

173 rbored low-grade dysplasia in 6 cases (16%), high-grade dysplasia in 31 cases (81%), and areas of inv

174 ersy with regard to the optimal treatment of high-grade dysplasia in Barrett's esophagus.

175 roach for suitable operative candidates with high-grade dysplasia in Barrett's esophagus.

176 creased microbial diversity in patients with high-grade dysplasia in comparison to control patients,

177 HRIs who underwent pancreatic resection had high-grade dysplasia in less than 3 cm intraductal papil

178 The risk of high-grade dysplasia in nonworrisome lesions smaller tha

179 id lesions (all tubulovillous adenomas, with high-grade dysplasia in one).

180 and in combination, for evaluating low- and high-grade dysplasia in patients with Barrett's esophagu

181 escence spectroscopy could be used to detect high-grade dysplasia in patients with Barrett's esophagu

182 The presence of high-grade dysplasia in serrated lesions was uncommon wh

183 excision of advanced adenomas, diagnosis of high-grade dysplasia in the rectum or pouch, or progress

184 t 25 percent villous elements or evidence of high-grade dysplasia, including carcinoma) did not diffe

185 ssification based on adenoma size >=20 mm or high-grade dysplasia (instead of the current high-risk c

186 The prevalence of synchronous polyps with high grade dysplasia is highest in patients with large f

187 Barrett's esophagus-associated high-grade dysplasia is commonly treated by endoscopy.

188 The presence of high-grade dysplasia is frequently associated with an un

189 ntramucosal adenocarcinoma or Barrett's with high-grade dysplasia is independent of the type of resec

190 Adenocarcinoma or high-grade dysplasia is present in 14.9% of resected pan

191 sion at the protein and transcript levels in high-grade dysplasias, its reappearance in grade 3 cance

192 The extent of high-grade dysplasia may not accurately predict cancer d

193 ells in normal cervix (N = 21), HIV-negative high-grade dysplasia (N = 21), and HIV-positive high-gra

194 h-grade dysplasia (N = 21), and HIV-positive high-grade dysplasia (N = 30).

195 res, including a villous component (n = 11), high-grade dysplasia (n = 4), and invasive cancer (n = 5

196 Indications for operation included high-grade dysplasia (n = 47) and cancer (n = 175).

197 geal cancer (n = 80), Barrett esophagus with high-grade dysplasia (n = 6), recalcitrant stricture (n

198 d adenoma, n = 4; tubulovillous adenoma with high grade dysplasia, n = 3; villous adenoma, n = 3), an

199 sk factors for malignancy (adenocarcinoma or high-grade dysplasia) occurring in the setting of an MCN

200 anal pain was independently associated with high-grade dysplasia (odds ratio, 6.42; 95% CI, 1.18-43.

201 ossessed a diagnostic accuracy for cancer or high-grade dysplasia of 78% (sensitivity 83%, specificit

202 The development of high-grade dysplasia only occurred in patients who were

203 nce of UDD in predicting advanced neoplasia [high grade dysplasia or invasive carcinoma (HGD/IC)] was

204 h risk adenomas (villous or tubulovillous or high grade dysplasia or size > 1 cm or > 3 adenomatous p

205 Ablation reduced the risk of progression to high-grade dysplasia or adenocarcinoma by 25.0% (1.5% fo

206 rimary outcome was neoplastic progression to high-grade dysplasia or adenocarcinoma during a 3-year f

207 pically visible lesion, and a biopsy showing high-grade dysplasia or adenocarcinoma has been question

208 of the patients with BE developed esophageal high-grade dysplasia or adenocarcinomas of the esophagus

209 No patient developed high-grade dysplasia or cancer in 410 patient-years of f

210 dentify patients at high risk for developing high-grade dysplasia or cancer.

211 ent throughout the colon of UC patients with high-grade dysplasia or cancer.

212 No patient progressed to high-grade dysplasia or cancer.

213 ytology was abnormal in all 11 patients with high-grade dysplasia or carcinoma but only 2 of 9 patien

214 Sensitivity of balloon cytology for high-grade dysplasia or carcinoma was 80% but only 25% f

215 lloon cytology detected 80% of patients with high-grade dysplasia or carcinoma when sampling was adeq

216 ients who are at a higher risk of developing high-grade dysplasia or carcinoma.

217 ve colitis progresses to advanced neoplasia (high-grade dysplasia or colorectal cancer) and whether s

218 cholangitis) and no history of advanced CRN (high-grade dysplasia or colorectal cancer) or colectomy.

219 iteria, 15 progressed to advanced neoplasia (high-grade dysplasia or colorectal cancer), and 65 progr

220 These patients may progress to high-grade dysplasia or develop adenocarcinoma.

221 tion rates of lesions suspected of harboring high-grade dysplasia or early adenocarcinoma, a novel gr

222 nical and endoscopic factors associated with high-grade dysplasia or esophageal adenocarcinoma and va

223 gy analysis, before RFA, 71% of patients had high-grade dysplasia or esophageal adenocarcinoma, 15% h

224 Patients with biopsy-proven high-grade dysplasia or esophageal cancer were enrolled

225 petent patients, AGWs of HIV+ MSM may harbor high-grade dysplasia or even invasive squamous cell carc

226 3% (5-27), whereas the probability of having high-grade dysplasia or intramucosal adenocarcinoma was

227 99% CI 96-100) and the probability of having high-grade dysplasia or intramucosal adenocarcinoma was

228 Of these, 376 had no dysplasia and 22 had high-grade dysplasia or intramucosal adenocarcinoma.

229 Patients found to have high-grade dysplasia or intramucosal cancer received end

230 alyses comprised esophagectomy management of high-grade dysplasia or intramucosal cancer, screening b

231 d 11q was significantly higher in IPMNs with high-grade dysplasia or invasion compared with PDAC.

232 Malignant disease was defined as high-grade dysplasia or invasive adenocarcinoma on resul

233 the presence of multifocal neoplasia (MFN) (high-grade dysplasia or invasive carcinoma).

234 Malignancies (high-grade dysplasia or invasive neoplasm) developed aft

235 Fifty-four patients had high-grade dysplasia or tumors confined to the mucosa wi

236 us histology (OR, 2.3; 95% CI, 1.5-3.7), and high-grade dysplasia (OR, 1.9; 95% CI, 1.2-3.1).

237 a polyp with villous histologic features or high-grade dysplasia), or a cancer.

238 pathologically advanced (villous component, high-grade dysplasia, or >/=1 cm); 21.5% (211 of 981) ha

239 or any adenoma with villous growth pattern, high-grade dysplasia, or >=10 mm in diameter).

240 adenoma with villous or serrated histology, high-grade dysplasia, or an invasive cancer.

241 /=1 cm; or with villous histologic findings, high-grade dysplasia, or cancer) during follow-up.

242 in diameter, villous adenomas, adenomas with high-grade dysplasia, or cancer) in men would be missed

243 villous histologic appearance, a polyp with high-grade dysplasia, or cancer), the DNA panel was posi

244 a polyp with villous features, a polyp with high-grade dysplasia, or cancer, among persons with dist

245 mpared the development of pancreatic cancer, high-grade dysplasia, or clinically worrisome features,

246 s >=10mm, adenomas with villous histology or high-grade dysplasia, or colorectal cancer [CRC]) and as

247 essed to any neoplasia (low-grade dysplasia, high-grade dysplasia, or colorectal cancer).

248 ors for advanced colorectal neoplasia (aCRN, high-grade dysplasia, or CRC) in patients with IBD.

249 age benign disease, Barrett's esophagus with high-grade dysplasia, or esophageal carcinoma limited to

250 sk PCLs were those with invasive carcinomas, high-grade dysplasia, or intestinal-type intraductal pap

251 adenoma with villous histology, adenoma with high-grade dysplasia, or invasive cancer.

252 greater, adenomas with villous histology or high-grade dysplasia, or invasive cancer.

253 definite for dysplasia, low-grade dysplasia, high-grade dysplasia, or invasive cancer.

254 diameter, a villous adenoma, an adenoma with high-grade dysplasia, or invasive cancer.

255 diameter, a villous adenoma, an adenoma with high-grade dysplasia, or invasive cancer.

256 diameter, a villous adenoma, an adenoma with high-grade dysplasia, or invasive cancer.

257 e cumulative incidence of pancreatic cancer, high-grade dysplasia, or worrisome features on pancreati

258 igh-grade dysplasia, and 40% of HIV-positive high-grade dysplasia (P < 0.001).

259 igh-grade dysplasia, and 50% of HIV-positive high-grade dysplasia (P = 0.001 normal versus high-grade

260 in endoscopically versus surgically treated high-grade dysplasia patients has led to a shift in trea

261 of concomitant occult invasive cancer among high-grade dysplasia patients undergoing esophagectomy a

262 and low-grade dysplasia and more than 80% in high-grade dysplasia patients, and the treatment appears

263 f adenoma progression (villous histology and high-grade dysplasia) rather than with adenoma growth.

264 Low- or high-grade dysplasia received surveillance every 6 or 3

265 gh incidence of esophageal adenocarcinoma in high-grade dysplasia renders chemoprevention cost-effect

266 ow-grade dysplasia samples as benign, 90% of high-grade dysplasia samples as premalignant, and 28% of

267 remalignant, and 28% of low-grade with focal high-grade dysplasia samples as premalignant.

268 mosomal aberrations, IPMNs with moderate and high-grade dysplasia showed frequent copy number alterat

269 The patient with high-grade dysplasia shows the highest concentrations fo

270 ratio [SIR] 2.07; 95% CI 1.40-2.93) or with high-grade dysplasia (SIR 0.79; 95% CI 0.39-1.41), where

271 dvanced lesions (> or =25% villous features, high-grade dysplasia, size > or =1 cm, or invasive cance

272 m non-dysplasia esophageal lesion to low and high grade dysplasia, suggesting that cyclin E plays an

273 ions, with a high ML consistently present in high grade dysplasia targets.

274 significantly higher in Barrett tissues with high grade dysplasia than without dysplasia.

275 patients with intramucosal adenocarcinoma or high grade dysplasia that had a vagal-sparing (n=49), tr

276 those patients with Barrett's esophagus and high-grade dysplasia, the ICER ranges between $3900 and

277 ett's metaplasia progresses through low- and high-grade dysplasia to invasive cancer.

278 percentage of positively staining nuclei in high-grade dysplasia versus low-grade dysplasia (54.8 +/

279 creased risk have either 3 or more adenomas, high-grade dysplasia, villous features, or an adenoma 1

280 age, 58.2 +/- 6.3 years; adenomas >/=10 mm, high-grade dysplasia, villous, or tubulovillous) and 400

281 increased tumor number, burden, and risk of high-grade dysplasia vs. WT mice.

282 of moderate risk; the probability of having high-grade dysplasia was 14% (9-21).

283 The rate of detection of polyps with high-grade dysplasia was 69.2% with DNA testing and 46.2

284 High-grade dysplasia was eradicated in all patients and

285 High-grade dysplasia was not associated independently wi

286 High-grade dysplasia was not associated with AA or NAA.

287 a, with any or low-grade dysplasia, and with high-grade dysplasia were 60.8 years, 65.6 years, and 70

288 t adenomas, adenomas >=20 mm in diameter and high-grade dysplasia were associated with increased risk

289 indices concurrently, all patients with any high-grade dysplasia were classified correctly.

290 diagnosed with colorectal adenocarcinoma or high-grade dysplasia were enrolled.

291 els in bronchial tissue specimens containing high-grade dysplasia were significantly higher than in t

292 nced neoplasia (cancer, adenoma >/=10 mm, or high-grade dysplasia) were calculated.

293 tic BE, 22 samples of LGD, and 34 samples of high-grade dysplasia) were identified, randomly assigned

294 29 of 71 invasive cancers plus adenomas with high-grade dysplasia, whereas Hemoccult II identified 10

295 can be detected at the pre-invasive stage of high-grade dysplasia with the novel Cytosponge device.

296 can be detected at the pre-invasive stage of high-grade dysplasia with the novel Cytosponge device.

297 or the treatment of Barrett's esophagus with high-grade dysplasia, with complete eradication of dyspl

298 High-grade dysplasia within Barrett's mucosa remains the

299 The recurrence rate of high-grade dysplasia within one year was significantly h

300 he Barrett's segments of 58 patients who had high-grade dysplasia without cancer.