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

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

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

7 of superficial esophageal adenocarcinoma or high-grade dysplasia.

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

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

10 patients with intramucosal adenocarcinoma or high-grade dysplasia.

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

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

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

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

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

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

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

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

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

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

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

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

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

24 endoscopic photodynamic therapy to eradicate high-grade dysplasia.

25 diagnosed as having Barrett's esophagus with high-grade dysplasia.

26 intraductal papillary mucinous neoplasm had high-grade dysplasia.

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

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

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

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

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

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

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

34 arm in 20 esophageal adenocarcinomas and two high-grade dysplasias.

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

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

37 17.7%), as well as low- (10.8% vs. 3.8%) and high-grade dysplasia (1.5% vs. 0%) were predominant in T

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

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

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

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

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

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

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

45 , 2.1-4.9 vs. tubular), and in adenomas with high-grade dysplasia (32.0% vs. 13.6%; OR, 3.0; 95% CI,

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

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

48 00 person-years among patients with baseline high-grade dysplasia (95% CI 4.2-12.5).

49 00 person-years among patients with baseline high-grade dysplasia (95% CI 8.8-20.7).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 between 1985 and 1995 with 11 patients with high-grade dysplasia arising in Barrett's esophagus diag

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

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

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

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

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

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

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

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

100 , 28.6% in low-grade dysplasia, and 57.1% in high-grade dysplasia-carcinoma in situ and invasive carc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 e spectroscopy has great potential to detect high-grade dysplasia in Barrett's esophagus when using t

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

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

162 High-grade dysplasia in columnar-lined (Barrett's) oesop

163 High-grade dysplasia in columnar-lined oesophagus can be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 3% (5-27), whereas the probability of having high-grade dysplasia or intramucosal adenocarcinoma was

210 99% CI 96-100) and the probability of having high-grade dysplasia or intramucosal adenocarcinoma was

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

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

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

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

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

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

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

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

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

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

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

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

223 /=1 cm; or with villous histologic findings, high-grade dysplasia, or cancer) during follow-up.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 High-grade dysplasia was eradicated in all patients and

260 High-grade dysplasia was not associated independently wi

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

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

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

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

265 Five patients with histologically confirmed high-grade dysplasia were treated with endoscopic photod

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

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

268 29 of 71 invasive cancers plus adenomas with high-grade dysplasia, whereas Hemoccult II identified 10

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

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

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

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

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

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