ライフサイエンスコーパス: HSIL

1 HSIL detection varied considerably by center (from 13% t

2 HSIL identified by any biopsy was the reference standard

3 HSIL recurrence was associated with a LEEP biopsy result

4 HSIL recurrence was associated with a LEEP biopsy result

5 HSIL was found in 26% and 18% of anal biopsies following

6 HSIL was significantly associated with E7-specific CD8(+

7 HSIL+ detection ranged from 7.5% (12 of 160) to 54.5% (6

8 Over 695.3 PY follow-up, 153 HSIL cleared (clearance 22.0, 95% CI 18.8-25.8 per 100 P

9 th increasing disease severity [LSIL] (20%), HSIL, (17%), and cancer patients (7%); X2 test P for the

10 status (Normal = 2/20,10%; LSIL = 11/52,21%; HSIL = 25/92,27%; ICC = 2/5,40%).

11 fidence interval: 168.2, 3,229.2) for CIN2-3/HSIL+ versus <CIN2-3/HSIL+; 92% of RRs were above 3.0.

12 cervical cancer (together designated CIN2-3/HSIL+) to evaluate the robustness of HPV persistence for

13 >12 months), wider testing intervals, CIN2-3/HSIL+, and use of an HPV-negative reference group were c

14 istently and strongly associated with CIN2-3/HSIL+, despite wide variation in definitions and study m

15 .2, 3,229.2) for CIN2-3/HSIL+ versus <CIN2-3/HSIL+; 92% of RRs were above 3.0.

16 t 18 men (16.8%) showed LSIL, and 25 (23.4%) HSIL.

17 tion rate was 33% (134 of 410), of which 48% HSILs were detected at baseline.

18 pithelial samples from 10 normal cervices, 7 HSILs, and 21 SCCs using high-density oligonucleotide mi

19 multivariate analyses, the odds of having A-HSIL were >6 times higher in women with anal hrHPV (adju

20 Thirteen (18%) anal biopsies identified A-HSIL.

21 igh-grade squamous intraepithelial lesion (A-HSIL) as the dependent variable.

22 accinated women may not be protected against HSIL and lesser dysplasia especially if they were vaccin

23 All HSIL cases occurred in individuals with anal hrHPV.

24 Only 2% of all HSILs diagnosed in the participants were detected by bio

25 Anal HSIL is common in HIV-infected women.

26 Anal HSIL was also associated with cervical cytohistopatholog

27 Anal HSIL was associated with cervical high-risk HPV, both in

28 Anal HSIL was diagnosed by histopathological examinations of

29 , PRs were similarly calculated for all anal HSIL and HPV16-positive anal HSIL.

30 hese data strongly suggest that not all anal HSIL detected in screening requires treatment.

31 s with human immunodeficiency virus and anal HSIL were randomly assigned 1:1:1 to receive treatment w

32 atios (ORs) of histologically confirmed anal HSIL in RTRs vs controls and risk factors for anal HSIL

33 we report outcomes and risk factors for anal HSIL following implementation of universal AC screening

34 the prevalence of and risk factors for anal HSIL in a US cohort.

35 Screening for anal HSIL in RTRs should be considered.

36 n RTRs vs controls and risk factors for anal HSIL in RTRs, stratified by sex and anal high-risk (hr)

37 CI, 1.53-11.48]) were risk factors for anal HSIL in RTRs.

38 l hrHPV infection were risk factors for anal HSIL in RTRs.

39 competent controls and risk factors for anal HSIL in RTRs.

40 significantly lower with treatment for anal HSIL than with active monitoring.

41 om prospective studies of treatment for anal HSIL to prevent anal cancer are lacking.

42 those with anal hrHPV, RTRs had higher anal HSIL prevalence than controls (33.8% vs 9.5%; aOR, 6.06

43 RTRs had higher anal HSIL prevalence than controls, both among men (6.5% vs 0

44 RTRs had increased risk of anal HSIL compared with immunocompetent controls, with partic

45 The causative HPV type of anal HSIL was determined in whole tissue sections (WTS) and b

46 ropositivity for HPV were predictors of anal HSIL, either in general or caused by the concordant HPV

47 LHIV aged >=18 years with no history of anal HSIL.

48 Prevalence of HPV16-positive anal HSIL was 23-25% in cervical HPV16-positive women older t

49 ed for all anal HSIL and HPV16-positive anal HSIL.

50 age or older and who had biopsy-proven anal HSIL were randomly assigned, in a 1:1 ratio, to receive

51 Among participants with biopsy-proven anal HSIL, the risk of anal cancer was significantly lower wi

52 terminant independently associated with anal HSIL, both in general and by concordant, causative HPV t

53 nfections were strongly associated with anal HSIL, in general as well as for the concordant HPV type.

54 itive MSM, 50 (26%) were diagnosed with anal HSIL.

55 ts) were compared with HPV genotypes in anal HSILs (222 lesions) determined by laser capture microdis

56 f ongoing viral replication, more so in anal HSILs.

57 IRC ablation of anal HSILs results in more clearance of HSILs than observatio

58 aged >=27 years with 1-3 biopsy-proven anal HSILs (index HSILs) without prior history of HSIL treatm

59 HPV16-positive HSIL+ (1.66, 1.36-2.03), and HSIL+ in HPV16-positive MSM (1.19, 1.04-1.37).

60 ed risk of CIN2+(OR=2.2; 95% CI=1.1-4.6) and HSIL+(OR=1.6; 95% CI=1.1-2.4).

61 35, 39, 45, 51, 52, 56, 58, 59, and 68), and HSIL or worse (HSIL+), were compared by use of adjusted

62 faction, human papillomavirus clearance, and HSIL recurrence.

63 ies of cervical determinants of anal HPV and HSIL published up to Aug 31, 2018.

64 st fold expression increase in both LSIL and HSIL compared to the other miRNAs.

65 Incident LSIL and HSIL were common during follow-up among HIV-positive MSM

66 The normal, LSIL, and HSIL cells were selected on the basis of the ratio of th

67 tags) that were overexpressed in tumors and HSIL tissues, 35 were confirmed using in situ hybridizat

68 Incident LSILs and HSILs were common during follow-up among HIV-positive MS

69 L) biopsies was shown to distinguish between HSIL with an increased and a low cancer risk, supporting

70 ary endpoint was methylation-positive biopsy HSIL (M+ HSIL), indicating increased cancer risk.

71 02 had an 8.2-fold increased risk for cancer/HSILs (95% CI, 1.8-37.2) and a 5.3-fold increased risk f

72 re associated with decreased risk for cancer/HSILs (odds ratio [OR], 0.4; 95% confidence interval [CI

73 The primary endpoint, cervical HSIL by histology or cytology at either week 26 or 52, w

74 The primary endpoint, cervical HSIL by histology or cytology at either week 26 or 52, w

75 Treatment for cervical HSIL reduces progression to cervical cancer; however, da

76 rmal cytology up to 22% [59/273] in cervical HSIL; PR 23.1, 9.4-57.0, p<0.0001) and HIV-positive wome

77 n improves response to treatment of cervical HSIL.

78 n improves response to treatment of cervical HSIL.

79 esburg, South Africa diagnosed with cervical HSIL by colposcopic biopsy.

80 sburg, South Africa, diagnosed with cervical HSIL by colposcopic biopsy.

81 We compared risk of CIN2+/HSIL+between multiple and single infections and assessed

82 h persistent HPV16 were less likely to clear HSIL and are more likely to benefit from effective HSIL

83 gorithms predicted HPV-16 as the most common HSIL-causative genotype, and proportions differed from L

84 A composite HSIL diagnosis (cytology histology) was used.

85 The cumulative HSIL detection rate was 33% (134 of 410), of which 48% H

86 Cytology HSIL+ had optimal performance for CIN2+/CIN3+ detection

87 and adjusted Poisson regression of cytology (HSIL) and histopathology (CIN2, CIN3, and CIN2+) outcome

88 Sensitivity of the algorithm to detect HSIL or worse was 85.4% (95% CI 81.0-89.6), with specifi

89 rall population, sensitivities for detecting HSIL increased from 60.6% (95% CI, 54.8% to 66.6%) from

90 y" samples and low sensitivity for detecting HSIL.

91 We examined the risk of developing HSIL among adolescents with and without HIV infection.

92 neoplasia grade 2 or more severe diagnoses (HSIL/AIN2+), and we estimated the 2- and 5-year cumulati

93 developed a pioneering CNN to differentiate HSIL and LSIL in HPV-related dysplastic lesions, during

94 Cigarette smoking more than doubled HSIL risk.

95 had AC. Cigarette smoking more than doubled HSIL risk.

96 nd are more likely to benefit from effective HSIL treatments.

97 assigned, in a 1:1 ratio, to receive either HSIL treatment or active monitoring without treatment.

98 in the eligible population and (2) estimated HSIL detection rate based on our current low-threshold c

99 atypical squamous cells that cannot exclude HSIL in 23%, 40%, 5%, and 1% of cases, respectively.

100 n the testing phase, performance metrics for HSIL were: sensitivity 99.0%, specificity 97.8%, PPV 97.

101 Improved treatments are needed for HSIL to reduce the burden of cervical cancer among women

102 The risk for HSIL associated with high concentrations of IL-12 may be

103 The heightened risk for HSIL associated with persistent LSIL underscores the nee

104 Adjusted RR for HSIL was 0.53 (95% CI, .43-.64), resulting in a VE of 47

105 he model achieved an average sensitivity for HSIL of 98.1% (IC95% 97.6-98.5%), specificity of 97.4% (

106 cancer, but current screening strategies for HSIL detection lack specificity.

107 serves as an independent screening test for HSIL and may help to determine the progressive potential

108 The sensitivity of HPV DNA testing for HSIL was equivalent to, if not greater than, that of the

109 anal cytology as a diagnostic indicator for HSILs, increasing the sensitivity from 91.2% to 96.6%, t

110 fferentiate low-grade (LSIL) and high grade (HSIL) squamous intraepithelial lesions, in the cervix an

111 (NILM), and low-grade (LSIL) and high-grade (HSIL) squamous intraepithelial lesions.

112 ithelial lesions (LSIL; n = 52), high-grade (HSIL; n = 92), invasive cervical cancer (ICC; n = 5) and

113 squamous intraepithelial lesion or greater (HSIL+) had best combination of sensitivity (CIN2+: 70.1%

114 uman immunodeficiency virus), 51 (38.1%) had HSIL.

115 Twenty-six participants had HSIL a mean of 1 year before measurement of T-cell respo

116 Adolescent Health Care) and who did not have HSIL on cytologic examination at study entry or at the f

117 1% and 10%, respectively, were found to have HSIL on biopsy.

118 These women have high HSIL recurrence rates after loop electroexcision procedu

119 The prevalence of anal histologic HSIL (hHSIL) was 27% (95% confidence interval [CI], 22%-

120 Sixty-five (6.7%) had histologic HSIL or cancer.

121 colposcopy increased detection of histologic HSIL, regardless of patient characteristics.

122 For women with histologic HSIL+, the HPV test was positive in 89.2% (95% confidenc

123 ate the age-specific prevalence of anal HPV, HSIL, and their combination, in men, stratified by HIV s

124 en with a high-grade colposcopic impression, HSIL cytology, and human papillomavirus (HPV) type 16 po

125 investigated the anal microbiome to improve HSIL screening.

126 tology and high-resolution anoscopy improved HSIL detection but did not fully compensate for between-

127 The vaginal microbiome in HSIL was characterised by higher levels of Sneathia sang

128 sociated with 23% (-17% to 48%) reduction in HSIL risk among those >/= 18 with no history of abnormal

129 l cervix and LSILs, is readily detectable in HSILs, and is very strongly expressed in nearly all inva

130 or partial clearance (clearance of >=1 index HSIL) occurred more commonly in the treatment group (82%

131 Complete index HSIL clearance occurred more frequently in the treatment

132 ry end point was complete clearance of index HSIL at month 12.

133 ars with 1-3 biopsy-proven anal HSILs (index HSILs) without prior history of HSIL treatment with infr

134 high-grade squamous intra-epithelial lesion (HSIL), and atypical squamous cells that cannot exclude H

135 high-grade squamous intraepithelial lesion (HSIL) (ASC-H).

136 high-grade squamous intraepithelial lesion (HSIL) and anal intraepithelial neoplasia grade 2 or more

137 high-grade squamous intraepithelial lesion (HSIL) biopsies was shown to distinguish between HSIL wit

138 high-grade squamous intraepithelial lesion (HSIL) in human immunodeficiency virus (HIV)-infected ado

139 high-grade squamous intraepithelial lesion (HSIL) or worse.

140 high-grade squamous intraepithelial lesion (HSIL) to carcinoma, and (iii) flexibility to model cance

141 high-grade squamous intraepithelial lesion (HSIL), frequently regresses spontaneously.

142 (high-grade squamous intraepithelial lesion [HSIL] on cytology) if availability is low.

143 high-grade squamous intraepithelial lesion [HSIL] with positive HPV test results), management consis

144 , low-grade squamous intraepithelial lesion, HSIL, and atypical glandular cells should be referred fo

145 g with HIV) and high grade cervical lesions (HSIL-CIN2+; 9288 women living with HIV).

146 high-grade squamous intraepithelial lesions (HSIL) and anal cancer (AC) compared with HIV-uninfected

147 high-grade squamous intraepithelial lesions (HSIL) and cervical cancer.

148 high-grade squamous intraepithelial lesions (HSIL) and cervical cancer.

149 high-grade squamous intraepithelial lesions (HSIL) and, hence, anal cancer.

150 high-grade squamous intraepithelial lesions (HSIL) grade 2 (CIN2, n = 8), and grade 3 (CIN3, n = 17).

151 high-grade squamous intraepithelial lesions (HSIL) in human immunodeficiency virus (HIV)-positive men

152 high-grade squamous intraepithelial lesions (HSIL) in men can inform anal cancer prevention efforts.

153 high-grade squamous intraepithelial lesions (HSIL) of the cervix will progress to invasive squamous c

154 High-grade squamous intraepithelial lesions (HSIL) or cervical intraepithelial neoplasia (CIN) grade

155 high-grade squamous intraepithelial lesions (HSIL), and 28 with invasive cervical cancer with 25 wome

156 high-grade squamous intraepithelial lesions (HSIL), and invasive cervical cancer (together designated

157 high-grade squamous intraepithelial lesions (HSIL), and the AIN classification in AIN1, AIN2 and AIN3

158 high-grade squamous intraepithelial lesions (HSIL).

159 r or high-grade squamous epithelial lesions (HSILs; n=365) or low-grade squamous epithelial lesions (

160 high-grade squamous intraepithelial lesions (HSILs) ablation may reduce the incidence of invasive can

161 high-grade squamous intraepithelial lesions (HSILs) as precursors to cancer in the anogenital area, a

162 high-grade squamous intraepithelial lesions (HSILs) diagnosed cytologically; 1198 with cervical intra

163 high-grade squamous intraepithelial lesions (HSILs) in men who have sex with men living with human im

164 of anal high-grade intraepithelial lesions (HSILs) in RTRs compared with immunocompetent controls an

165 high-grade squamous intraepithelial lesions (HSILs) in screening populations are identified from ASCU

166 high-grade squamous intraepithelial lesions (HSILs) precede anal cancer, and accurate studies of HSIL

167 high-grade squamous intraepithelial lesions (HSILs), among young MSM with HIV (MSMLWH).

168 high-grade squamous intraepithelial lesions (HSILs).

169 high-grade squamous intraepithelial lesions (HSILs).

170 high-grade squamous intraepithelial lesions (HSILs).

171 high-grade squamous intraepithelial lesions (HSILs).

172 high-grade squamous intraepithelial lesions (HSILs).

173 high-grade squamous intraepithelial lesions (HSILs; n=166), or low-grade squamous intraepithelial les

174 high-grade squamous intraepithelial lesions [HSIL]) associated with anal cancer.

175 high grade squamous intraepithelial lesions [HSILs]).

176 high-grade squamous intraepithelial lesions [HSILs]).

177 unconventional high surge impedance loading (HSIL) lines emerge as a potential game changer.

178 ing with HIV with undetectable PVL had lower HSIL-AIN2+ prevalence than those with detectable PVL (cr

179 No incident qHPV type-associated anal LSILs/HSILs were detected among men naive to that type, compar

180 cine-type HPV infection and associated LSILs/HSILs have not been studied.

181 son-years for HPV6,11,16,18-associated LSILs/HSILs, respectively, among those previously exposed to t

182 against incident qHPV type-associated LSILs/HSILs.

183 while maintaining a high sensitivity for M+ HSIL and detecting all cancers.

184 int was methylation-positive biopsy HSIL (M+ HSIL), indicating increased cancer risk.

185 e curve of 0.68-0.70 to detect underlying M+ HSIL.

186 Among HPV16-positive MSM, HSIL+ prevalence increased with age.

187 ese oncogenic HPV-negative women, 2 cases of HSIL+ were observed; an HIV-uninfected woman and an HIV-

188 LEEP biopsy result of HSIL and detection of HSIL at the margins of LEEP sample.

189 LEEP biopsy result of HSIL and detection of HSIL at the margins of the LEEP sample.

190 udy has quantified the improved detection of HSIL by taking multiple lesion-directed biopsies.

191 ificantly associated with the development of HSIL.

192 e primary outcome was cytologic diagnosis of HSIL confirmed by expert review.

193 produced a range of inaccurate estimates of HSIL attribution, with the proportional algorithm perfor

194 HSILs (index HSILs) without prior history of HSIL treatment with infrared coagulation (IRC).

195 Incidence of HSIL by the end of follow-up was higher for HIV-infected

196 The incidence of HSIL was alarmingly high in HIV-infected adolescent girl

197 The 5-year cumulative incidence of HSIL+ and CIN-2+ was similar in HIV-infected women and H

198 Substantial numbers of HSIL would have been missed by strictly adhering to exis

199 ogeneity, HIV was a significant predictor of HSIL+ (aPR 1.54, 95% CI 1.36-1.73), HPV16-positive HSIL+

200 cytology with HRA results, and predictors of HSIL pathology, and compared rates of HSIL pathology amo

201 ors of HSIL pathology, and compared rates of HSIL pathology among women meeting screening guidelines

202 imary outcome was histological resolution of HSIL.

203 was associated with a LEEP biopsy result of HSIL and detection of HSIL at the margins of LEEP sample

204 was associated with a LEEP biopsy result of HSIL and detection of HSIL at the margins of the LEEP sa

205 We evaluated the risk of HSIL in women concomitantly infected with multiple HPV g

206 We calculated the risk of HSIL in women infected with a single HPV genotype and th

207 or most types, we observed a greater risk of HSIL in women infected with multiple carcinogenic HPV ty

208 observed an increased but plateauing risk of HSIL in women infected with multiple types, compared wit

209 additive effects of HPV types on the risk of HSIL in women infected with multiple types.

210 The highest risk of HSIL was observed for HPV-16 (0.036), followed by HPV-33

211 In contrast, the risk of HSIL was similar in women infected with HPV-16 and other

212 ART was associated with a decreased risk of HSIL-CIN2+ incidence among 1830 women living with HIV (0

213 dual stain-negativity indicate a low risk of HSIL/AIN2+ for at least 2 years, compared with negative

214 imated the 2- and 5-year cumulative risks of HSIL/AIN2+ using logistic and Cox regression models.

215 The 2- and 5-year risks of HSIL/AIN2+ were highest for those testing HPV16/18- or H

216 gative had the lowest 2- and 5-year risks of HSIL/AIN2+.

217 precede anal cancer, and accurate studies of HSIL prevalence among WLHIV in the United States are lac

218 The highest increase in yield of HSIL was observed for women with a high-grade colposcopi

219 n of anal HSILs results in more clearance of HSILs than observation alone.

220 common reason for exclusion was detection of HSILs in 88/260 (34%).

221 d -1% (-44% to 29%) against the detection of HSILs, LSILs, and ASCUS, respectively.

222 Understanding the fractions of HSILs attributable to HPV genotypes is important to info

223 h a single biopsy can miss identification of HSILs.

224 Given their high prevalence of HSILs, there is an urgent need to vaccinate young MSMLWH

225 psy was also performed for suspected ongoing HSIL in the treatment group, annually in the active-moni

226 for HRA referral would have led to no HRA or HSIL detection.

227 cluded 88,073 frames, categorized as LSIL or HSIL based on pathological analysis.

228 likely to underlie the appearance of LSIL or HSIL soon after infection.

229 de squamous intraepithelial lesions (LSIL or HSIL).

230 ence interval [CI], 0.29-0.89) for cancer or HSILs and 0.58 (95% CI, 0.37-1.04) for LSILs, compared w

231 more, such as patients with HPV-16-positive HSIL, proceeding directly to excisional treatment is pre

232 cancers and detecting 79% of HPV-16-positive HSIL-AIN3.

233 (aPR 1.54, 95% CI 1.36-1.73), HPV16-positive HSIL+ (1.66, 1.36-2.03), and HSIL+ in HPV16-positive MSM

234 rch and initiatives targeting HPV16-positive HSIL+.

235 Algorithms developed for predicting HSIL-causative genotype fractions have never been compar

236 cell responses may be associated with recent HSIL regression.

237 Recurrent HSIL was high despite virologic suppression.

238 support HPV vaccination to prevent recurrent HSIL after LEEP in women living with HIV.

239 anal biopsies of suspected new or recurrent HSILs.

240 line, risk of progression to high-grade SIL (HSIL) and the clearance rate were estimated at lesion le

241 aepithelial lesions (LSIL), high-grade SILs (HSIL), and invasive carcinomas.

242 the risk of progression to high-grade SILs (HSILs) and the clearance rate were estimated at the lesi

243 helial lesions (LSILs), and high-grade SILs (HSILs).

244 The strongest HSIL determinants were baseline human papillomavirus 16

245 aled copy number increases of 3q, 63% of the HSIL (CIN2) lesions and 76% of the HSIL (CIN3) lesions s

246 3% of the HSIL (CIN2) lesions and 76% of the HSIL (CIN3) lesions showed extra copies of 3q.

247 Participants were randomized 1:1 to HSIL ablation with IRC (treatment) or no treatment (acti

248 .2%-91.9%) but lower specificity compared to HSIL+ (42.7%, 95% CI 38.4%-47.1%; relative specificity =

249 e second visit; 29 (16.4%) had progressed to HSIL.

250 155 fold expression from negative samples to HSIL, with the highest fold expression increase in both

251 ow-grade squamous intraepithelial lesions to HSILs and finally to cancer.

252 cond visit, and 29 (16.4%) had progressed to HSILs.

253 ated (and P < 0.001) in the SCCs relative to HSILs and normal cervix samples.

254 the performance of these new unconventional HSIL lines against lightning.

255 ines is sufficient when using unconventional HSIL lines in addressing shielding failure.

256 edominantly (93.9%) cisgender MSM undergoing HSIL screening with high-resolution anoscopy and anal bi

257 anal swabs was assessed to detect underlying HSIL with an increased cancer risk.

258 can help identify those who have underlying HSIL.

259 ts in the treatment group were treated until HSIL was completely resolved.

260 fferential expression in invasive SCC versus HSIL may contribute to tumor progression or may be usefu

261 ative (9.5%), 63 were LSIL (60%) and 32 were HSIL (30.5%) according to the LAST.

262 ed that T-cell responses are associated with HSIL regression.

263 e anal sex was significantly associated with HSIL.

264 there was some evidence of association with HSIL-CIN2+ (0.65, 0.40-1.06; I(2)=30%).

265 screening eligible) were ever detected with HSIL.

266 There were 129 men diagnosed with HSIL/AIN2+ during the study.

267 Triage of HPV-positive women with HSIL+ maintained high specificity but with some loss in

268 ed to HC2, triage of HC2-positive women with HSIL+ resulted in a 40% reduction in colposcopy referral

269 26.8% with any abnormal cytology (zero with HSIL) triggering HRA referral.

270 cobalamin were significantly associated with HSILs in both cohorts.

271 biome composition signatures associated with HSILs, but elevated levels of microbiome-encoded protein

272 Those without HSILs were vaccinated at 0, 2, and 6 months.

273 52, 56, 58, 59, and 68), and HSIL or worse (HSIL+), were compared by use of adjusted prevalence rati