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1                                              HSIL identified by any biopsy was the reference standard
2                                              HSIL was found in 26% and 18% of anal biopsies following
3                                              HSIL was significantly associated with E7-specific CD8(+
4 th increasing disease severity [LSIL] (20%), HSIL, (17%), and cancer patients (7%); X2 test P for the
5 status (Normal = 2/20,10%; LSIL = 11/52,21%; HSIL = 25/92,27%; ICC = 2/5,40%).
6 fidence interval: 168.2, 3,229.2) for CIN2-3/HSIL+ versus <CIN2-3/HSIL+; 92% of RRs were above 3.0.
7  cervical cancer (together designated CIN2-3/HSIL+) to evaluate the robustness of HPV persistence for
8 >12 months), wider testing intervals, CIN2-3/HSIL+, and use of an HPV-negative reference group were c
9 istently and strongly associated with CIN2-3/HSIL+, despite wide variation in definitions and study m
10 .2, 3,229.2) for CIN2-3/HSIL+ versus <CIN2-3/HSIL+; 92% of RRs were above 3.0.
11 pithelial samples from 10 normal cervices, 7 HSILs, and 21 SCCs using high-density oligonucleotide mi
12 accinated women may not be protected against HSIL and lesser dysplasia especially if they were vaccin
13                               Only 2% of all HSILs diagnosed in the participants were detected by bio
14                                         Anal HSIL is common in HIV-infected women.
15 we report outcomes and risk factors for anal HSIL following implementation of universal AC screening
16 f ongoing viral replication, more so in anal HSILs.
17 ed risk of CIN2+(OR=2.2; 95% CI=1.1-4.6) and HSIL+(OR=1.6; 95% CI=1.1-2.4).
18  tags) that were overexpressed in tumors and HSIL tissues, 35 were confirmed using in situ hybridizat
19 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
20 re associated with decreased risk for cancer/HSILs (odds ratio [OR], 0.4; 95% confidence interval [CI
21                    We compared risk of CIN2+/HSIL+between multiple and single infections and assessed
22 rall population, sensitivities for detecting HSIL increased from 60.6% (95% CI, 54.8% to 66.6%) from
23           We examined the risk of developing HSIL among adolescents with and without HIV infection.
24  had AC. Cigarette smoking more than doubled HSIL risk.
25          Cigarette smoking more than doubled HSIL risk.
26                                 The risk for HSIL associated with high concentrations of IL-12 may be
27                      The heightened risk for HSIL associated with persistent LSIL underscores the nee
28  serves as an independent screening test for HSIL and may help to determine the progressive potential
29       The sensitivity of HPV DNA testing for HSIL was equivalent to, if not greater than, that of the
30 ithelial lesions (LSIL; n = 52), high-grade (HSIL; n = 92), invasive cervical cancer (ICC; n = 5) and
31 uman immunodeficiency virus), 51 (38.1%) had HSIL.
32                  Twenty-six participants had HSIL a mean of 1 year before measurement of T-cell respo
33 Adolescent Health Care) and who did not have HSIL on cytologic examination at study entry or at the f
34 1% and 10%, respectively, were found to have HSIL on biopsy.
35             Sixty-five (6.7%) had histologic HSIL or cancer.
36 colposcopy increased detection of histologic HSIL, regardless of patient characteristics.
37                    For women with histologic HSIL+, the HPV test was positive in 89.2% (95% confidenc
38 en with a high-grade colposcopic impression, HSIL cytology, and human papillomavirus (HPV) type 16 po
39                    The vaginal microbiome in HSIL was characterised by higher levels of Sneathia sang
40 sociated with 23% (-17% to 48%) reduction in HSIL risk among those >/= 18 with no history of abnormal
41 l cervix and LSILs, is readily detectable in HSILs, and is very strongly expressed in nearly all inva
42  high-grade squamous intraepithelial lesion (HSIL) (ASC-H).
43  high-grade squamous intraepithelial lesion (HSIL) in human immunodeficiency virus (HIV)-infected ado
44  high-grade squamous intraepithelial lesion (HSIL), frequently regresses spontaneously.
45 , low-grade squamous intraepithelial lesion, HSIL, and atypical glandular cells should be referred fo
46 g with HIV) and high grade cervical lesions (HSIL-CIN2+; 9288 women living with HIV).
47 high-grade squamous intraepithelial lesions (HSIL) and anal cancer (AC) compared with HIV-uninfected
48 high-grade squamous intraepithelial lesions (HSIL) grade 2 (CIN2, n = 8), and grade 3 (CIN3, n = 17).
49 high-grade squamous intraepithelial lesions (HSIL) of the cervix will progress to invasive squamous c
50 high-grade squamous intraepithelial lesions (HSIL), and 28 with invasive cervical cancer with 25 wome
51 high-grade squamous intraepithelial lesions (HSIL), and invasive cervical cancer (together designated
52 r or high-grade squamous epithelial lesions (HSILs; n=365) or low-grade squamous epithelial lesions (
53 high-grade squamous intraepithelial lesions (HSILs) diagnosed cytologically; 1198 with cervical intra
54 high-grade squamous intraepithelial lesions (HSILs) in screening populations are identified from ASCU
55 high-grade squamous intraepithelial lesions (HSILs).
56 high-grade squamous intraepithelial lesions (HSILs).
57 high-grade squamous intraepithelial lesions (HSILs).
58 high-grade squamous intraepithelial lesions (HSILs; n=166), or low-grade squamous intraepithelial les
59 high-grade squamous intraepithelial lesions [HSILs]).
60 ese oncogenic HPV-negative women, 2 cases of HSIL+ were observed; an HIV-uninfected woman and an HIV-
61 udy has quantified the improved detection of HSIL by taking multiple lesion-directed biopsies.
62 ificantly associated with the development of HSIL.
63 e primary outcome was cytologic diagnosis of HSIL confirmed by expert review.
64                                 Incidence of HSIL by the end of follow-up was higher for HIV-infected
65                             The incidence of HSIL was alarmingly high in HIV-infected adolescent girl
66           The 5-year cumulative incidence of HSIL+ and CIN-2+ was similar in HIV-infected women and H
67                       Substantial numbers of HSIL would have been missed by strictly adhering to exis
68 cytology with HRA results, and predictors of HSIL pathology, and compared rates of HSIL pathology amo
69 ors of HSIL pathology, and compared rates of HSIL pathology among women meeting screening guidelines
70                     We evaluated the risk of HSIL in women concomitantly infected with multiple HPV g
71                    We calculated the risk of HSIL in women infected with a single HPV genotype and th
72 or most types, we observed a greater risk of HSIL in women infected with multiple carcinogenic HPV ty
73 observed an increased but plateauing risk of HSIL in women infected with multiple types, compared wit
74 additive effects of HPV types on the risk of HSIL in women infected with multiple types.
75                          The highest risk of HSIL was observed for HPV-16 (0.036), followed by HPV-33
76                     In contrast, the risk of HSIL was similar in women infected with HPV-16 and other
77  ART was associated with a decreased risk of HSIL-CIN2+ incidence among 1830 women living with HIV (0
78             The highest increase in yield of HSIL was observed for women with a high-grade colposcopi
79 d -1% (-44% to 29%) against the detection of HSILs, LSILs, and ASCUS, respectively.
80 h a single biopsy can miss identification of HSILs.
81 likely to underlie the appearance of LSIL or HSIL soon after infection.
82 de squamous intraepithelial lesions (LSIL or HSIL).
83 ence interval [CI], 0.29-0.89) for cancer or HSILs and 0.58 (95% CI, 0.37-1.04) for LSILs, compared w
84 cell responses may be associated with recent HSIL regression.
85 aepithelial lesions (LSIL), high-grade SILs (HSIL), and invasive carcinomas.
86 helial lesions (LSILs), and high-grade SILs (HSILs).
87 aled copy number increases of 3q, 63% of the HSIL (CIN2) lesions and 76% of the HSIL (CIN3) lesions s
88 3% of the HSIL (CIN2) lesions and 76% of the HSIL (CIN3) lesions showed extra copies of 3q.
89 ow-grade squamous intraepithelial lesions to HSILs and finally to cancer.
90 ated (and P < 0.001) in the SCCs relative to HSILs and normal cervix samples.
91  can help identify those who have underlying HSIL.
92 fferential expression in invasive SCC versus HSIL may contribute to tumor progression or may be usefu
93 ed that T-cell responses are associated with HSIL regression.
94 e anal sex was significantly associated with HSIL.
95  there was some evidence of association with HSIL-CIN2+ (0.65, 0.40-1.06; I(2)=30%).

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