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1                               Thirteen (18%) anal biopsies identified A-HSIL.
2 = 462) urological (bladder), 18.1% (n = 234) anal, and 5.7% had sarcoma (n = 74).The median age acros
3 s sarcoma (OR, 48.2; 95% CI, 22.0 to 105.6), anal (OR, 15.5; 95% CI, 11.0 to 21.9), and penile cancer
4                             Forty-nine (65%) anal cytology samples were abnormal, and 38 (51%) of ana
5   HPV (any type) was detected in 742 (71.8%) anal specimens and 101 (9.8%) oral specimens.
6 4 and/or microRNA124-2 was found in 69 (95%) anal samples and 19 (26%) cervical samples.
7 ; 208 women underwent HRA following abnormal anal cytology.
8             Thirty-nine percent had abnormal anal cytology on initial screen and 15% on secondary scr
9                       Among 61 MSW, abnormal anal cytology was detected in 12 (20%) and was associate
10                       Prevalence of abnormal anal cytology was 12.9% (95% CI, 9.2%-17.7%; 6 studies i
11 d not received systemic therapy for advanced anal cancer were randomly assigned 1:1 to intravenous ci
12 dge conducted in chemotherapy-naive advanced anal cancer.
13       We estimated the VE (>=1 dose) against anal HPV positivity of the bivalent vaccine, whose targe
14 dence for vaccine effectiveness (VE) against anal HPV infections among women is limited.
15 sults, PRs were similarly calculated for all anal HSIL and HPV16-positive anal HSIL.
16 lower in HIV-infected subjects engaged in an anal cytology screening program.
17 ntly lower in persons with HIV engaged in an anal cytology screening program.
18 nic visitors 16-24 years old who provided an anal swab sample as part of a repeated cross-sectional s
19 brow hairs (60.9%), oral mucosa (35.6%), and anal mucosa (33.3%).
20 tological and cytological abnormalities; and anal cancer incidence.
21 n, anal intraepithelial neoplasia (AIN), and anal cancer among people living with HIV.
22 ) showed remarkable performance for AIN3 and anal cancer detection (area under the curve [AUC] > 0.85
23 pants underwent high-resolution anoscopy and anal cytology and had anal and cervical samples collecte
24 ell carcinomas, gastroesophageal cancer, and anal cancer).
25 al adenocarcinoma, oropharyngeal cancer, and anal cancer.
26                                 Cervical and anal HPV infections were highly correlated.
27 a from 13 427 women with paired cervical and anal samples from 36 studies.
28             For HPV genotyping, cervical and anal samples were obtained at baseline and annually.
29 r pattern, associated with gas expulsion and anal sphincter relaxation, inferred to be associated wit
30 of HPV-16/18 vaccination against genital and anal infections.
31                   Risk for these genital and anal SPCs are high and a follow-up plan should be agreed
32 (cervical, other female and male genital and anal) and skin squamous cell CIS; additionally RRs were
33  methylation markers for detecting HGAIN and anal cancer.
34  high human immunodeficiency virus (HIV) and anal cancer incidence.
35 he natural history of anal high-risk HPV and anal lesion progression is not well established.
36  squamous intraepithelial lesions (HSIL) and anal cancer (AC) compared with HIV-uninfected women.
37 e squamous intraepithelial lesion (HSIL) and anal intraepithelial neoplasia grade 2 or more severe di
38 ight reduce anal high-risk HPV infection and anal cancer risk.
39  tracer was observed in liver metastases and anal cancer, with an SUV(max) of 9.1 and 13.9, respectiv
40 ajor causative agents of cervical, oral, and anal cancers.
41 tection in urine samples, oro-pharyngeal and anal swabs.
42  genital skin swabs, oral rinse samples, and anal swabs.
43                   Self-reported anal sex and anal symptoms were independently associated with anorect
44 including collection of cervical/vaginal and anal specimens, followed by high-resolution anoscopy wit
45                   Baseline prevalence of any anal 9v HR-HPV type among men who have sex with men (MSM
46                                           As anal cancer is potentially preventable, these important
47 ession levels was observed in HIV-associated anal SCCs (fold change, 12.69; P < .001).
48 preference, HIV status, and, when available, anal cytopathology.
49 Cox models, we assessed associations between anal cancer risk and various time-updated CD4 and HIV RN
50 entral cause of anal cancer, is increased by anal sexual intercourse and worsened by human immunodefi
51 study strengthens evidence that lung cancer, anal cancer, and myeloma are diagnosed at modestly young
52  history of the precursor to this carcinoma, anal squamous intraepithelial lesions (SILs).
53 aphrodites and larval males, the single cell anal depressor muscle, used for waste expulsion, contain
54 eviews, cervical/anal cytologic and cervical/anal HPV testing for 2 years.
55 uded questionnaires, chart reviews, cervical/anal cytologic and cervical/anal HPV testing for 2 years
56  tract infection caused by Escherichia coli, anal lymphogranuloma venereum infection, and a positive
57                               Self-collected anal swab and oral rinse specimens were assessed for 37
58 ic DCHR is pull-through transection and colo-anal anastomosis.
59 ted standardized incidence ratios to compare anal cancer incidence in people with HIV infection with
60                                  We compared anal high-risk HPV prevalence by HIV status, cervical hi
61 rformance of a composite endpoint comprising anal liquid-based cytology (aLBC) and high-risk human pa
62                               In conclusion, anal HPV-16 is more persistent than HPV-18, and its inci
63 xually transmitted infection, and condomless anal intercourse.
64  transmitted infection (STI), and condomless anal intercourse.
65 ine and tenofovir for MSM who had condomless anal sexual intercourse in the previous 3 months, a nega
66 ences in longitudinal patterns of condomless anal intercourse with nonsteady partners (nsCAI) in the
67 rs of follow-up, couples reported condomless anal sex a total of 76 088 times.
68 n and transgender women reporting condomless anal intercourse with >/=1 HIV-infected or unknown-seros
69 muL was the strongest predictor of consensus anal hHSIL diagnosis (adjusted odds ratio [aOR], 10.34 [
70                                        NG/CT anal, pharyngeal, and urine (APU) samples from MSM atten
71  the impact of a screening program to detect anal cancer precursors on the incidence of cases of inva
72  the impact of a screening program to detect anal cancer precursors on the incidence of cases of inva
73  AI may need additional strategies to detect anal chancres, to reduce transmission.
74 ex with men (MSM) are at risk for developing anal squamous cell carcinoma.
75                        Poorly differentiated anal neuroendocrine carcinomas (ANECs) are rare lesions
76                                  The dorsal, anal and caudal fins of vertebrates are proposed to have
77 crease the risk of blood-blood contacts (eg, anal sex and fisting), was initially found in human immu
78 y virus (HIV; PLWH) have a markedly elevated anal cancer risk, largely due to loss of immunoregulator
79 stantial and consistent evidence of elevated anal SCC incidence in SOTR.
80         We enrolled 256 women with evaluable anal pathology.
81 ulation, used Poisson regression to evaluate anal cancer incidence among subgroups of people with HIV
82 mine the role of Wnt pathway in the external anal sphincter (EAS) injury-related fibrosis and muscle
83 re aged 18-24 years, and median age of first anal sex was 18 years (IQR 17-21).
84    Imaging modalities such as fistulography, anal endosonography, perineal sonography, magnetic reson
85 nal cancer, 6.68 (95% CI, 3.64 to 12.25) for anal intraepithelial neoplasia grade 3, 4.97 (95% CI, 3.
86 3.8% for vaginal, 59% for bladder, 48.3% for anal, and 48.1% for sarcoma.
87 te ratios of 3.85 (95% CI, 2.32 to 6.37) for anal cancer, 6.68 (95% CI, 3.64 to 12.25) for anal intra
88 swabs collection to investigate STIs and for anal biopsy.
89 sidered when selecting the best approach for anal cancer screening programs.
90 in the cervix show promise as biomarkers for anal cancer screening in HIV+ and at-risk HIV-negative w
91 ponse evaluation after chemoradiotherapy for anal cancer.
92 87 patients treated by chemoradiotherapy for anal squamous cell carcinoma between October 2007 and Oc
93 Here we report outcomes and risk factors for anal HSIL following implementation of universal AC scree
94 luate the prevalence of and risk factors for anal HSIL in a US cohort.
95                               Guidelines for anal cancer recommend assessment of response at 6-12 wee
96 illomavirus (HPV) vaccines are indicated for anal cancer prevention, but evidence for vaccine effecti
97                        Screening methods for anal squamous intraepithelial lesions (SILs) are subopti
98 e shown good cross-sectional performance for anal precancer detection in human immunodeficiency virus
99 he past were generally better predictors for anal cancer risk than their corresponding more recent me
100 onfirming HIV-positive MSM as priorities for anal cancer prevention.
101 with patients in general, and profoundly for anal sex.
102 a continued structured screening program for anal cancer prevention.
103 ening and management of HIV+ MSM at risk for anal cancer.
104 rs provide long-term risk stratification for anal precancers.
105 ccurring in those having salvage surgery for anal cancer.Multivariable analysis showed R0 resection w
106  samples and 78.6% (95% CI: 69.4-87.7%) from anal samples; 2.7% (95% CI: 0.7-4.7%) for Epstein-Barr v
107 h T1 to T3 rectal adenocarcinoma <15 cm from anal verge, given Lap or Open and followed for a minimum
108               Median anastomotic height from anal verge was 3.0 +/- 2.0 cm with stapled techniques ac
109                                   High-grade anal intraepithelial neoplasia (AIN2/3; HGAIN) is highly
110 apillomavirus (HPV) genotypes-and high-grade anal intraepithelial neoplasia (HGAIN) in men who have s
111       At baseline, 75% had anal HPV, 51% had anal HR-HPV, 50% had cervical HPV, and 29% had cervical
112                         At baseline, 75% had anal HPV, 51% had anal HR-HPV, 50% had cervical HPV, and
113                                      All had anal cytology and a high-resolution anoscopy at baseline
114 esolution anoscopy and anal cytology and had anal and cervical samples collected.
115 onths, use of hormonal contraception, having anal sex in the past 3 months, and HIV status of 0.60 (9
116 urrent smokers, and 56% reported ever having anal sex with a man.
117 s intraepithelial lesions (HSIL) and, hence, anal cancer.
118 develops tone important for maintaining high anal pressure and continence.
119 seful markers for identifying PLWH at higher anal cancer risk.
120 iate analysis were conducted with histologic anal high-grade squamous intraepithelial lesion (A-HSIL)
121 marker panel that includes ZNF582 identifies anal cancer and HGAIN with a cancer-like methylation pat
122 ne was 10.5% [6.3% in urine samples, 4.3% in anal swabs and 0.5% in throat swabs] and remained unchan
123 d oral mucosa (9.2%), and HPV-76 (beta-3) in anal mucosa (14.9%).
124      Case numbers for CIS ranged from 330 in anal to 177,285 in cervical CIS.
125 cinogenesis, but have never been assessed in anal precancerous lesions.
126 gations of PD-1/PD-L1 checkpoint blockade in anal SCC, irrespective of patient HIV status.
127 0 cells per muL, there was a 40% decrease in anal cancer incidence (crude HR 0.60, 0.46-0.78; I(2) 21
128 uadrivalent vaccine-type HPV was detected in anal or oral specimens from 475 (26.9%) participants.
129 on of IC infiltration or PD-L1 expression in anal SCC.
130 ne silencing by promoter hypermethylation in anal carcinogenesis is needed.
131 he EAS resulted in significant impairment in anal canal pressure and EAS muscle L-T function.
132  consequence of staging misclassification in anal cancer that we have termed reduced prognostic discr
133                         HrHPV persistence in anal swabs was common, varying by hrHPV type between 3-2
134 ing for differences in sexual positioning in anal intercourse and condom use by partner type and fitt
135  IC subsets, and gene expression profiles in anal SCCs from HIV-positive vs HIV-negative patients.
136 ndings demonstrate an immune-reactive TME in anal SCCs from HIV-positive patients and support clinica
137 local tumor immune microenvironment (TME) in anal SCCs from HIV-positive and HIV-negative patients.
138                          The CRs of incident anal hrHPV infections had a median of 53.7 per 100 perso
139  (IRs) and clearance rates (CRs) of incident anal hrHPV infections were assessed by hrHPV type (types
140 s was significantly associated with incident anal hrHPV infections in multivariable analyses.
141 an papillomavirus-related cancers, including anal cancer (HR, 2.77; 95% CI, 1.29-5.96) and female gen
142 lts Among 447,953 people with HIV infection, anal cancer incidence was much higher than in the genera
143 r HIV-related factors on anal HPV infection, anal intraepithelial neoplasia (AIN), and anal cancer am
144 histopathology-predict anal HPV16 infection, anal high-grade squamous intraepithelial lesions (HSIL)
145        Aging-associated decrease in internal anal sphincter (IAS) tone (AADI) is a major contributor
146  in the regulation of basal tone in internal anal sphincter (IAS).
147                                 The internal anal sphincter (IAS) generates phasic contractions and t
148 m underlying tone generation in the internal anal sphincter (IAS) is controversial.
149                     KEY POINTS: The internal anal sphincter develops tone important for maintaining h
150 f anorectal resting pressure due to internal anal sphincter (IAS) dysfunctionality causes uncontrolle
151 ursors on the incidence of cases of invasive anal squamous-cell carcinoma (IASCC) in persons with HIV
152 ursors on the incidence of cases of invasive-anal-squamous-cell-carcinoma (IASCC) in HIV-1-infected s
153 nicians could consider combining loperamide, anal manometry-assisted biofeedback, and a standard educ
154                                     Magnetic anal sphincter augmentation is a novel surgical option i
155 mes improve significantly following magnetic anal sphincter augmentation.
156         All patients, who underwent magnetic anal sphincter augmentation procedure at a single center
157  are independent strong determinants of male anal HPV16 infection, confirming HIV-positive MSM as pri
158 e compounds present in 'pure' versus 'mixed' anal-gland secretions ('paste') of adult meerkats (Suric
159 s related to treatment were mild or moderate anal pain and bleeding.
160                                         Most anal HR-HPV types detected at 6 months (57%-93%) were pe
161                                     For MSM, anal HPV16 prevalence was significantly higher from stud
162 for at least 2 years, compared with negative anal cytology; however, the high positivity of HR-HPV in
163 s protective effects from maternal obstetric anal sphincter injuries.
164                    Higher rates of obstetric anal sphincter injury following vaginal birth were found
165             HSIL was found in 26% and 18% of anal biopsies following initial and secondary screening,
166 ology samples were abnormal, and 38 (51%) of anal samples were positive for at least 1 of 13 high-ris
167                              IRC ablation of anal HSILs results in more clearance of HSILs than obser
168 l CT positivity was common in the absence of anal sexual exposure.
169 (HIV)-infected women have a higher burden of anal high-grade squamous intraepithelial lesions (HSIL)
170 a systematic review describing the burden of anal squamous cell carcinoma (SCC), and its surrogates,
171                   We report a high burden of anal STIs with an unusual hrHPV type distribution among
172 on, most notably HPV16, the central cause of anal cancer, is increased by anal sexual intercourse and
173 med to assess the incidence and clearance of anal high-risk human papillomavirus (hrHPV) infections a
174 rary for studies of cervical determinants of anal HPV and HSIL published up to Aug 31, 2018.
175 at least 2,300 IU of HCV for the duration of anal intercourse.
176 histology, the pooled prevalence estimate of anal squamous intraepithelial lesions was 22.4% (95% CI,
177 agnosed by histopathological examinations of anal biopsies.
178 e in people with AIDS, with the exception of anal and lung cancers.
179 sed for vulvar/vaginal cancer in families of anal cancer patients.
180                                  Findings of anal cytologic tests were abnormal for 37% of women.
181 iral therapy (ART) on the natural history of anal high-risk HPV and anal lesion progression is not we
182 IV-related factors on the natural history of anal HPV-related disease in people living with HIV.
183 ere WLHIV aged >=18 years with no history of anal HSIL.
184   Prospective data on the natural history of anal human papillomavirus (HPV) infection are scarce in
185 224 men and 175 women reporting a history of anal receptive sexual intercourse.
186 ent infection include reporting a history of anal sex (adjusted odds ratio [aOR] 3.08, 1.11-8.57), ha
187     Groups with high cumulative incidence of anal cancer may benefit from screening.
188 s, and estimated the cumulative incidence of anal cancer to measure absolute risk.
189 -based meta-analyses evaluating incidence of anal SCC (standardized incidence ratio [SIR] vs general
190                              Irrespective of anal cytopathology, HPV16 prevalence was significantly h
191                                   The IRs of anal infections had a median of 5.2 per 100 person-years
192 16 being implicated in the large majority of anal cancer cases.
193  or current CD4 cell count) with outcomes of anal high-risk HPV prevalence, incidence, and persistenc
194 fy virological and serological predictors of anal high-grade squamous intraepithelial lesions (HSIL)
195 nd seropositivity for HPV were predictors of anal HSIL, either in general or caused by the concordant
196                            The prevalence of anal hHSIL in WLHIV in the United States was 27% in this
197                            The prevalence of anal histologic HSIL (hHSIL) was 27% (95% confidence int
198 absolute incidence rate [IR]), prevalence of anal squamous abnormalities, and human papillomavirus (H
199 eening might contribute to the prevention of anal cancer in women.
200 he high incidence and low clearance rates of anal HPV16 infection, compared to other hrHPV types, is
201 ce, incidence, progression, or regression of anal histological and cytological abnormalities; and ana
202                                  The risk of anal cancer due to high-risk human papillomavirus (HR-HP
203 d undetectable HIV PVL had 44% lower risk of anal cancer than those without (adjusted HR 0.56, 0.44-0
204  with HIV infection have an elevated risk of anal cancer.
205 n who have sex with men (MSM) are at risk of anal squamous cell carcinoma.
206                    The causative HPV type of anal HSIL was determined in whole tissue sections (WTS)
207 icant role during posttreatment follow-up of anal cancer.
208 tion of ART and other HIV-related factors on anal HPV infection, anal intraepithelial neoplasia (AIN)
209 l squamous intraepithelial lesions (ASIL) or anal intraepithelial neoplasia (AIN) are precancerous le
210 fected women reporting condomless vaginal or anal intercourse with at least 1 man with HIV infection
211 subject, we measured exhaled H2 and CH4, oro-anal transit time, and the severity of psychological and
212 = 132), foot (n = 59), leg (n = 58) and peri-anal (n = 34) wounds were common.
213 ression was used to study whether persistent anal HPV infections, HPV viral loads, and seropositivity
214                                       Pooled anal HPV16 prevalence was 3.6% (95% CI, 1.6%-7.8%; 4 stu
215 -treated and sham) remained affected by poor anal hygiene, lower resting pressure, and reduced RAIR t
216                 Prevalence of HPV16-positive anal HSIL was 23-25% in cervical HPV16-positive women ol
217 culated for all anal HSIL and HPV16-positive anal HSIL.
218  significantly higher in women with positive anal methylation.
219  similar muscle cell populations in the post-anal tail are generated from tailbud, declining Fgf sign
220  after total proctocolectomy and ileal pouch anal anastomosis is usually treated with antibiotics.
221 stomy, and 1172 (47.3%) received ileal pouch-anal anastomoses.
222 re surgical outcome of transanal ileal pouch-anal anastomosis (ta-IPAA) with transabdominal minimal i
223                         Although ileal pouch-anal anastomosis is recommended after colectomy for UC,
224 ery among patients who underwent ileal pouch-anal anastomosis was associated with higher 90-day posto
225 disease, ulcerative colitis, and ileal pouch-anal anastomosis.
226 mbined total proctocolectomy and ileal pouch-anal anastomosis.
227 mous intraepithelial lesions (HSILs) precede anal cancer, and accurate studies of HSIL prevalence amo
228 ata on the natural history of the precursor, anal squamous intraepithelial lesions (SIL), are limited
229 nd/or HIV-1 RNA level (HIV RNA) best predict anal cancer risk.
230 PV) infection and cytohistopathology-predict anal HPV16 infection, anal high-grade squamous intraepit
231 he efficacy of screening programs to prevent anal cancer in HIV-1-infected subjects is unclear.
232 he efficacy of screening programs to prevent anal cancer in persons with human immunodeficiency virus
233 dults aged >=27 years with 1-3 biopsy-proven anal HSILs (index HSILs) without prior history of HSIL t
234 RG-TFV rectal gel before and after receptive anal intercourse (RAI; or at least twice weekly in the e
235 e more likely to report condomless receptive anal sex in the prior 12 months (OR 2.44, 95% CI 2.05-2.
236  When adjusted for age, condomless receptive anal sex, depression, interpersonal stigma, law enforcem
237 eraction of gender with condomless receptive anal sex, the odds of HIV infection for transgender wome
238 teria for screening nor history of receptive anal sex was significantly associated with HSIL.
239 mary syphilis who did not practice receptive anal intercourse almost always (92%) had their primary s
240 mpared to MSM who did not practice receptive anal intercourse.
241 ard transmission.Men who practiced receptive anal intercourse (AI) were more likely to present with s
242 The finding that MSM who practiced receptive anal intercourse more commonly presented with secondary
243 ypothesized that MSM who practiced receptive anal intercourse were more likely to present with second
244 philis if they reported practicing receptive anal intercourse (adjusted odds ratio 3.90; P < .001) af
245  (24%) men reported not practicing receptive anal sex.
246 mary syphilis who did not practise receptive anal intercourse almost always (92%) had their primary s
247 mpared to MSM who did not practise receptive anal intercourse.
248 The finding that MSM who practised receptive anal intercourse more commonly presented with secondary
249 e sex with men (MSM) who practised receptive anal intercourse were more likely to present with second
250 philis if they reported practising receptive anal intercourse (adjusted odds ratio 3.90, p<0.001) aft
251  (24%) men reported not practising receptive anal sex.
252 ha diversity, which is linked with receptive anal intercourse in both males and females.
253 iation at high nadir CD4 counts might reduce anal high-risk HPV infection and anal cancer risk.
254 ciated with approximately 90% of HPV-related anal cancers.
255   This review summarizes clinically relevant anal sphincter anatomy, imaging methods, classification
256                                     Reported anal and oral sex (vs neither) was independently associa
257  = 185) of women had an indication (reported anal sex or symptoms), 72.5% (n = 689) did not have an i
258 ance of the initial infection; none reported anal sex.
259                                Self-reported anal sex and anal symptoms were independently associated
260       Testing on indication of self-reported anal sex or symptoms is used to manage anorectal Chlamyd
261                                    High-risk anal human papillomavirus (HPV) infection is prevalent a
262 onths (S2); APU samples every 6 months (S3); anal and pharyngeal (AP) samples every 6 months (S4); an
263                       For targeted secondary anal cancer prevention in high-risk groups, HIV-negative
264       Annually, providers collected separate anal swabs for HPV detection and cytopathologic examinat
265 ly those older than 45 years, have a similar anal cancer risk profile to that of HIV-positive women.
266 ic review and meta-analysis of type-specific anal HPV prevalence in men, compared according to sexual
267  screening programmes might help to stratify anal cancer risk, irrespective of HIV status.
268 at loperamide is equivalent to placebo, that anal exercises with biofeedback is equivalent to an educ
269 ere: 1 cm decrease in tumor height above the anal verge (OR = 1.290, 95% CI: 1.101,1.511); and an ASA
270 ctal cancer, with a median distance from the anal verge of 5.0 cm.
271  rectal adenocarcinoma within 12 cm from the anal verge, T3/4 and/or node positive, were randomly ass
272 e bulk of the lesion is below 15 cm from the anal verge, will be randomised between either a TAMIS or
273 astomotic height was 3.5 +/- 1.9 cm from the anal verge.
274  and the type-specific HPV viral load in the anal swabs was determined.
275 from in vitro cultures and injected into the anal pore of unfed uninfected Ixodes scapularis nymphal
276               Squamous cell carcinoma of the anal canal (SCCA) is a rare malignancy associated with i
277       Purpose Squamous cell carcinoma of the anal canal (SCCAC) is characterized by high locoregional
278 ge II/III rectal cancer, within 12 cm of the anal verge (T1-3, N0-2, M0) in patients who received neo
279 T3 rectal adenocarcinoma within 12 cm of the anal verge with no evidence of metastasis.
280 tained from high-risk patients, submitted to anal cancer screening from July 2016 to January 2017.
281                         To better understand anal cancer development and prevention, we determined wh
282             Treatment participants underwent anal biopsies of suspected new or recurrent HSILs.
283  behavior including frequency of unprotected anal intercourse, number of partners, and incidence of s
284  of participants reported recent unprotected anal intercourse.
285 m malformation, caudal regression, vertebral-anal-cardiac-tracheo-esophageal fistula-renal-limb (VACT
286 ble solid tumour (eligible tumour types were anal, biliary, cervical, endometrial, mesothelioma, neur
287 uited from a longitudinal study during which anal self-swabs and serum were collected at up to 5 bi-a
288                  ART was not associated with anal cancer incidence when adjusted for years living wit
289           DNA methylation is associated with anal carcinogenesis.
290 ly determinant independently associated with anal HSIL, both in general and by concordant, causative
291 HPV infections were strongly associated with anal HSIL, in general as well as for the concordant HPV
292          We assessed factors associated with anal precancer in HIV+ and at-risk HIV-negative women fr
293              Our results are consistent with anal cancer promotion by severe, prolonged HIV-induced i
294 V-positive MSM, 50 (26%) were diagnosed with anal HSIL.
295              Tissue samples of HIV+ men with anal cancer (n = 26), AIN3 (n = 24), AIN2 (n = 42), AIN1
296 a from women who underwent AC screening with anal cytology from April 2009 to July 2014 were analyzed
297 e was significantly higher from studies with anal cytopathology, suggesting population sampling effec
298                        Among 3255 women with anal cytohistopathology results, PRs were similarly calc
299 ng A-HSIL were >6 times higher in women with anal hrHPV (adjusted odds ratio [aOR], 6.08 [95% confide
300                       In HIV-negative women, anal HPV16 prevalence was 41% (447/1097) in cervical HPV

 
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