ライフサイエンスコーパス: HPV

1 HPV (any type) was detected in 742 (71.8%) anal specimen

2 HPV could be inhibited by mitochondrial superoxide inhib

3 HPV E6 and E7 also enhanced the ability of HR proteins t

4 HPV E6 and E7 proteins suppress the levels of miR-424, a

5 HPV oncogene expression in the cervical epithelium elici

6 HPV replication factories formed in the nucleus are loca

7 HPV-16-specific CD8(+) T cell responses were significant

8 HPV-6 B1 variants prevalence was increased in GWs and ge

9 HPV-6 variants distribution differed between countries a

10 ts, type-specific concordance for at least 1 HPV type was found in only 35 (3.4%) participants.

11 ccine effectiveness for HPV types 16 and 18, HPV types 31, 33, and 45, other high-risk types, and any

12 determined based on 8 (6 HPV-positive and 2 HPV-negative) control samples.

13 es were seropositive for at least 1 of the 4 HPV types.

14 type assignment was determined based on 8 (6 HPV-positive and 2 HPV-negative) control samples.

15 eWGS identified 7 HPV types not included in the LA genotyping.

16 cal cancer, and risk behaviors for acquiring HPV.

17 In Africa, HPV 16 accounted for 13% of HPV-positive WHIV with norma

18 mory, suggesting possible protection against HPV vaccine types after a single dose of 4vHPV.

19 ropose that LKB1 acts as a safeguard against HPV-stimulated aerobic glycolysis and tumor progression.

20 ce in CIN2+ detection rate in LBC versus all HPV-screened women, with p = 0.62 between HPV screening

21 ifference in referral rate in LBC versus all HPV-screened women; p = 0.003 for difference in CIN2+ de

22 t high-risk genus human Alphapapillomavirus (HPV) infections cause nearly every cervical carcinoma an

23 Although HPV was detected in specimens from both anatomical sites

24 valence was also significantly reduced among HPV-16/18-vaccinated (4.1%) compared with unvaccinated s

25 Anal HPV is highly prevalent in women living with HIV, and ty

26 s, cervical/anal cytologic and cervical/anal HPV testing for 2 years.

27 At baseline, 75% had anal HPV, 51% had anal HR-HPV, 50% had cervical HPV, and 29%

28 We analyzed HPV DNA types detected in self-collected cervicovaginal

29 revalence (from ARTISTIC, PHE, Natsal-3) and HPV-related disease incidence (from National Cancer Regi

30 ing of all cervical screening (cytologic and HPV testing) and any cervical, vulvar, and vaginal histo

31 rence in referral rate between cytology- and HPV-screened women was not significant.

32 utes to cellular membrane depolarization and HPV.

33 of HPV integration in the human genome, and HPV-associated histone enrichment sites upstream of canc

34 L) who were triaged with tests for hrHPV and HPV 16/18 to find cervical intraepithelial neoplasia (gr

35 reated or estrogen-treated nontransgenic and HPV-transgenic mice.

36 Enhanced expression of MUC16, SIRPA and HPV-16-E7 protein was detectable in the circulating exos

37 ometric mean titers for anti-HPV-16 and anti-HPV-18.

38 tes and 3D/2D geometric mean titers for anti-HPV-16 and anti-HPV-18.

39 (excluding a decrease of 1.5 times) of anti-HPV 6, 11, 16, and 18 geometric mean titres (GMT).

40 , 33, and 45, other high-risk types, and any HPV were calculated using logistic regression.

41 The prevalence of any HPV genotype was 45.3% on the penis, 11.2% in the oral c

42 The overall prevalence of any HPV infection was 45.2% (95% confidence interval [CI], 4

43 Prevalence of any HPV was 12.5% in 14-19 year olds and was higher in older

44 The prevalence of any HPV was 42.2% (95% confidence interval [CI], 38.3%-46.1%

45 n papillomavirus 16/18 AS04-adjuvanted (AS04-HPV-16/18) vaccine schedules at months 0 and 6 (2D_M0,6)

46 The AS04-HPV-16/18 vaccine administered as a 2-dose schedule was

47 oproteins may be the best approach to assess HPV-disease for clinical outcome because it is associate

48 e role of HF keratinocyte stem cells in beta-HPV-induced skin carcinogenesis, we utilized a transgeni

49 Prevalence of beta-HPV varied by anatomic site of infection.

50 rated similar histology associated with beta-HPV reactivation and nuclear p63 expression within the H

51 ll HPV-screened women, with p = 0.62 between HPV screening groups).

52 28 days following a single dose of bivalent HPV vaccine (2vHPV; Cervarix, GlaxoSmithKline).

53 oses (at 0, 1, and 6 months) of the bivalent HPV vaccine were identified in the vaccination registrat

54 after vaccination suggests that the bivalent HPV-16/18 vaccine has protective efficacy in men.

55 ccine types 16, 18, 6, or 11 was compared by HPV vaccination status, as measured by self-reported rec

56 round of HPV screening, possibly dampened by HPV vaccine effect; in this study, although the point es

57 he extent of gene expression dysregulated by HPV E7-induced DNA methylation, we analyzed parallel glo

58 The impairment of HR by HPV oncogenes may be targeted for treatment of HPV(+) ma

59 causal HPV infections by age, stratified by HPV genotype (HPV16 vs. other HPV genotypes), and the di

60 R assay for the detection of 13 carcinogenic HPV types (the H13 assay; Hybribio, Hong Kong) that is m

61 we estimated the cumulative number of causal HPV infections by age, stratified by HPV genotype (HPV16

62 , 50% and 75% of women acquired their causal HPV infection by ages 20.6 (range: 20.1-21.1) and 30.6 (

63 he age at which women acquire their "causal" HPV infection that develops into cervical cancer is poor

64 l HPV, 51% had anal HR-HPV, 50% had cervical HPV, and 29% had cervical HR-HPV.

65 Conclusion HPV vaccination was associated with reduction in vaccine

66 Conclusion HPV vaccine initiation rates in cancer survivors are low

67 having cT1-2 N1-2b pathologically confirmed HPV-negative OPSCC in 2010 to 2012 were identified using

68 Correspondingly, HPV-infected cells heat-treated at 44 degrees C showed a

69 H13 is a lower-cost HPV DNA test that might be useful for primary screening

70 dominant negative inhibitor of E2-dependent HPV replication.

71 ulting from chromatin alterations that drive HPV-related tumorigenesis.

72 ibute to virus-induced immune evasion during HPV persistence.

73 stimates for referral rates in women in each HPV-screened group were 41%-44% higher than in cytology-

74 f cervical and head and neck cancers, enable HPV-positive cancer cells to escape from these regulator

75 At enrollment, HPV infection was detected in 54% of HIV-negative women,

76 We estimated HPV prevalence in the prevaccine (2003-2006) and vaccine

77 creases in proportion seropositive for every HPV type across all age groups, many statistically signi

78 To examine HPV-associated changes in the keratinocyte transcriptome

79 HIV status, the majority of couples exhibit HPV concordance over 2 years.

80 of RAD51 away from DSBs in cells expressing HPV E6 and E7 hinders HR through a distinct mechanism.

81 population-level impact in males from female HPV vaccination.

82 anging from 0.79 for HPV 33 down to 0.38 for HPV 56.

83 ormal ratios in Africa ranging from 0.79 for HPV 33 down to 0.38 for HPV 56.

84 20/1,992 (1.0% [95% CI 0.6%-1.5%]); and for HPV+DS triage, these were 79/2,008 (3.9% [95% CI 3.1%-4.

85 th England [PHE]) and fitting it to data for HPV prevalence (from ARTISTIC, PHE, Natsal-3) and HPV-re

86 Estimates of vaccine effectiveness for HPV types 16 and 18, HPV types 31, 33, and 45, other hig

87 for whether women had been age-eligible for HPV vaccination or not.

88 women </=33 years had been age-eligible for HPV vaccination, with 3-dose uptake across age cohorts b

89 en and to examine potential risk factors for HPV infection.

90 To evaluate the accuracy of genotyping for HPV types 16 and 18 and its utility as a second triage s

91 p16 is used as a surrogate marker for HPV infection.

92 ent of adsorption assays based on nfGNPs for HPV detection and cervical cancer prevention.

93 Samples positive for HPV-DNA were screened for viral oncoprotein expression u

94 scopy referral and CIN2+ detection rates for HPV-screened versus cytology-screened women in Australia

95 nctional relevance of superoxide release for HPV.

96 During the decades required for HPV-associated tumorigenesis, the cellular genome become

97 (0.1% [95% CI 0.0%-0.6%]), respectively; for HPV+LBC triage, these were 75/1,992 (3.8% [95% CI 3.0%-4

98 tudy shows a long-lasting increased risk for HPV-related carcinomas and premalignancies of the anogen

99 n CIN among cohorts partially vaccinated for HPV may be considered when clinical practice guidelines

100 Further, HPV E6 attenuates repair by causing RAD51 to be mislocal

101 prevalence among men with concurrent genital HPV infection was 4-fold greater (19.3%) than among thos

102 population prevalence data for male genital HPV infection is not well known, while the HPV vaccinati

103 The prevalence of genital HPV infection and the HPV vaccination coverage rate amon

104 To estimate the prevalence of genital HPV infection and the HPV vaccination rate in the United

105 The overall genital HPV infection prevalence was 45.2% (95% CI, 41.3%-49.3%)

106 .68-56.51) against cross-reactive genotypes (HPV 31, 33, 45), respectively.

107 Overall, our results suggest that high HPV prevalence and diversity can be explained by a combi

108 We have now determined how HPV oncogenes and estrogen treatment affect genome-wide

109 val [CI], 38.3%-46.1%) and of high-risk (HR) HPV was 23.4% (95% CI, 21.3%-25.6%).

110 Subsequently, all cases of high-risk (hr) HPV-associated high-grade lesions and carcinomas in the

111 Most anal HR-HPV types detected at 6 months (57%-93%) were persistent

112 baseline, 75% had anal HPV, 51% had anal HR-HPV, 50% had cervical HPV, and 29% had cervical HR-HPV.

113 0% had cervical HPV, and 29% had cervical HR-HPV.

114 er due to high-risk human papillomavirus (HR-HPV) is higher in women living with human immunodeficien

115 om UK patients for the presence of twelve HR-HPV types DNA using PCR and Sanger sequencing.

116 Data obtained showed the presence of HR-HPVs in 42% of breast tissues of which the viral activit

117 However, it is unclear if HPV status is of high value for cancers of the larynx an

118 ssist policy makers considering implementing HPV vaccination programs.

119 rtant function in HPV replication.IMPORTANCE HPV infections are an important driver of many epithelia

120 Analysis of ASE in HPV-related OPSCC identified multiple alterations likely

121 en Rint1 and E2 has an important function in HPV replication.IMPORTANCE HPV infections are an importa

122 omparisons revealed substantial increases in HPV vaccination during this time period, and more modest

123 l growth, and cell migration and invasion in HPV-transformed cells.

124 and A3G in a temperature-dependent manner in HPV-infected cells.

125 limited redundancy for NSD family members in HPV-negative HNSCCs and suggest a potential role for imp

126 wed accumulated G-to-A or C-to-T mutation in HPV E2 gene.

127 Our goal was to examine the role of p16 in HPV-related favorable treatment outcomes and to investig

128 on distinctly alters methylation patterns in HPV-associated cancer.

129 E7 are the primary transforming proteins in HPV that drive tumor progression.

130 hoc study, a highly significant reduction in HPV prevalence 4 years after vaccination suggests that t

131 NA that has been reported to be repressed in HPV-positive cancers of the cervix and oropharynx is miR

132 age repair, CHK1 and Wee1, are suppressed in HPV-positive cells, providing an explanation for why thi

133 anation for why this microRNA is targeted in HPV-positive cells.IMPORTANCE We describe here for the f

134 rgeting chromatin regulators is warranted in HPV-negative HNSCCs driven by aberrant H3K36 methylation

135 demonstrated, that this is due to increasing HPV prevalence in the unvaccinated population.

136 Because intratumoral HPV oncoproteins upregulate immune checkpoint proteins s

137 The findings suggest that lower HPV seroprevalence in older US women primarily reflects

138 FGFR3 depletion in cell lines that maintain HPV-31 episomes increased viral copy number.

139 The test set was chosen to include many HPV-positive specimens.

140 sitive tumors, many recurrent and metastatic HPV-positive tumors exhibited a molecular profile more s

141 w Mexico Administrative Code, the New Mexico HPV Pap Registry, a statewide public health surveillance

142 After the onset of mitosis, HPV-harboring transport vesicles bud from the TGN, follo

143 ibes the inhibition of infection of multiple HPV types, including oncogenic types, by treatment with

144 Although new HPV infections and precancers can occur throughout a wom

145 We used a novel HPV whole-genome sequencing technique to evaluate an exc

146 genome deregulation in the genesis of 13% of HPV-negative HNSCCs.

147 In Africa, HPV 16 accounted for 13% of HPV-positive WHIV with normal cytological findings, but

148 (95% confidence interval [CI], 6.3-21.9%) of HPV DNA detections in genital samples were attributable

149 cost-effective way of reducing the burden of HPV-related disease in MSM.

150 ous and immunotherapy-directed clearances of HPV-related disease.IMPORTANCE High-risk-type human papi

151 For detection of HPV types, a Roche Linear Array test was performed.

152 vasive assisting technology for diagnosis of HPV-associated malignancies, especially, at primary heal

153 monstrates evidence of high effectiveness of HPV prophylactic vaccines at an individual level, suppor

154 f interest was the age-adjusted incidence of HPV-related cancer (both cervical and non-cervical) in a

155 a pre-existing disparity in the incidence of HPV-related cancer by ethnicity, partly due to herd immu

156 The incidence of HPV-related oropharyngeal squamous cell carcinoma (OPSCC

157 Viral integration of HPV into the host genome is not required for the viral l

158 Our study suggests that the introduction of HPV vaccination in England will initially widen a pre-ex

159 ctors for miR-424 reduced both the levels of HPV genomes in undifferentiated cells and amplification

160 pression in the cervical microenvironment of HPV-transgenic mice compared with nontransgenic mice.

161 We developed an individual-based model of HPV transmission and disease, parameterising it with the

162 ify high-risk groups for broad monitoring of HPV-associated cancers in resource-constrained settings.

163 Endpoints included noninferiority of HPV-16/18 antibodies for 2D_M0,6 versus 3D_M0,1,6; 2D_M0

164 regression was used to estimate the odds of HPV infection.

165 The prevalence of HPV among other demographic groups and other anatomic si

166 ogram has had an impact on the prevalence of HPV types 6, 11, 16, and 18 among males.

167 morbidities; we estimated the prevalence of HPV vaccine initiation in cancer survivors versus the US

168 complementary strategy for the prevention of HPV-related diseases, especially since tender negotiatio

169 A substantial proportion of HPV DNA detections may be depositions due to recent unpr

170 itical role for miR-424 in the regulation of HPV replication.

171 nlikely to occur through the Y102 residue of HPV E2.IMPORTANCE The papillomavirus (PV) is a double-st

172 To determine the role of HPV in the regional perfusion redistribution in bronchoc

173 are important gaps in evidencing the role of HPV persistence in the invasiveness of BC.

174 To explore the role of HPV tumor status among women and nonwhites with OPSCC an

175 poscopy referral rates in the first round of HPV screening, possibly dampened by HPV vaccine effect;

176 The pooled sensitivity of HPV 16/18 genotyping for CIN3+ was about 70% for women w

177 specific gene expression variation, sites of HPV integration in the human genome, and HPV-associated

178 V oncogenes may be targeted for treatment of HPV(+) malignancies.

179 Studies evaluating the presence of HPVs in breast cancer (BC) have generated considerable c

180 nd 134 (56%) were positive for any oncogenic HPV type (ISH+).

181 otection as much as women from a female-only HPV vaccination program with high coverage.

182 erosexual males in settings with female-only HPV vaccination.

183 Oral HPV infection with vaccine types 16, 18, 6, or 11 was co

184 Oral HPV prevalence among men with concurrent genital HPV inf

185 observed association between penile and oral HPV infections.

186 The predicted probability of high-risk oral HPV infection was greatest among black participants, tho

187 sociated with reduction in vaccine-type oral HPV prevalence among young US adults.

188 he Myc protein and, in contrast to all other HPV-positive cervical cancer cell lines, they harbored a

189 1.31-5.96), whereas the prevalence of other HPV types was significantly higher only between ages 20-

190 stratified by HPV genotype (HPV16 vs. other HPV genotypes), and the direct age-specific reduction in

191 Overall HPV DNA prevalence was also significantly reduced among

192 Overall HPV prevalence increased with increasing age: the preval

193 k cancers positive for human papillomavirus (HPV) are exquisitely radiosensitive.

194 Methylation of the human papillomavirus (HPV) DNA has been proposed as a novel biomarker.

195 s in the prevalence of human papillomavirus (HPV) genotypes 6, 11, 16, and 18 in women and girls aged

196 stituted funded female human papillomavirus (HPV) immunization in 2007, followed by a targeted male v

197 alence data on genital human papillomavirus (HPV) in males in the United States, using findings from

198 nce risk of persistent Human Papillomavirus (HPV) infection and cervical carcinogenesis.

199 Human papillomavirus (HPV) infection distinctly alters methylation patterns in

200 Human Papillomavirus (HPV) infection has been recognized as the main etiologic

201 Human Papillomavirus (HPV) infection involves multiple steps, from cell attach

202 Although new human papillomavirus (HPV) infections can occur at all ages, the age at which

203 The human papillomavirus (HPV) replication cycle is tightly linked to epithelial c

204 land, UK, will change: human papillomavirus (HPV) screening will be the primary test for cervical can

205 logy-based measures of human papillomavirus (HPV) status are routinely obtained in the care of head a

206 (PD-L1) expression and human papillomavirus (HPV) status.

207 st-treatment high-risk human papillomavirus (HPV) testing.

208 ve and easy-to-perform human papillomavirus (HPV) tests are needed for primary cervical cancer screen

209 outine vaccination for human papillomavirus (HPV) types 16 and 18, targeted at 12-13-year-old girls,

210 cinogenic potential of human papillomavirus (HPV) types among women infected with human immunodeficie

211 e designed a universal human papillomavirus (HPV) typing assay based on target enrichment and whole-g

212 Human papillomavirus (HPV) vaccination is still not reaching many high-risk po

213 Uptake of human papillomavirus (HPV) vaccine among girls in the Dutch immunization progr

214 Human papillomavirus (HPV) vaccine was recommended in 2006 for routine vaccina

215 prophylactic bivalent human papillomavirus (HPV) vaccine.

216 reated DCs pulsed with human papillomavirus (HPV)-16 E6/E7 peptides significantly inhibited the tumor

217 gammadelta T cells in human papillomavirus (HPV)-associated uterine cervical SCC, the third-leading

218 y of cancers including human papillomavirus (HPV)-caused cervical cancer.

219 icantly upregulated in human papillomavirus (HPV)-infected cell lines and tissues.

220 Human papillomavirus (HPV)-negative oropharyngeal squamous cell carcinoma (OPS

221 Patients with human papillomavirus (HPV)-positive head and neck squamous cell carcinoma (HNS

222 Compared to primary human papillomavirus (HPV)-positive tumors, many recurrent and metastatic HPV-

223 determine the risk of human papillomavirus (HPV)-related carcinomas and premalignancies in women dia

224 s are at high risk for human papillomavirus (HPV)-related morbidities; we estimated the prevalence of

225 Human papillomaviruses (HPV) replicate their genomes in differentiating epitheli

226 tions with high-risk human papillomaviruses (HPVs) are a major cause of anogenital and oropharyngeal

227 Oncogenic human papillomaviruses (HPVs) are closely linked to major human malignancies, in

228 Infection by human papillomaviruses (HPVs) has been implicated in the aetiology of a variety

229 on Survey and had results of oral and penile HPV DNA testing were examined.

230 ve was to determine the prevalence of penile HPV infection in the United States.

231 estimate the population prevalence of penile HPV infection.

232 Our findings indicate that penile HPV is common among men in the United States.

233 In the development of cancer, persistent HPV infections induce E6 and E7 oncoproteins, which prom

234 Since preventative HPV vaccines have not been widely used in many countries

235 quadrivalent vaccine (4vHPV), which prevents HPV-6, -11, -16, and -18 infection.

236 Introduction of primary HPV screening from 2019 could reduce age-standardised ra

237 Prophylactic HPV vaccine is available for primary prevention.

238 Quadrivalent HPV vaccination during pregnancy was not associated with

239 Quadrivalent HPV vaccination of MSM via GUM clinics is likely to be a

240 with zero, 1, 2, or 3 doses of quadrivalent HPV vaccine (4vHPV; Gardasil, Merck) 6 years previously.

241 revealed that the prevalence of quadrivalent HPV vaccine types (4vHPV), types 6, 11, 16, and 18, was

242 ist regarding the safety of the quadrivalent HPV vaccine in this context.

243 tched analyses, exposure to the quadrivalent HPV vaccine was not associated with significantly higher

244 CCs after the first dose of the quadrivalent HPV vaccine.

245 enografts from human papillomavirus-related (HPV(+)) head and neck squamous cell carcinoma (HNSCC) sa

246 ociation of ART with prevalence of high-risk HPV (6537 women living with HIV) and high grade cervical

247 genetic downregulation of HLA-E by high-risk HPV E7 may contribute to virus-induced immune evasion du

248 By contrast, the prevalence of high-risk HPV genotypes other than 16 and 18 remained the same acr

249 al sex partners, the prevalence of high-risk HPV infection was 22.2% (CI, 9.6% to 34.8%).

250 Our studies demonstrate that high-risk HPV oncogenes profoundly reprogram the tumor microenviro

251 ociation of ART with prevalence of high-risk HPV or prevalence, incidence, progression, or regression

252 on excisional treatment; however, high-risk HPV post-treatment predicts treatment failure more accur

253 A negative high-risk HPV test post treatment was associated with a risk of CI

254 HIV on ART had lower prevalence of high-risk HPV than did those not on ART (adjusted odds ratio [aOR]

255 rature review and meta-analysis of high-risk HPV-type distribution in 19883 HIV-positive women was pe

256 ersus cytology-screened women in Australia's HPV-vaccinated population (by 2014, resident women </=33

257 xual orientation, with the exception of some HPV- and HIV-associated cancers.

258 Y chromosome DNA predicted type-specific HPV concordance in univariate analyses, but in multivari

259 It is widely assumed that HPV-positive cancer cells are under selection pressure t

260 We have recently reported that HPV E7-dependent promoter hypermethylation leads to down

261 We show that HPV E6 and E7 allow HR to initiate at an inappropriate p

262 The HPV life cycle is tightly regulated and intimately linke

263 prevalence of genital HPV infection and the HPV vaccination coverage rate among adult men.

264 prevalence of genital HPV infection and the HPV vaccination rate in the United States among adult me

265 rom males aged 14-59 years, we estimated the HPV DNA prevalence and prevalence ratios (PRs) with resp

266 ssigned to and 2,008 analysed (99.8%) in the HPV+DS triage group.

267 ssigned to and 1,992 analysed (99.8%) in the HPV+LBC triage group; and 2,012 assigned to and 2,008 an

268 Among vaccine-eligible men, the HPV vaccination coverage was 10.7% (95% CI, 7.8%-14.6%).

269 reported receipt of at least one dose of the HPV vaccine.

270 is of RNA transcripts detected fusion of the HPV/Myc genes, arising from apparent microhomologous rec

271 We show that the HPV E2 protein targets Rad50-interacting protein 1 (Rint

272 f blood vessels in the dermis underlying the HPV-induced lesions.

273 l HPV infection is not well known, while the HPV vaccination coverage is low in the United States.

274 e intervals for the risk of GWs according to HPV-6 variants were calculated.

275 ed mitotic defects that likely contribute to HPV-mediated cancer progression.

276 plasia grade 2/3, vaginal cancer) related to HPV 31, 33, 45, 52, and 58 and non-inferiority (excludin

277 vical, vulvar and vaginal disease related to HPV 31, 33, 45, 52, and 58 was 0.5 cases per 10 000 pers

278 milar immunogenicity profile with respect to HPV 6, 11, 16, and 18.

279 xhibited a molecular profile more similar to HPV-negative tumors, including enriched frequencies of T

280 ars were 20.0% higher in those who underwent HPV testing, resulting in more CIN2+ and CIN3+ detection

281 e clinically-relevant human papilloma virus (HPV) 16 E7 oncoprotein induces cytotoxicity against pept

282 r among patients with human papilloma virus (HPV)-positive tumors.

283 pathogenic strains of human papilloma virus (HPV).

284 ence interval [CI] = 90.22-98.32) against VT HPV and 38.37% (95% CI = 12.68-56.51) against cross-reac

285 be observed at the cancer stage (SCC), where HPV oncoproteins are highly expressed, supporting the cl

286 both transient and persistent DSBs, whereas HPV E7 is only capable of impairing RAD51 localization t

287 We assessed whether HPV L1 gene methylation can predict the presence of high

288 rvations illuminate important means by which HPVs can cause cancer through alterations in the tumor m

289 relatively poor prognosis in comparison with HPV-positive disease, with decreased locoregional contro

290 Among couples with HPV results at all visits, >/=1 of the same genotypes we

291 chemotherapy (IC) could select patients with HPV-associated OPSCC for reduced radiation dose as a mea

292 urther study in favorable-risk patients with HPV-associated OPSCC.

293 overall survival rates than do patients with HPV-negative HNSCC, but the mechanisms underlying this p

294 onal study, OS was similar for patients with HPV-negative OPSCC when treated with primary surgery vs

295 sociated with poor survival in patients with HPV-positive HNSCC.

296 N3+ detection was much shorter in those with HPV testing vs those without testing (median, 103 vs 393

297 lesions were detected in 2.49% of women with HPV testing vs 2.15% of women without HPV testing (P = .

298 grade 1 was detected in 11.6% of women with HPV testing vs 6.6% without testing (relative risk, 1.76

299 n with HPV testing vs 2.15% of women without HPV testing (P = .23).

300 e necessary for cellular transformation, yet HPV integration is frequently reported in cervical and h