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1 to influence the likelihood of conversion to cervical cancer.
2 al hysterectomy in patients with early stage cervical cancer.
3 mavirus (HPV) infections cause most cases of cervical cancer.
4 cervical intraepithelial neoplasia (CIN), or cervical cancer.
5 h HIV have a significantly increased risk of cervical cancer.
6 incidence rates (ASIRs) of HIV-attributable cervical cancer.
7 squamous intraepithelial lesions (HSIL) and cervical cancer.
8 ict the future incidence rates and burden of cervical cancer.
9 anti-cancerous properties of ormeloxifene in cervical cancer.
10 neoplasias (CINs) need be treated to prevent cervical cancer.
11 women, who are at a known, increased risk of cervical cancer.
12 1 months to not reached) among patients with cervical cancer.
13 umour activity against recurrent or advanced cervical cancer.
14 gy and Obstetrics staging system for uterine cervical cancer.
15 reatment, cure and prevention of HPV related cervical cancer.
16 PV) is a prerequisite for the development of cervical cancer.
17 her oncogenic types, the causative agents of cervical cancer.
18 ninvasive methods for the early detection of cervical cancer.
19 igh-risk human papillomavirus (hrHPV) causes cervical cancer.
20 linical trial of the secondary prevention of cervical cancer.
21 es (HPVs) are implicated in the aetiology of cervical cancer.
22 lated PAX1 associated with poor prognosis in cervical cancer.
23 ressor genes, is an important risk factor in cervical cancer.
24 extremely rare and aggressive neuroendocrine cervical cancer.
25 ts from the cohort of patients with advanced cervical cancer.
26 lity of antiangiogenesis therapy in advanced cervical cancer.
27 port of having ever had a screening test for cervical cancer.
28 (HPV) screening will be the primary test for cervical cancer.
29 including human papillomavirus (HPV)-caused cervical cancer.
30 preservation of women treated surgically for cervical cancer.
31 l hysterectomy for patients with early stage cervical cancer.
32 ng the association between HIV infection and cervical cancer.
33 of hypoxia levels in patients with tumors of cervical cancer.
34 d cancer registries to estimate incidence of cervical cancer.
35 omaviruses (HPV) are the causative agents of cervical cancer.
36 t a novel therapeutic target for HPV-induced cervical cancer.
37 However, not all infected women develop cervical cancer.
38 and treatment for pre-invasive and invasive cervical cancer.
39 NCT02285192) in 23 patients with uterine or cervical cancer.
40 ting dysregulation of these two microRNAs in cervical cancer.
41 women aged 20-29 years who were screened for cervical cancer.
42 forms of HPV16, the cause of the majority of cervical cancers.
43 were breast (33.3%), urothelial (12.5%), and cervical cancer (10.4%).Grade 3 adverse events were cons
45 east cancer, 10.2 (8.0-12.4) in survivors of cervical cancer, 18.9 (16.6-21.1) in survivors of testic
46 st cancer, 15.8% (14.8-16.7) in survivors of cervical cancer, 20.2% (18.9-21.5) in survivors of testi
50 cancer survival, we estimated stage-specific cervical cancer 5-year net survival in 200 countries and
51 y of care could substantially improve global cervical cancer 5-year net survival, with quality of car
53 rica, 63.8% (95% CI 58.9-68.1) of women with cervical cancer (9200 new cases, 95% CI 8500-9800) were
54 ncluding self-sampling-has potential to make cervical cancer a rare disease in the decades to come.
55 f human papillomavirus-associated metastatic cervical cancer after tumor-infiltrating adoptive T cell
58 evalence in abnormal cytology (from ASCUS to cervical cancer) among Mexican women which were undergoi
59 distant metastasis was 13.7% (21 of 153) for cervical cancer and 11.8% (24 of 203) for endometrial ca
60 e rates were 26.3% (95% CI, 9.1 to 51.2) for cervical cancer and 20.0% (95% CI, 0.5 to 71.6) for vagi
62 k stratification of women when screening for cervical cancer and inform HPV vaccination strategies.
63 her odds of pancreatic, kidney, uterine, and cervical cancer and lower odds of esophageal cancer and
64 Benefits increased with advanced stage of cervical cancer and more efficient scale up of radiother
65 elial neoplasia of grade 2 or 3 and cases of cervical cancer and noncervical HPV-associated cancer by
66 elial neoplasia of grade 2 or 3 and cases of cervical cancer and noncervical HPV-associated cancer by
67 est for gliomas and sarcomas and highest for cervical cancer and oropharyngeal head and neck cancer.
69 on of women living with HIV among women with cervical cancer and population attributable fractions an
71 than half a million women are diagnosed with cervical cancer and the disease results in over 300 000
73 l immunisation, and screening for breast and cervical cancers) and four treatment indicators (skilled
74 a 2+ [CIN2+]) is an effective way to prevent cervical cancer, and recommendations exist for the monit
75 ccination coverage, changes in screening for cervical cancer, and risk behaviors for acquiring HPV.
76 or advanced HPV-positive (HPV-16 or HPV-18) cervical cancer, and who had progressed after available
82 study aimed to assess the existing burden of cervical cancer as a baseline from which to assess the e
84 ng, and treatment interventions to eliminate cervical cancer as a public health problem during the 21
85 loping a global strategy towards eliminating cervical cancer as a public health problem, which propos
88 isk human papillomaviruses (HR-HPVs) promote cervical cancer as well as a subset of anogenital and he
89 2019 could reduce age-standardised rates of cervical cancer at ages 25-64 years by 19%, from 15.1 in
91 nce were performed on 30 women with advanced cervical cancers at three time points (within 2 weeks be
93 wanted to examine whether IPSA could improve cervical cancer brachytherapy plans giving D90 < 6 Gy (w
96 d updates to demography, disability weights, cervical cancer burden estimates resulted in a 26% incre
97 obal Burden of Disease (GBD) 2017 study, and cervical cancer burden from the Global Cancer Incidence,
98 Africa, where a substantial HIV-attributable cervical cancer burden has added to the existing cervica
99 hods for demography, disability weights, and cervical cancer burden, and generated revised estimates
104 Although current methods of treatment for cervical cancer can ablate lesions, preventing metastati
106 nt thresholds, and to estimate the number of cervical cancer cases averted on the path to elimination
107 tion and screening coverage on the number of cervical cancer cases averted over the 50 years from 202
108 e potential to avert up to 12.5-13.4 million cervical cancer cases by 2069, and could achieve average
109 er intervention, there would be 44.4 million cervical cancer cases diagnosed globally over the period
111 Health impact was presented in terms of cervical cancer cases, deaths, or disability-adjusted li
113 to prevent 1 anogential warts (AGW) case or cervical cancer (CC) was similar for routine + catch-up
115 l line (Human Dermal Fibroblasts, HDF) and a cervical cancer cell line (HeLa), as a function of time
117 r loss of expression of the two microRNAs in cervical cancer cell lines and primary tumors, indicatin
118 cidates its possible mechanisms of action on cervical cancer cell lines CaSki and HeLa positive for H
119 1 was found overexpressed in HPV-16 positive cervical cancer cell lines in an HPV-16 E6-dependent man
120 hsa-miR-34a or hsa-miR-449a in HeLa and SiHa cervical cancer cell lines resulted in DNA damage respon
121 n and, in contrast to all other HPV-positive cervical cancer cell lines, they harbored a gain-of-func
124 of human cervical cancer cells in vitro and cervical cancer cell xenograft in vivo in nude mice, and
126 ormeloxifene induces radio-sensitization in cervical cancer cells and caused potent tumor growth inh
127 next-generation sequencing (NGS) analysis of cervical cancer cells and their EVs compared with cervic
128 sing MKN-45 gastric or FOLR1-expressing HeLa cervical cancer cells confirmed noninterference of the a
131 nergistically to inhibit the growth of human cervical cancer cells in vitro and cervical cancer cell
132 ted tumorigenic and metastatic properties of cervical cancer cells via arresting cell cycle at G1-S t
138 s, with male circumcision protecting against cervical cancer, cervical dysplasia, herpes simplex viru
142 a point-of-care test and treat programme for cervical cancer control in Papua New Guinea, improving t
144 Australia, Centre for Research Excellence in Cervical Cancer Control, Canadian Institute of Health Re
146 een HPV vaccination and the risk of invasive cervical cancer, controlling for age at follow-up, calen
148 umans study of PLG in women with uterine and cervical cancer demonstrates its feasibility and its abi
151 an papillomaviruses (HPV) cause over 500 000 cervical cancers each year, most of which occur in low-r
152 present study aimed to investigate the anti-cervical cancer effects of metformin, a first-line thera
153 PV vaccination coverage of girls can lead to cervical cancer elimination in most LMICs by the end of
156 n regions in which all countries can achieve cervical cancer elimination with girls-only vaccination,
159 vical specimens from the Study to Understand Cervical Cancer Endpoints and Early Determinants (SUCCEE
160 pelvic examination for conditions other than cervical cancer, gonorrhea, and chlamydia, for which the
161 r any gynecologic cancer or condition except cervical cancer, gonorrhea, and chlamydia, which are cov
162 mavirus (HPV) infection is the main cause of cervical cancer has resulted in the development of proph
163 that dispose certain individuals to develop cervical cancer has the potential to enable the developm
164 any malignancies, including locally advanced cervical cancer, head and neck cancer, and lung cancer.
168 eductions and will be necessary to eliminate cervical cancer in countries with the highest burden.
169 In the next 25 years, the epidemiology of cervical cancer in England, UK, will change: human papil
170 logy, with a prevalence of 44% [101/228] for cervical cancer in HIV-negative women (PR vs normal cyto
171 tion in the rate of premature mortality from cervical cancer in LMICs is possible, contributing to th
172 We estimated age-specific absolute risks of cervical cancer in the absence of screening (derived fro
173 than 44 million women will be diagnosed with cervical cancer in the next 50 years if primary and seco
174 rnal-beam radiotherapy and brachytherapy for cervical cancer in upper-middle-income, lower-middle-inc
175 omavirus 58 (HPV58) is found in 10 to 18% of cervical cancers in East Asia but is rather uncommon els
177 ot yet been defined, but an absolute rate of cervical cancer incidence could be chosen for such a thr
178 2020 onwards would result in average annual cervical cancer incidence declining to less than six new
180 dicted to reduce the median age-standardised cervical cancer incidence in LMICs from 19.8 (range 19.4
181 cer cases by 2069, and could achieve average cervical cancer incidence of around four per 100 000 wom
182 ds examined were an average age-standardised cervical cancer incidence of four or fewer cases per 100
183 predefined criteria, projected reductions in cervical cancer incidence over time in 78 LMICs for thre
185 ge, vaccination yielded a 22.9% reduction in cervical cancer incidence, with 38.4 million requiring e
186 ancer-specific mortality among patients with cervical cancer, independent of tumor characteristics an
187 standardised incidence and mortality rate of cervical cancer, indirectly standardised incidence ratio
188 wever, the significance of LKB1 mutations in cervical cancer initiation and progress has not been exa
191 asts increased IL23 production in cocultured cervical cancer-instructed mDCs, which mediated subseque
194 ir "causal" HPV infection that develops into cervical cancer is poorly understood and practically uno
200 0.71]; I(2)=97.58% and no publication bias), cervical cancer (k=23; 0.89 [0.84-0.95]; I(2)=98.47% and
201 lness, 1 023 288 in the general population), cervical cancer (k=29; 295 688 with mental illness, 3 54
202 ication among patients with locally advanced cervical cancer (LACC) and paraaortic lymph node (PALN)
203 treatment of patients with locally advanced cervical cancer (LACC), 40% of patients present with dis
204 f hsa-miR-34a and hsa-miR-449a expression in cervical cancer leads to overexpression of PACS-1 and su
206 for their anticancer activity against HeLa (cervical cancer), MCF-7 (breast cancer), HL-60 (Human pr
207 n of the Th17-promoting cytokine IL23 in the cervical cancer micromilieu and found CD83(+) mature den
208 , our study defines a mechanism by which the cervical cancer micromilieu supports IL23-mediated Th17
209 the 90-70-90 triple-intervention targets on cervical cancer mortality and deaths averted over the ne
210 of the WHO elimination strategy would reduce cervical cancer mortality by almost 99% and save more th
211 Reductions in age-standardised rates of cervical cancer mortality in 78 low-income and lower-mid
213 ccination alone would have minimal impact on cervical cancer mortality, leading to a 0.1% (0.1-0.5) r
219 cal cancer cells and their EVs compared with cervical cancer patient plasma EV-derived small RNAs, we
222 utcomes and circulating neutrophil counts in cervical cancer patients treated with definitive chemora
223 rotein mixtures extracted from the tissue of cervical cancer patients was also utilized to validate t
224 programmed death ligand 1-positive advanced cervical cancer, pembrolizumab demonstrated antitumor ac
225 ess around the time of diagnosis of invasive cervical cancer places patients at a higher risk of canc
226 regional collaborative approaches, enhancing cervical cancer prevention, improving cancer surveillanc
227 e impact of potential scale-up scenarios for cervical cancer prevention, in order to predict the futu
231 2070 to identify the earliest years by which cervical cancer rates could drop below two absolute leve
233 gement in HIV clinics, especially for KS and cervical cancer, remain important priorities in the curr
234 n screening and development of HPV vaccines, cervical cancer remains one of the deadliest malignancie
238 of 1848 Slovenian women attended 2 rounds of cervical cancer screening 3 years apart and provided dat
239 in the self-reported lifetime prevalence of cervical cancer screening among countries within regions
240 s time period, and more modest reductions in cervical cancer screening and sexual risk behaviors.
242 sting may be a promising approach to improve cervical cancer screening coverage, especially among wom
247 However, evidence on prevalence levels of cervical cancer screening in low- and middle-income coun
248 en and treat is the recommended approach for cervical cancer screening in low-resource settings, but
249 lomavirus (HPV) tests are needed for primary cervical cancer screening in lower-resource regions.
250 ong Mexican women which were undergoing from cervical cancer screening in the Salud Digna clinics in
252 tential use of DNA methylation detection, in cervical cancer screening or triage of mildly abnormal c
257 tion of the cervix with acetic acid (VIA) as cervical cancer screening strategy in resource-poor sett
263 r patients with pancreatic, renal, lung, and cervical cancers showed that high-level expression of MC
265 frequently among survivors of breast cancer, cervical cancer, testicular cancer, and Hodgkin lymphoma
266 survived at least 30 years from diagnosis of cervical cancer, testicular cancer, Hodgkin lymphoma in
267 sion, which was demonstrated to be higher in cervical cancer than the normal surrounding tissue.
268 xually transmitted infection associated with cervical cancer that frequently occurs as a coinfection
269 3H-AS1 was also found to be altered in human cervical cancer tissues and high expression of this lncR
271 IV prevalence and GLOBOCAN 2018 estimates of cervical cancer to calculate the proportion of women liv
272 erties that are associated with HPV-positive cervical cancer transformed cells such as rapid growth a
276 The estimated age-standardised incidence of cervical cancer was 13.1 per 100 000 women globally and
278 Globally, the average age at diagnosis of cervical cancer was 53 years, ranging from 44 years (Van
280 ol mice treated with 17beta-estradiol alone, cervical cancer was absent in the MPA-treated mice.
283 umab for patients with recurrent or advanced cervical cancer was safe and treatment-related adverse e
286 model that simulates the natural history of cervical cancer, we estimated the cumulative number of c
289 n many forms of cancer, including breast and cervical cancers, were significantly increased during th
290 rogrammes have been successful for colon and cervical cancers, where subsequent surgical removal of p
291 ents an alternative therapeutic modality for cervical cancer which may have rapid clinical translatio
292 over time in HPV16 infections progressing to cervical cancer, which could influence risk stratificati
293 se was observed in a patient with metastatic cervical cancer who received 2.7 x 10(9) cells (ongoing
294 ients with recurrent or advanced, inoperable cervical cancer, who were aged 18 years or older with Ea
295 ancers, we describe the burden of breast and cervical cancer, with an emphasis on global and regional
296 for the treatment of recurrent or metastatic cervical cancer, with an overall response rate of 14.3%.
297 is developing a global strategy to eliminate cervical cancer, with goals for screening prevalence amo
298 a statistical analysis of existing trends in cervical cancer worldwide using high-quality cancer regi
300 d we assumed that 50% of women with invasive cervical cancer would receive appropriate surgery, radio