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1 ns targeting the vasculature in premalignant cervical dysplasia.
2 lear staining of beta-catenin in 18 cases of cervical dysplasia.
3 umerous HPV types, and frequently results in cervical dysplasia.
4 s also evidence for reduced gap junctions in cervical dysplasia.
5  may improve sensitivity in the detection of cervical dysplasia.
6 equired some form of destructive therapy for cervical dysplasia.
7  important early event in the development of cervical dysplasia.
8  was also found in a subset of 10 high-grade cervical dysplasias.
9 nts with invasive cervical cancer, 1361 with cervical dysplasia and 841 healthy controls.
10 uman papillomavirus infection and subsequent cervical dysplasia and a decrease in the abundance of La
11 human papillomavirus types and prevalence in cervical dysplasia and cancer in HIV-infected women sugg
12 wn to have diagnostic utility in identifying cervical dysplasia and carcinoma.
13 on of E7 caused the regression of high-grade cervical dysplasia and established cervical tumors, indi
14 critical role in development of precancerous cervical dysplasia and progression to invasive cervical
15 a potentially important marker of high-grade cervical dysplasia and squamous cell carcinoma (SCC).
16 included clinical sensitivity for high grade cervical dysplasia and usability.
17 screening was dependent on the prevalence of cervical dysplasia and/or HPV infection or vaccination i
18 F of most patients with untreated high-grade cervical dysplasia but disappeared if the dysplasia was
19 tion of persistent cervical infection and of cervical dysplasia by these major oncogenic types.
20                                   High-grade cervical dysplasia caused by human papillomavirus (HPV)
21 inated against HPV have a lower incidence of cervical dysplasia compared to unvaccinated women.
22 , chondrodysplasia punctata, coronal clefts, cervical dysplasia, congenital cataracts, profound postn
23 countries, up to 80% of women diagnosed with cervical dysplasia do not return for follow-up care, pri
24 genic HPV infection predicted progression of cervical dysplasia from normal to abnormal SIL (HR, 2.8;
25 ry of any anogenital cancer or treatment for cervical dysplasia, had no hysterectomy, and were not pr
26  human papillomavirus (QHPV) vaccine against cervical dysplasia has not been estimated using populati
27 umcision protecting against cervical cancer, cervical dysplasia, herpes simplex virus type 2, chlamyd
28  intracervical injections as a treatment for cervical dysplasia in low- and middle-income countries.
29 the school-based HPV immunization program on cervical dysplasia in women in British Columbia, Canada.
30 een and treat women for preinvasive disease, cervical dysplasia, is the key factor leading to the red
31 ts in lower risk of preterm birth given that cervical dysplasia itself is associated with higher risk
32 ubjects, at least 25% of HPV16(+) high-grade cervical dysplasia lesions undergo complete regression.
33 V) in the cervix, the proportion of cases of cervical dysplasia missed, or the false-negative rate, h
34 e (n = 31) without dysplasia, diagnosed with cervical dysplasia (n = 38), or newly diagnosed with inv
35 , and 7.4% of the methylprednisolone group), cervical dysplasia (seen in 11% of the cyclophosphamide
36  in these women suggests that the associated cervical dysplasia should be managed conservatively.
37 ent human papillomavirus (HPV) infection and cervical dysplasia than do HIV-uninfected women.
38 fectiveness (VE) of the QHPV vaccine against cervical dysplasia using data collected routinely in Man
39 shold of microvessel leakage associated with cervical dysplasia was <17 kDa and highlighted the poten
40 ical sensitivity for detection of high-grade cervical dysplasia was 95.8% (95% CI, 86.0%-98.8%; 46 of