European Journal of Obstetrics & Gynecology and Reproductive Biology
Plenary session 4 — screening for cervical cancer precursorsSpontaneous evolution of intraepithelial lesions according to the grade and type of the implicated human papillomavirus (HPV)
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Preventing cancer: The role of Papillomavirus vaccination in the general population
2020, Bulletin du CancerFluorescence microscopy of H&E stained cervical biopsies to assist the diagnosis and grading of CIN
2018, Pathology Research and PracticeCitation Excerpt :In addition to not being able to always predict the biologic behavior of CIN lesions, the histopathological classification of cervical biopsies is problematic. This occurs because the criteria for CIN diagnosis is subjective and has high inter and intra-observer variability [18,19]. A study by Stoler et al. showed that the concordance rate of diagnosing CIN1 was 38.2% between community pathologists and an expert panel of gynecological pathologists, while rate for CIN2 was 38% and CIN3 68% [20].
Antiviral activity of Ellagic acid and Annona Muricata in cervical HPV related pre-neoplastic lesions: A randomized trial
2017, Journal of Functional FoodsEstimation of the epidemiological burden of HPV-related anogenital cancers, precancerous lesions, and genital warts in women and men in Europe: Potential additional benefit of a nine-valent second generation HPV vaccine compared to first generation HPV vaccines
2015, Papillomavirus ResearchCitation Excerpt :By extrapolating these data to countries without or with less organized screening, we overestimated the detected burden in those countries. However these lesions do exist, even if not detected, and have a high potential to develop to cancer if not recognized and treated: 5% of CIN2 and more than 12% of CIN3 progress to invasive cancer [29]. Mc Credie et al. found that the cumulative 30 year incidence of invasive cancer in women with CIN3 was 30% and increased to 50% in women with persistent CIN3 [30].
SOX1 suppresses cell growth and invasion in cervical cancer
2013, Gynecologic OncologyCitation Excerpt :The E6 and E7 oncoproteins, encoded in high-risk HPV types, inactivate p53 and retinoblastoma (Rb) proteins and cause abnormal transformation [3]. However, HPV infection is necessary but is not enough to cause cervical cancer [4], and the molecular mechanisms underlying cervical carcinogenesis remain elusive. Genetic changes and epigenetic changes play important roles in the complex signaling pathways involved in cervical cancer development [5–10].
Structured Literature Review to Identify Human Papillomavirus’s Natural History Parameters for Dynamic Population Models of Vaccine Impacts
2024, Infectious Diseases and Therapy