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The review highlights likely cellular origins at the squamocolumnar junction, HPV-type dependent progression patterns, and the role of human immune responses in both progression and regression, and summarizes mechanisms, CIN management, and current 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\n[https://doi.org/10.1007/s10147-023-02337-7](https://doi.org/10.1007/s10147-023-02337-7)  \nCarcinogenesis and management of human papillomavirus‑associated cervical cancer  \nMisako Kusakabe1 · Ayumi Taguchi1,2 · Kenbun Sone1 · Mayuyo Mori1 · Yutaka Osuga1  \nReceived: 1 March 2023 / Accepted: 1 April 2023 / Published online: 9 June 2023 © The Author(s) 2023  \nAbstract  \nApproximately 95% of cervical cancer are caused by human papillomavirus (HPV) infection. Although it is estimated that HPV-associated cervical cancer will decrease with the widespread use of HPV vaccine, it may take time for HPV-associated cervical cancer to be eliminated. For the appropriate management of HPV-associated cervical cancer, it is important to understand the detailed mechanisms of cervical cancer development. First, the cellular origin of most cervical cancers is thought to be cells in the squamocolumnar junction (SCJ) of the uterine cervix. Therefore, it is important to understand the characteristics of SCJ for cervical cancer screening and treatment. Second, cervical cancer is caused by high risk HPV (HRHPV) infection, however, the manner of progression to cervical cancer differs depending on the type of HR-HPV: HPV16 is characterized by a stepwise carcinogenesis, HPV18 is difficult to detect in precancerous lesions, and HPV52, 58 tends to remain in the state of cervical intraepithelial neoplasia (CIN) . Third, in addition to the type of HPV, the involvement of the human immune response is also important in the progression and regression of cervical cancer. In this review, we demonstrate the carcinogenesis mechanism of HPV-associated cervical cancer, management of CIN, and the current treatment of CIN and cervical cancer.  \nKeywords Human papillomavirus · Cervical cancer · Squamocolumnar junction  \nAbbreviations  \nCIN Cervical intraepithelial neoplasia  \nCGP Cancer genome profiling  \nHLA Human leukocyte antigen  \nHR-HPV High risk human papillomavirus  \nHSIL High-grade squamous intraepithelial lesion IFN Interferon  \nIRF Interferon regulatory factor  \nMHLW The Ministry of Health, Labor and Welfare NKT Natural killer T  \nSCJ Squamocolumnar junction  \nTAM Tumor-associated macrophages  \nMisako Kusakabe and Ayumi Taguchi contributed equally.  \n* Ayumi Taguchi [TAGUCHIA-GYN@h.u-tokyo.ac.jp](TAGUCHIA-GYN@h.u-tokyo.ac.jp)  \n1 Department of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655, Japan  \n2 Laboratory of Human Single Cell Immunology, World Premier International Immunology Frontier Research Center (WPI-IFReC), Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan  \nTIL Tumor-infiltrating lymphocyte  \nTLR Toll-like receptors  \nTreg Regulatory T cells  \nTZ Transformation zone  \nEpidemiology of cervical cancer  \nand the introduction of HPV vaccination  \nHuman papillomavirus (HPV) infection is the main cause of cervical cancer. Despite the recent introduction of an HPV vaccination, cervical cancer remains the fourth most commonly diagnosed cancer among women worldwide and the fourth leading cause of cancer-related death [1] . Approximately 10,000 patients were newly diagnosed with cervical cancer in 2019 in Japan, and the number is growing slightly [2] . Cervical cancer is classified into two major histologic types, squamous cell carcinoma (72.6%) and adenocarcinoma (21.8%) [3] and the 5-year survival rates by histologic type are 81.4% for squamous cell carcinoma and 75.8% for adenocarcinoma, with adenocarcinoma having a worse prognosis than squamous cell carcinoma [3] . More than 80% of cervical adenocarcinoma are HPV associated, but 10–15%  \nof them, such as gastric-type adenocarcinoma and clear cell carcinoma, have been reported to be HPV independent [4] . However, squamous cell carcinomas, which comprise the majority of cervical cancers are mostly caused by HPV infection, and approximately 95% of cervical canc","cbCaiga7NJgfsN1o","https://ap.wps.com/l/cbCaiga7NJgfsN1o","pdf",2459368,"English","# Abstract\n## Epidemiology of cervical cancer and the introduction of HPV vaccination\n## Cellular origins and squamocolumnar junction (SCJ)\n## Type-dependent progression of high-risk HPV\n## Immune response and CIN regression/progression\n## Management and current treatments of CIN and cervical cancer","[{\"question\":\"What proportion of cervical cancer cases are linked to HPV infection?\",\"answer\":\"About 95% of cervical cancer is caused by human papillomavirus (HPV) infection.\"},{\"question\":\"Why can HPV-associated cervical cancer take time to be eliminated after vaccination?\",\"answer\":\"Even with widespread HPV vaccination, elimination may take time, so detailed mechanisms of cervical cancer development are important for appropriate management.\"},{\"question\":\"How does progression to cervical cancer differ by high-risk HPV type?\",\"answer\":\"Progression patterns vary by HPV type: HPV16 shows stepwise carcinogenesis, HPV18 is difficult to detect in precancerous lesions, and HPV52/58 tend to remain in cervical intraepithelial neoplasia (CIN).\"},{\"question\":\"Which factors beyond HPV type influence progression and regression?\",\"answer\":\"In addition to HPV type, involvement of the human immune response is important for both progression and regression of cervical cancer.\"}]","Carcinogenesis and management of human papillomavirus-associated cervical cancer | PDF",1790245130,25]