Uterine Cervical Neoplasms

The dominant known cause is persistent human papillomavirus (HPV) infection, which is described as the well-established etiology of cervical cancer. The disease is largely driven by HPV, and HPV is diagnosed in more than 90% of cervical cancers.

Persistent HPV infection contributes to cervical carcinogenesis through molecular pathogenesis and immune evasion. The tumor immune microenvironment is implicated in progression and therapeutic response, with roles for tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells, alongside HPV-mediated immune suppression.

HPV infection is the main risk factor supported by the grounding. The literature also notes that HPV-related disease burden varies by HPV genotype, regional conditions, study population, and anatomical site sampled, and that HPV-related diseases are more prevalent in developing countries.

Treatment is described at the modality and drug-class level as surgery for selected early-stage disease, radiotherapy, and systemic drug therapy for advanced or recurrent disease. Systemic options include platinum-based chemotherapy such as cisplatin, fluorouracil-based therapy, immune checkpoint inhibitors such as pembrolizumab, anti-angiogenic therapy such as bevacizumab, and antibody-drug conjugates such as tisotumab vedotin.