Background/Objectives: Cervical cancer remains a major cause of morbidity and mortality among women worldwide, marked by stark geographic and socioeconomic disparities. Preventable via HPV vaccination and screening, progress toward elimination varies widely across and within countries. This narrative review synthesizes the epidemiology, including incidence, mortality, survival, and stage distribution, as well as risk factors and the coverage/equity of HPV screening and vaccination programs. Methods: Comprehensive searches were performed in PubMed, Web of Science, Scopus, and Google Scholar (no date restrictions; English only). Included were original epidemiological studies, systematic reviews, meta-analyses, and international reports on burden, risk factors, or prevention indicators. Data were qualitatively synthesized into three themes: epidemiological patterns, risk factors, and screening/prevention programs. Results: Persistent high-risk HPV infection causes nearly all cervical cancers, predominantly HPV16/18, with regional variation in other types. Strong co-factors include HIV immunosuppression, early sexual debut, multiple partners, high parity, long-term oral contraceptive use, and smoking. Inequalities in incidence, late diagnosis, and survival are driven by socioeconomic disadvantages, low education, rural residence, and poor health system access. Screening ranges from cytology/VIA to primary HPV testing, but coverage is low and inequitable in high-burden settings. HPV vaccination has expanded yet faces major gaps in low- and middle-income countries. Conclusions: Cervical cancer burden concentrates in low-resource and marginalized populations. Global elimination demands accelerated, equitable scale-up of HPV vaccination and screening, alongside health system strengthening and barrier reduction.

Background/Objectives: Most HPV infections are transient, but persistent high-risk infection, particularly with HPV16, is among the most important determinants of progression to HPV-associated precancer and cancer. The role of genotype, infection persistence, and anatomical site varies across cervical, oropharyngeal, anal, vaginal, vulvar, and penile cancers. This review synthesizes evidence to clarify how these factors shape cancer risk and prevention. Methods: This structured narrative review used iterative, topic-specific searches in PubMed, Scopus, Web of Science, and Google Scholar without a publication-year restriction and was limited to English-language sources. Search terms were adapted to each database and thematic question. Original empirical studies and secondary data analyses informed direct quantitative discussion, whereas reviews, meta-analyses, guidelines, consensus statements, and authoritative reports were used principally for context. Evidence was synthesized qualitatively because study designs, populations, anatomical sites, assays, outcomes, and clinical purposes differed substantially; no new meta-analysis was performed. Results: The most developed longitudinal and screening evidence concerned cervical cancer, whereas evidence for several non-cervical sites was smaller and more heterogeneous. HPV16 was the most important genotype in most cancers examined. The role of HPV18 and other high-risk genotypes varied depending on the cancer site, tissue type, and geographic region. Most transient infections do not lead to cancer; however, persistent high-risk HPV infection, particularly HPV16, was associated with high-grade lesions and an increased risk of cancer. Vaccination was associated with a reduction in high-grade lesions and invasive cancer in population-based studies. Self-sampling and urine testing had practical value when individuals with positive results proceeded to triage, treatment, and follow-up. Conclusions: Three key questions exist for assessing the risk of HPV-associated cancers: Where has the persistent infection occurred? Which genotype is involved? And can the healthcare system intervene before progression to cancer? In cervical cancer, vaccination, screening, triage, and treatment are linked within the most developed prevention pathway. For anal cancer, prevention is more strongly focused on high-risk groups and diagnostic capacity. In oropharyngeal cancer, HPV is important for understanding etiology and prognosis, but there is still no established population screening pathway. Evidence for vaginal, vulvar, and penile cancers must be interpreted separately by site.

Background: Declining age standardized rates conceal differences in gastric cancer by age, sex, anatomical subsite, histological type, and region. This review examines these patterns alongside risk factors, Helicobacter pylori eradication, screening, and surveillance. Methods: PubMed, Web of Science, and Scopus were searched iteratively for literature available through January 2026. Google Scholar and reference lists were used to identify additional relevant sources. One reviewer selected sources, and findings were interpreted qualitatively according to study design, population, confounding, precision, and geographic applicability. Results: Standardized rates have fallen in many countries, while absolute case numbers continue to rise. Increases reported in some younger groups do not establish a uniform global trend because age definitions and registry coverage differ. Helicobacter pylori is a major causal factor, but mucosal damage, hereditary susceptibility, and other exposures affect risk. Randomized trials support eradication for reducing primary and metachronous cancer incidence. Screening associations with earlier diagnosis and lower mortality are largely observational and concentrated in East Asia. Conclusions: Prevention requires treatment of Helicobacter pylori and confirmation of cure. Advanced or extensive atrophy or intestinal metaplasia, autoimmune gastritis, and defined hereditary syndromes require the appropriate surveillance or specialist assessment. Family history, migration background, and behavioral exposures inform further assessment but are not equivalent indications for surveillance. Population screening and targeted assessment should follow local disease burden, antimicrobial resistance, and endoscopy capacity.