Molecular Genetic Basis of Cervical Cancer

Background: Cervical cancer is a cancer that occurs in the cells of the cervix–the lower part of the uterus that connects it to the vagina and represents a global public health problem. In 2008, 530,000 new cases and 275,000 deaths from cervical cancer were recorded worldwide, and in 2018, an increase to 570,000 new cases and 311,000 deaths was recorded. For many years, it has been known that the main cause of preinvasive lesions and cervical cancer is the human papillomavirus–HPV. The total prevalence of HPV in the cervix in the general population of women is 10%. In developing countries, this prevalence is higher and describe most frequent clinical manifestations in the praxis. Objective: The aim of this study was to analyze and describe molecular genetic basis of cervical cancer and the most frequent clinical manifestations in the praxis. Methods: This is cross-sectional study based on meta-analysis of the facts published in scientific literature stored in indexed databases Medline, PubMed Central, Scopus, Hinari, etc., about molecular genetic basis of the cervical cancer with description of clinical manifestations and its consequences describing morbidity and mortality rate in the population worldwide. Results and Discussion:  In 2008, 530,000 new cases and 275,000 deaths from cervical cancer were recorded worldwide, and in 2018, an increase to 570,000 new cases and 311,000 deaths was recorded. The main cause of preinvasive lesions and cervical cancer is the human papillomavirus–HPV. HPV infection is most common in young, sexually active women under the age of 25, but cervical cancer is more common in older women. Oncogenic types of human papillomavirus 16 and 18 together with HPV 45 and 31 are the causative agents of 80% of cervical cancer cases. HPV 16 has the highest oncogenic potential. Epigenetic changes include DNA methylation and post-translational modifications of histones, such as: methylation, acetylation, phosphorylation, ubiquitination and sumoylation. Cervical intraepithelial (CIN / SIL) lesion is a premalignant change of the cervix that occurs due to chronic infection with high-risk types of HPV. Persistent infection with oncogenic types of HPV causes almost all cases of cancer. HPV DNA was detected in 99.7% of cancer samples. Conclusion: There are four main steps in the development of cervical cancer: infection of the metaplastic epithelium of the transformation zone, viral persistence, progression towards precancerous lesions and invasion of the basement membrane. Histologically, in about 80% of cases, squamous cell carcinomas arise from preexisting dysplasias. Adenocarcinoma accounts for about 15-20% of cancer cases. HPV 16 is the main cause of squamous cell carcinoma, unlike HPV 18 which is typically associated with adenocarcinoma.