**1. Introduction**

According to WHO, in 2020, an estimated 604,000 females were diagnosed with cervical cancer worldwide, and about 342,000 females died from the disease [1]. Every year in the United States, about 13,000 new cases of cervical cancer are diagnosed, and about 4000 women die of cervix cancer. Hispanic females have the highest rates of developing cervical cancer, and Black females have the highest rates of dying from cervical cancer [2]. The highest incidences occur in populations with a high prevalence of human papillomavirus (HPV) infection and inadequate screening rates. The mortality rates for cervical cancer range from less than 2 per 100,000 in western Asia, Western Europe, and Australia to more than 20 per 100,000 in central America, Melanesia, and the majority of Africa due to these factors, plus variances in access to effective therapies [3]. Most covariables traditionally associated with an increased risk of cervical cancer appear to be surrogates for sexually transmitted HPV infection. The results of tumor DNA analysis show that practically all squamous or adenocarcinoma of the cervix cases integrate DNA from at least one of multiple high-risk HPV

subtypes. HPV16, HPV18, HPV31, HPV33, and HPV45 are high-risk subtypes; the most prevalent are HPV16 and HPV18, which account for around 70% of cervical malignancies. Risk factors for cervix cancer and its intraepithelial precursors include early coitus, multiple sexual partners, and a history of other sexually transmitted infections [4]. Although some researchers have observed a link between cervical cancer with continued oral contraceptive usage, various confounding risk factors and changes in diagnostic criteria make it challenging to demonstrate a causal relationship [5].
