Abstract
Cervical cancer develops through persistent infection with high-risk human papilloma virus (hrHPV) and is a leading cause of death among women worldwide and in the United States. Periodic surveillance through hrHPV and Pap smear-based testing has remarkably reduced cervical cancer incidence worldwide and in the USA. However, considerable discordance in the occurrence and outcome of cervical cancer in various populations exists. Lack of adequate health insurance appears to act as a major socioeconomic burden for obtaining cervical cancer preventive screening in a timely manner, which results in disparate cervical cancer incidence. On the other hand, cervical cancer is aggressive and often detected in advanced stages, including African American and Hispanic/Latina women. In this context, our knowledge of the underlying molecular mechanism and genetic basis behind the disparate cervical cancer outcome is limited. In this review, we shed light on our current understanding and knowledge of racially disparate outcomes in cervical cancer.
Highlights
Other than CC, the evaluation of preneoplasic cervical lesions identified increasing mtDNA D-loop sequence variants in low grade squamous intraepithelial lesion (LGSIL, 17%) and high grade squamous intraepithelial lesion (HGSIL, 29%), whereas no mutations were detectable in the normal tissues and tissues with atypical squamous cells of undetermined significance (ASCUS) cytology [54]
The HPV-integrated cervical epithelial cells with more pronounced changes compared to CINI are regarded as high-grade squamous intraepithelial lesions (HGSILs) or CIN2, CIN2/3, or CIN3 depending on the degree of severity of the pathologic changes
Women diagnosed with cervical intraepithelial lesions (CINs)-2 or more advanced lesions would receive further treatment depending on age, pregnancy status, and fertility situation
Summary
Cervical cancer (CC) is one of the leading causes of death among women worldwide, with approximately 530,000 new cases and 275,000 deaths annually [1,2,3]. In the United States, it was estimated that 13,240 new cases of CC would be diagnosed in 2018 with an estimated death of 4170 women [4]. The major risk factors associated with CC development include high-risk human papilloma virus (hrHPV) infection, age, smoking, childbirth, use of oral contraception, and diet [1,3,5,6,7,8]. The hrHPV may remain undetected if not screened in a timely manner and manifest oncogenic transformation leading to CC development [8,9]
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