Abstract

Cervical cancer is one of the most common cancers in women worldwide. During their life time the vast majority of women become infected with human papillomavirus (HPV), but interestingly only a small portion develop cervical cancer and in the remainder infection regresses to a normal healthy state. Beyond HPV status, associated molecular characterization of disease has to be established. However, initial work suggests the existence of several different molecular classes, based on the biological features of differentially expressed genes in each subtype. This suggests that additional risk factors play an important role in the outcome of infection. Host genomic factors play an important role in the outcome of such complex or multifactor diseases such as cervical cancer and are also known to regulate the rate of disease progression. The aim of this review was to compile advances in the field of host genomics of HPV positive and negative cervical cancer and their association with clinical response.

Highlights

  • Human papillomavirus (HPV) is one of the most widely publicized and researched pathogenic DNA viruses

  • Cervical cancer is one of the most common cancers in women worldwide. During their life time the vast majority of women become infected with human papillomavirus (HPV), but interestingly only a small portion develop cervical cancer and in the remainder infection regresses to a normal healthy state

  • Host genomic factors play an important role in the outcome of such complex or multifactor diseases such as cervical cancer and are known to regulate the rate of disease progression

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Summary

Introduction

Human papillomavirus (HPV) is one of the most widely publicized and researched pathogenic DNA viruses. HPV research has focused on transforming viral activities in cervical cancer (Allie et al, 2014). Cervical cancer is the most common cancers in women worldwide and Genomic instability is a hallmark of human cancers, including the 5% caused by human papillomavirus (HPV) (Keilo et al, 2013). Cancer of the cervix is the second most common life-threatening cancer among women worldwide and both incidence and mortality rates are likely to be underestimated in developing countries. HPV high risk strains play at least the major if not an absolutely necessary role in the etiology (Behtash and Mehrdad, 2006). Persistent infection by ‘high risk’ genotypes of human papilloma virus (HPV) is necessary but not sufficient for the development of over 98% of cervical cancers (Ursula et al, 2006)

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