Molecular Basis of Cervical Oncogenesis

Abstract

Over the last decades the incidence and mortality by cervical cancer have decreased. Early diagnosis and treatment of precursory lesions are in part responsible for these results. In this paper the molecular basis to understand the cervical oncogenesis is presented. Several studies have shown that not taking routinely pap smears sets patients at higher risk to develop cervical cancer. The cell cycle is controlled by proliferative and supressive genes. When mutations take place, proto-oncogenes turn into oncogenes (carcinogenic) and cause excessive cellular multiplication. On the other hand, supressor genes contribute to cancer development when inactivated, and this leads the cells to inadequate growth. Virus such as the human papiloma virus (HPV) can affect this orchestrated cell cycle. Of special interest in the cervical carcinogenesis are the HPV subtypes 16 and 18. How HPV transforms the cervical cells is not fully understood. Real advances have been made in the application of molecular biology techniques for the understanding of this mechanism. It is already feasible to identify high and low risk HPV subtypes through hybrid capture and polymerase chain reaction. Once established, these techniques are easy to perform; however, they are still too expensive and require well equipped laboratories.