MOLECULAR DETERMINANTS OF HOSTVIRAL INTERACTION OF CERVICAL CANCER IN SUDAN

Abstract

Strong epidemiologic evidence indicates that infections by certain human papillomaviruses (HPVs) types are causally linked to cervical cancer development. Among the high risk HPV types, HPV 16 and 18 are recognized as the main causes of invasive cervical cancer and its precursor lesions. Little is known, however, regarding HPV prevalence in cancerous and normal women in Sudan, a country with high cervical cancer incidence. It is also known that HPV infection alone is not sufficient for progression to cervical cancer, additional genetic changes such as loss of distinct chromosomal regions, inactivation of tumor suppressor genes and activation of oncogenes, must occur in order for malignant transformation to take place. It is known that p53, a tumor suppressor gene, has a common polymorphism encoding proline (Pro) or arginine (Arg) at residue 72; produces marked change in the structure of p53. Retinoblasoma gene, another tumor suppressor gene, its mutation is not uncommon in different types of cancer. The oncogenic potentiality of HPV oncogenes (E6 and E7) is due to the reduction of the products of these tumor suppessor genes in HPV infected cells.