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.