About this research group
This group's ambition is to improve the nationwide cervical cancer screening, with the possibility of using self sampling. Important herein is research on the use of new triage methods for hrHPV positive women, by using HPV genotyping or molecular biomarkers. read moreAbout this research group
This group's ambition is to improve the nationwide cervical cancer screening, with the possibility of using self sampling. Important herein is research on the use of new triage methods for hrHPV positive women, by using HPV genotyping or molecular biomarkers.
Background
Worldwide 450,000 new cases of invasive cancer of the cervix are diagnosed every year. In developing countries, cancer of the cervix is the most frequent female malignancy and is responsible for about 24% of all cancers in women. Although screening programs, to identify precursor lesions of cervical cancer, have significantly reduced the mortality and morbidity of this disease, still more than 700 women have to be treated for cervical cancer in the Netherlands.
Human papillomaviruses (HPV) infections are prevalent in the general population. Obviously, not every women infected with a high-risk HPV type will develop cervical cancer. In fact, cervical cancer can be considered a very rare complication of a cervical infection with high-risk HPV. Clearly, additional virological, environmental, behavioral, immunological or ill-defined genetic factors must be implicated in the pathogenesis and progression of this cervical disease.
Aims
Studies to the biological behavior of Human papillomaviruses (HPV) infected cervical lesions, identified multiple HPV genotypes in different biopsies of the uterine cervix of the same patient. Multiple HPV genotypes were detected in all patients with severe dysplasia, while only a single HPV genotype was detected in patients with invasive carcinoma. The distribution of single and multiple HPV genotypes within the cervix seems to depend on the stage of the disease.
The presence of multiple HPV genotypes within a single biopsy indicates that monoclonality may be a late event in carcinogenesis. The presence of multiple HPV types in a single patient indicates that a difference between HPV infections must exist to explain the oncogenic behavior of a specific virus strain. It is suggested that viral persistence and the viral load may play a role in this respect.
So when does an HPV infection become oncogenic? The presence of only HPV cannot be considered sufficient for oncogenesis; other risk factors must play an important role. Hard evidence is difficult to obtain to determine whether an HPV infection, or in fact, whether an HPV induced cervical lesion will regress or progress.
Among the possibilities available, we hypothesize that the viral persistence, viral load and genetic predisposition, are objective criteria which are possibly involved in the pathogenesis of cervical cancer development. There is sufficient reason to consider that either one of these aspects, or a combination of these, do determine the behavior of a cervical lesion or in the HPV integration event, as an important step to carcinogensis. Therefore current studies are directed to obtain insight into the regressive/progressive behavior of cervical lesions related to HPV infections.