Cooperation with fatal outcome
Do viruses and bacteria have to cooperate for cervical cancer to develop? I am glad to share that my group will investigate this question in our project the German Research Foundation is funding. Cervical cancer is the fourth most common tumor in women. In 2020 around 604,237 women were diagnosed with cervical cancer globally, and about 341,843 died from the disease. The fact that viruses contribute to the malignancy in approximately 90 percent - should have been common knowledge since 2007. Vaccination is offered for girls aged 9 to 14 to protect them against cervical cancer. The vaccine is directed against the trigger: the human papillomavirus (HPV). The virus alone does not lead to cancer The fact that HPV is responsible for most cancers does not mean that infection with the virus necessarily results in disease: Although about 80 percent of all women experience an infection during their lifetime. Yet only 1.6 percent of them develop cervical cancer. So, it's clear that HPV infection alone is unlikely to cause cervical cancer. Many co-factors are suggested to increase the risk of developing cervical cancer, including co-infections with other sexually transmitted pathogens; their relative contribution is yet to be determined. Tissue alterations after infections are one of my group's main areas of research. To this end, we are developing, among other things, lifelike organ replicas - 3D organoids - using which we are investigating the disease processes. In this project, we will investigate which factors collaborate with HPV to initiate cancer development over the next three years. Many sufferers are also infected with Chlamydia Patients who develop cervical cancer are not only infected with the HPV but are often also with the bacterial pathogen Chlamydia at the same time. In earlier work, we showed that Chlamydia causes damage to the genetic material in infected cells without starting the otherwise usual repair mechanisms of the cells. The bacterium also suppresses programmed cell death, which the organism uses typically to prevent degenerate cells from multiplying uncontrollably. Despite these clear links between HPV and chlamydial infections and the development of cervical cancer, their role in cancer development has not been studied. Now we want to change that in the new research project. We employ unique 3D organoid and mouse models that give a good picture of what happens when both HPV and Chlamydia occur in cervix tissue. We rely on the latest technologies in studying these processes, such as genetic lineage analysis, single-cell RNA sequencing, and spatial transcriptomics. This way, we hope to gain new insights into the development of cervical cancer in the coming years and - in addition to the HPV - identify other factors that must be added for the tissue to actually degenerate.
