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Human papilloma viruses promote the development of white skin cancer
Every year around 260,000 new cases of white skin cancer (also called lighter skin cancer) occur in Germany. The most important risk factors for this type of cancer include intensive UV radiation from the sun and solarium as well as sunburns. Human papilloma viruses (HPV) can also cause white skin cancer.
As the University of Cologne reports in a recent release, human papilloma viruses (HPV) are not only the cause of genital cancers and head and neck tumors, but also cause white skin cancer. Immune-weakened people, for example people with an organ transplant, are particularly susceptible to the development of such tumors.
The most common forms of skin cancer
“Light skin cancer” (also called “white skin cancer”) includes squamous cell carcinoma and basal cell carcinoma.
According to the "ONKO Internet portal" of the German Cancer Society, the two subspecies are the most common forms of skin cancer. Every year, an average of 99,000 people contract squamous cell carcinoma and 159,200 people develop basal cell carcinoma. That is a total of almost 260,000 new cases of light skin cancer.
The cellular processes that lead to tumor development are still not fully understood. The working group led by Univ.-Prof. As part of a research project, Baki Akgül from the Institute of Virology at the University Hospital Cologne was able to uncover previously unknown mechanisms by which the HP virus influences infected cells.
Certain groups of people are particularly vulnerable
HPV are small pathogens that can infect both the human mucosa and keratinized skin. This can lead to both benign and malignant changes in the infected tissue. The viruses are divided into different subgroups. For certain types of cancer, such as cervical and tonsil cancer (almond cancer), the connection between HPV infection and the so-called alpha group has been proven.
Viruses of the so-called beta-HPV group are very widespread and colonize the human skin in the first weeks after birth. As explained in the release, beta-HPV are efficiently kept in check by the immune system so that virus replication takes place at a very low level and has no clinical impact.
As a result, there is little awareness among the population that this subgroup can also be responsible for the development of skin cancer. Abnormal proliferation of beta-HPV in the skin occurs especially in people who have received an organ transplant and who therefore have to permanently suppress the immune system to prevent rejection of the donor organ.
This favors the formation of skin cancer precursors and thus ultimately the development of light skin cancer. This also applies to people who suffer from a chronic immune deficiency. How the viruses promote cancer is not yet understood in detail.
Molecular mechanisms revealed
Prof. Akgül's group was able to show that HPV influences infected cells by means of a hitherto unknown mechanism and influences both the production of cellular proteins and their stability.
The researchers used 2D cell culture systems, 3D skin culture models and transgenic mice for their investigations and were able to show that the presence of the viral protein E7 alone is sufficient to reprogram infected skin stem cells into cancer stem cells.
In this way, the scientists were able to uncover molecular mechanisms by which virus-positive cells leave their tissue structure, migrate into other tissue layers and develop cancer cell-like behavior.
This process of cell invasion is based on the one hand on the ability of the protein E7 to weaken cell-cell contacts of infected skin cells, which is the basic prerequisite for detachment from the tissue.
On the other hand, the team showed an interaction between a family of cell surface proteins, the so-called integrins, and the connective tissue protein fibronectin. The researchers succeeded in proving that this mutual influence is also beneficial for the development of cancer.
Prerequisite for the development of therapies and vaccination approaches
The working group was also able to show that the virus influences the gene expression of infected cells. The researchers also succeeded in discovering a completely new mechanism by which the virus affects the stability of important cellular proteins that play a key role in cell division and DNA repair.
For the first time, the scientists were able to demonstrate a cooperation of the viral proteins E6 and E7, which apparently influence the stability of important cellular regulators via the protein degradation process of so-called autophagy.
The clarification of other tumorigenic mechanisms is the subject of ongoing research. As stated in the release, this work is imperative to develop therapies and vaccination approaches for HPV-caused white skin cancer.
The original publications to date have been published in the specialist journals "Journal of General Virology", "Oncogene", "Virology", "International Journal of Cancer" and "Virus Genes". (ad)
Author and source information
This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
- Cologne University Hospital: Human papilloma viruses promote the development of skin cancer, (accessed: December 14, 2019), Cologne University Hospital
- German Cancer Society: HELLER SKIN CANCER - AN UNDERESTIMATED DISEASE ?, (accessed: December 14, 2019), ONKO Internet portal
- Journal of General Virology: The levels of epithelial anchor proteins β-catenin and zona occludens-1 are altered by E7 of human papillomaviruses 5 and 8, (accessed: December 14, 2019), Journal of General Virology
- Oncogene: The fibronectin / α3β1 integrin axis serves as molecular basis for keratinocyte invasion induced by βHPV, (access: December 14, 2019), Oncogene
- Virology: HPV8 activates cellular gene expression mainly through Sp1 / 3 binding sites, (access: December 14, 2019), Virology
- International Journal of Cancer: Human papillomavirus type 8 oncoproteins E6 and E7 cooperate in downregulation of the cellular checkpoint kinase-1, (access: December 14, 2019), International Journal of Cancer
- Virus Genes: BetaHPV E6 and E7 colocalize with NuMa in dividing keratinocytes, (access: December 14, 2019), Virus Genes