DNA damage response mechanism inhibits viral tumour growth

By Redazione

Researchers at the University of Helsinki, Finland, have found that virus-induced tumour growth may be arrested by the human DNA damage response mechanism. This, however, only applies to the
early stages of tumour development, as this is when DNA damage checkpoints become activated, recent findings suggest.

A similar mechanism has been observed in oncogene-induced cancers: Oncogenes trigger DNA hyper-replication and can thus lead to cellular deterioration. Together with the oncogene-induced DNA
damage checkpoint, this functions as an early anti-cancer barrier.

The research group of Päivi Ojala from the Genome-scale biology research programme of the University of Helsinki studied the Kaposi’s sarcoma herpesvirus (KSHV). KSHV is a human tumour
virus and causes Kaposi’s sarcoma (KS). Nowadays, KS is the most common kind of tumour found in sub-Saharan Africa, as infection with both KSHV and human immunodeficiency virus (HIV) is
widespread. There is currently no effective treatment for KSHV-induced tumours.

In the early stage of the KSHV infection, the virus imitates a number of cellular proteins. One of these viral proteins, viral cyclin, leads to replicative stress in the cells that line the
interior of blood vessels (endothelial cells). This, in turn, triggers cellular deterioration and hence activation of the DNA damage response. So, tumour growth may be stopped by the repair
mechanism initiated by its own protein. However, DNA damage checkpoints are only activated in the early stages of tumour growth, the Finish scientists emphasise. Later in development, KSHV
infected cells may be imposed to overcome this checkpoint.

The project involves various universities and research institutes from Finland and Sweden. It was partly funded by the EU’s INCA (The role of chronic infections in the development of cancer)
project, which investigates certain types of cancer caused by viruses. The study was published on 28 September 2007 in the open access journal Public Library of Science (PLoS) Pathogens.

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