Sunday, November 6, 2011

Viral molecule aids in treating lymphoma

A mouse study revealed that a peptide that is derived from viruses can kill cancer cells by targeting a specific protein inside the cell. According to the scientists that conducted the study, the molecule they used as treatment could be more effective than what is currently used in the clinic to treat lymphoma, a cancer of white blood cells. The viral molecule targets an enzyme in our cells that functions by inhibiting a protein called P53, that is important in regulating many cellular functions. P53 is the most well-known tumour-suppressor, and  loss of P53 is found in almost all cancers. By inhibiting the inhibiting factor of P53, the scientists found that the levels of the tumour-suppressor rise which in turn lead to death of the cancer cell. The benefits of this type of treatment is that there seem to be less side-effects than conventional attempts.

The enzyme that inhibits P53 in our body is called HAUSP. A viral protein was found to bind 200 times more than P53, which rendered HAUSP unable to assert it's degrading effects on P53. This causes levels of P53 to rise. The mice that were found to have restored levels of the protein also showed a decrease in tumour size, while common side-effects were absent.

Because the P53 protein is important in regulating  various processes, such as the cell cycle and DNA repair. It is commonly regarded as the "guardian of the genome", because when the cell's genetic code gets damaged, it's P53 that stops the cell cycle, preventing the cell from dividing, and thus proliferating. This way, damaged cells can't turn into cancer cells. Instead, they will activate internal pathways that cause a cell to kill itself. Because of this, most cancers are found with dysfunctional P53, which lets them escape the guarding functions of the protein.  By re-activating the protein in mice that already had formed a tumour, they found increased death of cancer cells.
P53 is activated due to stress factors, which stops the cell cycle or kills the cell.
Curiously, the viral protein that was studied is derived from a virus that is known to cause lymphoma, which makes it even more remarkable that a viral molecule is able to decrease the tumour size in lymphoma. It does however explain why the viral molecule is able to specifically and effectively bind to a factor in the body found to be involved with cancer: it is likely that the virus itself, with an expansive set of peptides, has an overall effect that negatively impacts the function of tumour-suppressors like P53.

Recently, scientists have revealed how genetic instability that arised during development can causer cancer. They studied translocations, which basically are pieces of genetic code that broke off the chromosomes, and attach to an other one. The resulting combination can induce uncontrolled growth, and this disease process is found to underly lymphoma. However, cells can also become cancerous by DNA damage, leading to mutations in the genome itself, without breaking it. Changes in the genetic code for a gene, for example for P53, could render the corresponding protein to be dysfunctional. On the other hand, a mutation could cause a growth factor to become more active, leading to undesirable growth, eventually forming a tumour if the cell, with its tumour-suppressors, is unable to repair the damage.

The study in mice shows that the viral peptide could be a potent treatment for lymphoma. Of course, studies in human patients are necessary to confirm the efficacy of the treatment. Showing a functional effect in mice is a good step in the right direction. It is also interesting to find out if the viral therapy could be used in a cocktail with currently available drugs to treat lymphoma.

It is not the first time that viruses are used for treatment of cancer. A study with a virus called VSV revealed that it is able to kill cancer cells by exclusively infecting them. The observation that some viruses can cause cancer, and some of them are able to help us in curing it, is quite remarkable.

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