Sudden transgene causes the tumors to shrink

Scientists have discovered that making a major gene work again abruptly can provide a very effective new way of treating cancer. Many cancers are thought to be due to a ' flaw ' in the p53 tumor suppressor gene.

Two groups of US researchers re-activated the gene in the laboratory and found that enough to cause many different types of tumors to shrink.Nature 's studies offer hope for a new generation of anticancer drugs that are effective when boosting the activity of the p53 gene.

The gene p53 is altered and deactivated in most human cancers. It is one of the most widely studied genes in cancer and researchers have identified compounds that can restore its function.

But until now, it was not known whether such activity actually repelled the growth of tumors in tumors that had formed. Two research groups from New York's Cold Spring Harbor Laboratory and from the Massachusetts Institute of Technology (MIT) in Cambridge seem to have the answer.

Significant shrinkage

A tumor in the rat shrinks after the gene is reactivated.(Photo: BBC)

In animal experiments, they showed that even when re-activated for a short time, the gene significantly reduced the number of tumors, reducing it by 100% in some cases. The mechanism behind that repulsion seems to vary depending on the type of tumor.

The Massachusetts Institute of Technology team found that leukemia cells were "seduced to commit suicide" while polyps (a type of connective tissue cancer) began to become aging and losing their ability to divide.

The New York team, studying liver cancer, found that the cell aging process caused by the p53 gene is involved in the immune system's response that ' witnesses ' an increase in activity. The dynamics of molecules help clear cancer cells.

The researchers are not sure why these two cancers are affected in different ways but have begun to identify other genes that are activated in each type of tumor when the p53 gene is active again.

Dr. Andrea Ventura, a member of the Massachusetts Institute of Technology research team, said: 'This study provides important evidence of genetics that in order for a tumor to exist, inhibition is needed. constantly a gene that blocks that tumor. '

Key role

In normal cells, the p53 gene controls the cell cycle. When functioning properly, it activates DNA repair mechanisms and prevents the division of cells with damaged DNA. If DNA damage is irreversible, the p53 gene will cause cells to self-destruct by undergoing cell separation or programmed cell destruction.

When the p53 gene is stopped by mutation or deletion, cells are more likely to get cancer because they will divide uncontrollably as soon as DNA is damaged. The researchers used genetically altered mice that had inactive p53. But, they also introduced a gene ' switch ' that allowed researchers to make p53 work again after tumors developed.

The study also showed that activation of the p53 gene had no damaging effects in normal cells. Researchers were worried that the p53 gene could kill normal cells because it never showed up in those cells.

Ed Yong of the UK Cancer Research Center said: 'It is encouraging that cancers in mice can be treated by re-activating the p53 gene. Because the p53 gene is often "turned off" in human cancers, reactivating it may be able to create an effective cure for the disease in the future. But before this can happen, scientists need to prove that the same solution can be applied to human cancer. '

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