They have found out that the lack or inhibition of the protein it represents decreases the speed at which neoplasias occur, as it prevents the inflammation that contributes to the proliferation of cancer cells. Part of the conclusions of this research work are published in the June edition of the journal 'Cancer Research'.
Experts have used a model of experimental carcinogenesis, that is, have caused cancer in normal experimental mice and also in mice knocked out in that specific gene. After many experiments, they have found out that apart from collaborating to the DNA repair, the parp-1 gene has an influence on the growth of the carcinoma. Moreover, the gene’s lack of expression obstructs the angiogenesis process, which causes the creation of new blood vessels that allow sick cells to survive by receiving nourishment from the host organism.
The novelty of this finding is the possibility of designing new strategies that inhibit protein parp-1 activity in order to stop the progression of cancer. The next step consists of checking in experimentation models the efficacy of inhibitors in the treatment of cancer processes. So far, experts have used molecular medicines to carry out this delay process.
Researchers are trying to find more efficient therapeutical strategies that reinforce the action of antitumoral agents and decrease the administered radiation or chemotherapy doses. This way, the side effects will also decrease.
USA-based scientists have recently proven that this enzyme which repairs sick cells and keeps cell energy could be useful for the treatment of Huntington’s disease and other pathologies characterised by a low level of energy in cells. This is what an article published in the Chemistry & Biologyen’s August edition reveals, written by researchers of the Institute for Neurodegenerative Disease of Massachusetts General Hospital. These experts describe a new inhibitor of polymerase Parp1 which protects the cells affected by the Huntington’s disease in a lab.
Ismael Gaona | alfa
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