Scientists from Cancer Research UK explained how a class of common painkillers, including ibuprofen, can interact with a key protein that feeds the growth of many different types of cancer. Ibuprofen is one of several Profen - Particular group of drugs non-steroidal anti-inflammatory drugs (NSAIDs) - which are being investigated because of the ability to prevent cancer.
A research team from the University of Bath carried out an analysis of the same class of ibuprofen and found that all are processed by the body exactly the same way: through a protein called AMACR, which converts the drug into its active form. The AMACR is overactive in nearly all cancers and some prostate tumors of the gut, among others.
It is believed that it stimulates the growth of disease by increasing the supply of energy for cells. Therefore, according researchers to understand how drugs like ibuprofen can alter the activity of AMACR may help to better understand how they can block cancer growth.
"Our study is the first to test other drugs of the same family as ibuprofen and systematically show that they are all handled by the same protein in the body. Some previous laboratory studies have suggested that high doses of ibuprofen can stop the growth of prostate cancer cells but the reasons for this are not well understood, "says the study's lead author, Matthew Lloyd. According to scientist, to understand more about how this protein is to act in the cells and which molecules interact could provide important clues about how this process works, possibly opening new avenues of investigation for the treatment of prostate cancer in the future.
"This research is part of an international effort to understand how drugs such as ibuprofen may prevent or delay the development of cancer. But there are risks and prolonged use of these drugs can have side effects such as bleeding and stomach ulcers. Understanding more about how these drugs act at a molecular level is a crucial step in order to develop more targeted medications with fewer side effects in the future, "explains the researcher Julie Sharp.
Source: http://www.pop.eu.com
0 comments:
Post a Comment