(RxWiki News) Non-Hodgkin lymphoma is a cancer that starts in the lymphatic system, that’s made up of tiny tubes that run throughout the body. One subtype of non-Hodgkin lymphoma (NHL) – mantle cell lymphoma – needs more treatment options and research is under way to find those solutions.
Researchers in Israel have re-opened the debate about the possibility that one protein, which is seen in high levels in mantle cell leukemia, could be a suitable target for drugs to attack and kill as a means of treating the disease.
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Mantle cell lymphoma (MCL) is seen in about 7 percent of the roughly 70,000 Americans who are diagnosed with NHL every year.
The cancer typically appears in the lymph nodes, bone marrow and spleen. The GI tract – esophagus, stomach and intestines – are also sometimes involved.
The disease is usually identified by the presence of a protein called cyclin D1 which controls the multiplication of cells. Unfortunately, there are no cures for MCL.
Prof. Dan Peer of Tel Aviv University's Department of Cell Research and Immunology, is leading a collaborative effort between academia and industry to develop a new class of drugs designed to kill off faulty proteins and reprogram cells to behave normally.
Past efforts to disable Cyclin D1 in a search for an effective means of treating MCL. But Prof. Peer isn’t ready to give up on this theory.
He and his team worked with two companies, Alnylam Pharmaceuticals in Cambridge, Massachusetts and Integrated DNA Technologies in Iowa, to find a way to cripple cyclin D1.
In a pre-clinical laboratory study, researchers found that these experimental drugs were effective in shutting down the out-of-control cyclin D1.
Using a method called RNA interference, the researchers were able to target and kill off the protein.
"Ultimately, we want to be able to cure this disease, and I think we are on the way," Prof. Peer said in a press release. He wants these results to trigger new enthusiasm in working with cyclin D1 to find new therapies.
This study was published in the journal PLoS One. The research was supported by the Lewis Trust and the Israeli Science Foundation.
