New epigenetic drug against mantle cell lymphoma
Universitat de Barcelona Research News Jun 17, 2018
A new study, led by Manel Esteller, professor of genetics of the UB, ICREA researcher, and director of the Epigenetics and Cancer Biology Program (PEBC) of the Bellvitge Biomedical Research Instiutute (IDIBELL), presents an epigenetic drug able to slow down a cancer—mantle cell lymphoma—known for its aggressive behavior. The results of this research, published in the journal Haematologica, from the European Haematology Society (EHA), respond to the medical need of finding new drugs to increase long-term survival regarding this disease.
“Our laboratory is interested in finding new compounds with epigenetic activity and antitumor effects. Working with organic chemists and Quimatryx company, we got a molecule that inhibits the HDAC6 gene, a protein that chemically modifies other proteins through acetylation,” says Esteller, main author of the study. The research was also carried out with the clinical collaboration of the Haematology Services of the Catalan Institute of Oncology (ICO) in Hospitalet and Badalona, as well as the Josep Carreras Institute (IJC).
“While studying several types of cancer, we realized the efficiency of the new molecule was at its peak in this kind of lymphoma. This beneficial effect was observed in cultured cells, murine studies, and cells that were extracted from patients. In addition, the substance is very specific when it comes to its action target, with apparent little toxicity for healthy cells in the same patient, such as type T lymphocytes,” adds Esteller.
About 12% of cancers worldwide are linked to blood cells, be it leukemia, lymphoma, or myeloma, and a new patient is diagnosed with it every 2 minutes. Although some of these hematological oncologic processes are curable, there are others for which the treatments are not effective enough.
“What makes us especially happy in this case is the fact that the possible uses of the drug in clinical trials are to be considered for next year,” concludes Esteller.
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