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Combination of Introgen’s Nanoparticles Show Increased Efficacy in the Treatment of Metastatic Lung Cancer
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Two powerful tumor suppressor genes, p53 and FUS1, administered intravenously in nanoparticle formulations were capable of shrinking metastatic tumors in models of human lung cancer, according to investigators at The University of Texas M. D. Anderson Cancer Center.
Molecular cancer therapies using these genes, p53 and FUS1, are in clinical-stage development by Introgen Therapeutics. The technologies are included in a broad portfolio of properties licensed exclusively to Introgen from M. D. Anderson Cancer Center and other institutions.
The study, published in the January 15 issue of the journal Cancer Research, found that each of the nanoparticle tumor suppressors was effective therapy but more powerful results were observed when the treatments were combined.
Systemic therapy with combined p53 and FUS1 nanoparticles in disseminated, metastatic lung cancers decreased the number of human lung tumors by 75 percent and cut their size by 80 percent. The studies also showed that the nanoparticle treatments had no demonstrable adverse effects on normal cells.
This treatment strategy, the first time that two functional tumor suppressor genes have been used in a nanoparticle treatment, may offer a promising clinical treatment for lung and other cancers, according to lead author Lin Ji, Ph.D., assistant professor in the Department of Thoracic & Cardiovascular Surgery research at M. D. Anderson.
Robert E. Sobol, M.D., Introgen’s senior vice president, Medical and Scientific Affairs stated, “These results further support our continued clinical development of p53 and FUS1 tumor suppressor therapies. These nanoparticle formulations facilitate treatment of disseminated cancers and validate the important concept of combining tumor suppressors selected to work synergistically in killing cancer cells while leaving normal cells unharmed.”
In this study, the researchers tested the combined FUS1/p53 nanoparticles against four different human lung cancers as well as in normal non-cancerous cells. The treatment inhibited tumor cell growth in all four lung cancers tested, they said. It also induced cell death in the tumors, likely through the activation of p53 and FUS1 mediated gene functions that resulted in the killing of cancer cells but not normal cells.
