Northwestern Medicine scientists have discovered why Huntington's is so toxic to cancer cells and harnessed it for a novel approach to treat cancer, a new study reports.
Huntington's is caused by an over abundance of a certain type of repeating RNA sequences in one gene, huntingtin, present in every cell. The defect that causes the disease also is highly toxic to tumor cells. These repeating sequences -- in the form of so-called small interfering RNAs -- attack genes in the cell that are critical for survival. Nerve cells in the brain are vulnerable to this form of cell death, however, cancer cells appear to be much more susceptible.
Molecule - Assassin - Tumor - Cells - Author
"This molecule is a super assassin against all tumor cells," said senior author Marcus Peter, the Tom D. Spies Professor of Cancer Metabolism at Northwestern University Feinberg School of Medicine. "We've never seen anything this powerful."
Huntington's disease deteriorates a person's physical and mental abilities during their prime working years and has no cure.
Study - Feb - Journal - EMBO - Reports
The study will be published Feb. 12 in the journal EMBO Reports.
To test the super assassin molecule in a treatment situation, Peter collaborated with Dr. Shad Thaxton, associate professor of urology at Feinberg, to deliver the molecule in nanoparticles to mice with human ovarian cancer. The treatment significantly reduced the tumor growth with no toxicity to the mice, Peter said. Importantly, the tumors did not develop resistance to this form of cancer treatment.
Peter - Thaxton - Delivery - Method - Efficacy
Peter and Thaxton are now refining the delivery method to increase its efficacy in reaching the tumor. The other challenge for the scientists is figuring out how to stabilize the nanoparticles, so they can be stored.
First and co-corresponding author Andrea Murmann, research assistant professor in medicine at Feinberg, also used the molecule to treat human and mouse ovarian, breast, prostate, liver, brain, lung, skin and colon cancer cell lines. The...
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