BLOG: Working toward a “sunblock” for mutation in ovarian cancer

BLOG: Working toward a “sunblock” for mutation in ovarian cancer


6.17.15 This year, MOCA provided a record $662,320 to 7 Minnesota ovarian cancer researchers, with projects focused on ovarian cancer prevention or treatment. We’ve asked each MOCA-funded researcher to author a blog post detailing their projects.

This post is provided from Reuben Harris, Ph.D., from the University of Minnesota. MOCA awarded Harris a $100,000 grant for his project titled: Stopping Enzyme-Catalyzed Ovarian Cancer Evolution.

Many mutations are essential to convert a normal cell into a tumor.  Ovarian cancer is no exception with some tumors bearing hundreds, to an eye-popping tens-of-thousands, of mutations.

Most of these mutations are inconsequential, but a significant proportion drives disease emergence, fuels tumor progression, and undermines therapeutic efforts through resistance. The sources and origins of most of these mutations are unclear.

The Harris lab at the University of Minnesota has discovered a protein in our bodies that normally functions to stop viral infections, which becomes over-active in ovarian cancer cells and inflicts mutations. This protein is called APOBEC3B (pronounced: apo-bek three bee).

A major goal of the Harris lab is to determine methods to stop this rogue DNA mutating protein and improve cancer treatments.

Recent work from the Harris lab has uncovered a cellular communication system responsible for APOBEC3B activity. Remarkably, this system had been previously linked to cancer, and drug companies have even developed small molecules to interfere with this communication system.

The Harris lab has been able to show these molecules stop APOBEC3B expression in model cell-based systems. MOCA-supported work has just begun to see if these molecules can be repurposed to stop tumor formation in living mice.

If successful, these efforts could lead to clinical trials to determine whether stopping APOBEC3B makes ovarian cancer more treatable with existing drugs.

A useful analogy for understanding this process is UV-rays in sunshine. A scientific understanding of UV-rays as harmful mutation-causing agents that lead to the development of melanoma actually prompted advances in the cosmetic industry (sunscreen) to protect people from these harmful effects.

Similarly, now that APOBEC3B is recognized as a significant source of mutation in ovarian cancer (as well as other cancers), analogous chemical innovations could provide the “sunblock” to APOBEC3B mutagenesis and ultimately revolutionize many cancer treatments.

Would you like more information about this research project or others that MOCA funds? Contact the MOCA office at (612) 822-0500 for more information.