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Archive - Jul 6, 2015

Georgetown Scientists Seek to Block Function of Ezrin Protein to Prevent Metastasis of Osteosarcoma

The investigation of a simple protein has uncovered its uniquely complicated role in the spread of the childhood cancer, osteosarcoma. It turns out that the protein, called ezrin, acts like an air traffic controller, coordinating multiple functions within a cancer cell and allowing it to endure stress conditions encountered during metastasis. It's been known that ezrin is a key regulator of osteosarcoma's spread to the lungs, but its mechanism was not known. Osteosarcoma is a tumor of bone that afflicts children, adolescents, and young adults. In most cases, the tumor is localized in the extremities and can be completely removed by surgery or amputation. "The main cause of death in osteosarcoma patients is not the tumor on their limbs, but the failure of their lungs when the cancer spreads there," explains Aykut Üren, M.D., Professor of Oncology at Georgetown Lombardi Comprehensive Cancer Center in Washington, D.C. Dr. Üren and his colleagues have developed molecules that block ezrin's function and prevent osteosarcoma spread in mouse models. In an attempt to explain the molecular mechanisms underlying ezrin-mediated cancer metastasis, the researchers discovered this previously unrecognized role for ezrin. Their finding is published online today in the journal Molecular and Cellular Biology. "Conventionally ezrin was believed to be functioning only on the inner surface of cancer cells," Dr. Üren says, "but our new discovery indicates that ezrin may operate deeper in the core of the cell and regulate expression of critical genes that are important for cancer's spread." The scientists say that ezrin functions in a new capacity that is unusual for its family of proteins.

iPSCs Derived from Rod Photoreceptors Better Than Fibroblast iPSCs at Producing Retinal Cells to Treat Retinal Degeneration; Epigenetic Switch May Play Important Role

By growing two types of stem cells in a "3-D culture" and measuring their ability to produce retinal cells, a team lead by St. Jude Children's Research Hospital researchers has found one stem cell type to be better at producing retinal cells. The research not only reveals which stem cell type might be better for treating retinal degeneration, but it also demonstrates a standardized method for quantifying the effectiveness of different stem cells for such therapies. The research was led by Michael Dyer, Ph.D., a member of the St. Jude Department of Developmental Neurobiology and a Howard Hughes Medical Institute (HHMI) investigator. The findings were published in the July 2, 2015 edition of the journal Cell Stem Cell. The article is titled “Quantification of Retinogenesis in 3D Cultures Reveals Epigenetic Memory and Higher Efficiency in iPSCs Derived from Rod Photoreceptors.” Stem cells are immature cells that can differentiate into more specialized cells in the body. In early clinical trials, researchers are testing whether stem cells can be differentiated into cells to replace those that are defective and die off in diseases such as age-related macular degeneration, retinitis pigmentosa, and Stargardt's disease. Such degeneration is the leading cause of vision loss, affecting more than 10 million people in the U.S.--more than cataracts and glaucoma combined. While such clinical trials have shown early promise, there are many scientific questions to be answered. "One important question is whether it makes a difference where the stem cells come from," Dr. Dyer said.