Researchers have translated a cutting-edge tactic for treating genetic disorders into a fresh approach for potentially stymying cancer.
Cell division is the generative spark of nearly every lifeform on Earth. But if healthy growth goes unchecked, cell division can turn lethal, overwhelming the organism. Such is the case with so-called oncogenes. When altered by a mutation, these growth-moderating genes go haywire, producing a geyser of cancer cells as a result.
But the findings have wider applications as well."That's the really exciting part," says Neumayer."This is proof of concept that siRNAs can be used for FLC, as well as adult liver cancers, which are much more common, and other tumor types elsewhere in the body.", which produces an enzyme called kinase A that's key to cellular metabolic function. The resulting fusion, known as DNAJB1::PRKACA, brings together the proteins and a catalytic subunit of the kinase.
Having shown that quelling the fused oncogene killed tumor cells, they decided to experiment with derailing kinase A activity, which research indicated was driving tumor growth.The problem was, fused kinase A and its"wild type" form are nearly identical, so"any drug you developed that blocks fused kinase A activity would affect all kinase A, including in normal cells," Neumayer says."In other words, you would incur a host of problematic side effects.
GalNAc conjugate therapies, which attach siRNA molecules to the ligand to deliver therapies inside cells, are already on the market for conditions such as hereditary transthyretin-mediated amyloidosis and atherosclerotic cardiovascular disease. The team wondered if they could use the same approach to thwart the kinase driving FLC tumors.
Neumayer says the findings suggest that siRNAs may be effective beyond FLC, capable of treating tumors throughout the body with a high degree of specificity:"I think siRNA medicines as a class will have a big impact over time as a new kind of genetic therapy."Christoph Neumayer, Denise Ng, David Requena, Caroline S. Jiang, Adam Qureshi, Roger Vaughan, Thazha P. Prakash, Alexey Revenko, Sanford M. Simon.
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