Recent research has been showing how the blue-stained nervous system appears at the center of most cases of an anti-myeloid disease, called Acute Myeloid Leukemia. Now, there’s some research published in EBioMedicine that may suggest how that interplay is going to play out.
In a study, Marcia Wijker-Brettler’s team found that the progenitor cells of the myeloid’s nucleus have five different “scars” that can both “snow” them to allow for safe entry into the nucleus, while also “scraping” these scarring treatments that allow them to have a chance to mature (the hollow scar stripes allow cells to be pushed through the hole). These spots seem to offer a tremendous amount of security against risk of infection, keeping the cells protected from things like viruses that would destroy the cellular connections needed to secrete special chemicals and red and white blood cells.
The result was that four out of five genes that are trafficked through the nucleus showed increase in activity, which is generally associated with cancer and other abnormal functions (since we do tend to have more disease with increased activity). But just because cells have no pain in the nucleus doesn’t mean they’re perfectly stable. Still, it’s not at all clear how the pool of mutated genes will be contained, and what treatments are necessary to use them in effectively.
What is clear, though, is that there’s an interesting principle at play here, says Oatley Smith, MD, PhD, an attending professor of neurobiology, physiology and anatomy at Washington University.
“You can see a potentially promising new class of technology being developed to go after this,” Smith says. “It’s called genome modification, or genetic engineering, and we have enough technology to go around to modify the genomes of cells.”