We talk about "hard wiring" the brain but our central nervous system is a work in progress. From the first neuron through childhood and adolescence, the neuronal network grows in complexity and size but also prunes out unneeded connections using molecules like the recently characterized enzyme, fidgetin, which makes strategic cuts in the microtubule scaffolding that holds up the cell's cytoskeleton and supports these connections. The ability of nerves to grow and prune diminishes as we mature until our adult neurons have mostly lost the power to reshape themselves.
A whimsically named fly gene, Sunday Driver, a.k.a. syd, and its mammalian analog, JIP3, seem to be in the driver's seat when it comes to parking the multiple nuclei of a skeletal muscle cell in their correct places, say researchers at the Sloan Kettering Institute (SKI). Getting that wrong and having mispositioned nuclei is a classic diagnostic sign of human congenital myopathies, a string of inherited muscle diseases such as Emery-Dreifuss muscular dystrophy (EDMD).
Glioblastoma multiforme (GBM) is the most common and the most deadly adult primary brain tumor, with an average survival of just 14 months following diagnosis. Even with aggressive treatment by surgery, radiation, and chemotherapy, most therapeutic approaches targeting the glioma cells in GBM fail. Faced with this bleak picture, Johanna Joyce and colleagues at Memorial Sloan Kettering Cancer Center (MSKCC) in New York City looked for an alternative strategy and turned to non-tumor cells that are part of the glioma microenvironment, the cancer's cellular neighbors. In particular, they zeroed in on tumor-associated macrophages and microglia (TAMs). The results were startling.
As we have learned more about the biology of cancer, it has become obvious that, aside from changes to the cancer genome, there are many other factors that determine tumor outcomes. Epigenetics, influences from the microenvironment, exosomes, and interplay with the immune system are now all recognized major players in cancer progression. Fresh evidence from Alain Silk, Melissa Wong, and colleagues at Oregon Health & Science University (OHSU) in Portland implicates a century-old observation—fusion of cancer cells with macrophages—as a new potentiator of cancer progression.