When the artificial intelligence boom began, it did not start as an open, interconnected utopia. From day one, it was built in silos.
Yoo et al. demonstrate that Z-RNA binding-deficient ADAR1 triggers aberrant multicellular type I interferon production, especially from astrocytes, and induces marked periventricular encephalopathy in mice. Blocking type I interferon signaling fully rescues the pathology, indicating that ventricular accumulation of type I interferon is the central driver of periventricular encephalopathy.
NVIDIA CEO Jensen Huang says his daily success comes from a simple habit, starting each morning by completing his highest priority task first. Speaking at the California Institute of Technology graduation ceremony, he explained that this approach gives him a sense of achievement early in the day and frees up time to focus on others.
Understanding which cells within a tumor will go on to form metastases remains one of the major challenges in cancer research. A study led by the Cell Plasticity in Development and Disease laboratory, headed by Ángela Nieto at the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and Miguel Hernández University (UMH) of Elche, offers an unexpected answer: The cells that will give rise to metastases can already be identified within the primary tumor.
The study, published in Nature Communications, combines the analysis of a mouse model of breast cancer with patient data. The results show that, at the invasive front of the tumor, there is a specific population of cells capable of both invading and either proliferating or entering a dormant state. This balance determines whether cells that escape the tumor can initiate new tumor growths in distant organs, the feared metastases.
Nieto’s team has been studying the epithelial-to-mesenchymal transition (EMT) for decades, a program that controls cell migration during embryonic development and is reactivated in tumors to enable cancer cells to spread and form metastases.