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Aberrant multicellular interferon signaling underlies Adar1 mutation–driven Aicardi-Goutières syndrome-like encephalopathy

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.

Nvidea CEO Jensen Huang follows just one rule to maximise daily productivity. ‘I do this every single morning, exactly the same way.’

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.

Within primary breast tumors, a high-risk cell state may seed future metastases

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.

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