Early Alzheimer’s leaves its mark long before neurons falter. Kong et al. use AtlasXomics spatial ATAC-seq to chart chromatin accessibility across the mouse brain, exposing region-specific microglial and astrocytic shifts that ignite inflammation and disrupt glial homeostasis—insights that could redefine early-stage AD therapy

Single-cell ATAC-seq exposes a critical twist in medulloblastoma’s story: after broad chromosomal hits spark tumor birth, late-emerging MYC-amplified subclones ignite aggressive progression—proof that tracking chromatin in real time can uncover the hidden drivers of relapse.

Chromosomal chaos doesn’t just accelerate tumor growth—it rewires the neighborhood. In esophageal adenocarcinoma, high CIN sparks patch-by-patch immune suppression and stromal remodeling, hinting that taming genomic instability could open the door to more effective, TME-targeted therapies.

Elevated chromatin accessibility pinpoints GSTM1 as a driver of aggressive NF-κB/STAT3 signaling in glioblastoma—linking its high expression to shorter survival and spotlighting a fresh, epigenetically defined target for therapy.

Abila et al. turn ordinary H&E slides into “tissue clocks,” training neural networks on 25,000 images to read each organ’s biological age and expose hidden, organ-specific aging patterns long before clinical symptoms appear.