Cells must constantly repair damage to their DNA that, if left unfixed, can lead to cell death, cancer, or accelerated ageing. EMBL researchers and their collaborators show that the Golgi complex, an organelle best known as the cell's sorting and shipping centre, stores DNA-repair proteins and dispatches them to the nucleus when damage occurs. When DNA is damaged,  the cell recruits the relevant repair proteins from the Golgi to the nucleus, matched to the type of damage, and clears the proteins it doesn’t need out of the nucleus, sequestering them back at the Golgi. This work reveals a new layer of regulation of DNA repair pathways from outside the nucleus, opening up new opportunities to modulate these pathways and to target related diseases such as cancer. 

Anti-angiogenic therapies targeting VEGF signaling have limited clinical efficacy due to inevitable resistance. Researchers constructed a pancancer single-cell atlas of 1.24 million cells across 13 cancer types, revealing that pericytes (PCs) and PC-derived PGF/ANGPT2 are more prominent pro-angiogenic regulators than the classical VEGFA-centric model. Tumor-educated MCAM+ immature PCs (imPCs) were identified as the primary source of PGF/ANGPT2, driving alternative angiogenesis and anti-VEGFR resistance. Combining anti-VEGFR with MCAM-targeting antibody-drug conjugates achieved superior tumor control through dual EC/PC inhibition.