Signaling in Oncogenesis, Angiogenesis, and Permeability

LASER couples damage sensing to ESCRT assembly for lysosome repair Nature volume 656, pages 216–226 (2026) Abstract Lysosomal membrane integrity is essential for cell survival, but how damage sensing is spatiotemporally coupled to repair remains poorly understood. Recruitment and assembly of endosomal sorting complex required for transport (ESCRT) I–III rapidly counteracts membrane damage, but it is unclear how ESCRT-I recognizes defective lysosomal membranes. Here, leveragin

BAK and BAX form a multiprotein complex to drive mtDNA efflux and caspase-independent cell death Science 22 Oct 2026 Vol 394, Issue 6822 Structured Abstract INTRODUCTION Mitochondria have a pivotal role in mammalian cell death. In response to apoptotic signals, activator BH3-only proteins activate BAX and BAK, leading to mitochondrial outer membrane permeabilization (MOMP), cytochrome c release, apoptosome assembly, and caspase-mediated apoptosis. In cells lacking apoptosome

Nature volume 655, pages 506–515 (2026) Abstract Ubiquitin signalling covers a wide range of protein modifications, but its scope may still be underestimated, owing to the ubiquitination of non-proteinaceous substrates, such as sugars, lipids and nucleotides1. The breadth of ubiquitinated non-protein substrates, their abundance and their cellular roles are currently unclear, as current ubiquitinomic and proteomic techniques do not detect non-proteinaceous modifications. Here

Cancer Cell Volume 44, Issue 6p1160-1178.e8June 08, 2026 Highlights • High-throughput scFCM profiling of TME linking CSCs to immunosuppression in TNBC • CSC-derived EVs-TSPAN8+ interact with CD103 to activate LKB1-AMPK-FOXP3 axis in Tregs • FOXP3 upregulates CD103 expression, a feedback loop driving CD103+FOXP3+ Treg formation • Neutralizing EVs-TSPAN8+ synergizes with anti-PD-1 therapy in TNBC preclinical models Summary Tumor cells evade anti-tumor immunity by reprogramming

Science 3 Sep 2026 Vol 393, Issue 6815 pp. 1036-1044 Editor’s summary Reactive oxygen species (ROS) have a paradoxical role in cancer. Low to moderate ROS levels can stimulate tumor growth, whereas excessive ROS accumulation triggers oxidative stress and DNA damage. Antioxidant therapies aim to neutralize free radicals and reduce oxidative stress, but clinical trials have not (yet) demonstrated improved cancer survival. Wesolowski et al. report that tumors can turn ROS depend

Nature (2026) Abstract Tyrosine kinase inhibitors (TKIs) targeting anaplastic lymphoma kinase (ALK) have transformed the treatment landscape of ALK fusion-positive non-small-cell lung carcinoma (ALK-positive NSCLC), but the limited options for patients who progress on approved TKIs highlight a continued need for an orthogonal therapeutic approach1,2. TRI-611 is a potent, brain-penetrant molecular glue degrader of ALK fusion proteins with the potential to address this need. TR

Cell Volume 189, Issue 14p4295-4309.e6July 09, 2026 Highlights • Distinct senescent states arise across brain-barrier cell lineages • Endothelial cells and macrophages engage a transient inflammatory senescent state • Choroid plexus epithelium maintains a persistent non-inflammatory senescent state • Senescent cell ablation alters vascular patterning and CSF homeostasis Summary Establishment of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier requires

Cell Death Diff Abstract The cGAS-STING pathway is an evolutionarily conserved DNA-sensing mechanism that triggers innate immune responses. cGAS and STING play dual roles in tumorigenesis, promoting antitumor immunity and cell death while fueling tumor growth and metastasis. However, the mechanisms fine-tuning this pathway remain elusive. Using complementary proteomic approaches, we report that Casein Kinase 1 alpha (CK1α) operates as a bimodal regulator of the cGAS-STING pat

Signal Transduction and Targeted Therapy volume 11, Article number: 264 (2026) Abstract Glycoprotein (GP) VI is a platelet-specific activating receptor for collagen and fibrin(ogen), and a promising target for antithrombotic therapy. Inhibitory Fab fragments against GPVI provide robust protection in mouse models of arterial thrombosis and ischemic stroke without impairing hemostasis in mice or humans. However, their short in vivo half-life limits their suitability for long-te