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cs.AI, q-bio.NC updates on arXiv.org
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RAAP: Retrieval-Augmented Affordance Prediction with Cross-Image Action Alignment
arXiv:2603.29419v1 Announce Type: cross Abstract: Understanding object affordances is essential for enabling robots to perform purposeful and fine-grained interactions in diverse and unstructured environments. However, existing approaches either rely on retrieval, which is fragile due to sparsity and coverage gaps, or on large-scale models, which frequently mislocalize contact points and mispredict post-contact actions when applied to unseen categories, thereby hindering robust generalization.
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Nature - Issue - nature.com science feeds
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DNA damage burden causes selective CUX2 neuron loss in neuroinflammation
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10310-3DNA damage burden and inadequate repair in CUX2+ cortical layer 2/3 excitatory neurons contributes to selective vulnerability in neuroinflammatory injury.
DNA damage burden causes selective CUX2 neuron loss in neuroinflammation
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10310-3
DNA damage burden and inadequate repair in CUX2+ cortical layer 2/3 excitatory neurons contributes to selective vulnerability in neuroinflammatory injury.-
Nature - Issue - nature.com science feeds
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Expansion of outer cortical CUX2 neurons requires adaptations for DNA repair
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10290-4The transcription factor ATF4 is shown to regulate double-stranded DNA repair within vulnerable CUX2+ upper-layer 2/3 cortical neurons, enabling their survival during development.
Expansion of outer cortical CUX2 neurons requires adaptations for DNA repair
Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10290-4
The transcription factor ATF4 is shown to regulate double-stranded DNA repair within vulnerable CUX2+ upper-layer 2/3 cortical neurons, enabling their survival during development.-
(Multiomics OR Omics) AND (Pancreatic)
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Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.ABSTRACTIntratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8
Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.
ABSTRACT
Intratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8% of tumors by existing subtyping systems. To overcome this, we identify a low-intratumor-heterogeneity/high-intertumor-variability (LIHV) gene set and develop an ITH-insensitive classification system defining five subgroups: inflammatory (SI), metabolic (SII), atypical (SIII-1), immune-silent (SIII-2), and neurodegenerative (SIII-3). These subgroups exhibit distinct clinical outcomes, molecular features, immune landscapes, and therapeutic vulnerabilities. GPRC5A and VTCN1 serve as robust immunohistochemical biomarkers for SI and SIII tumors, while serum CEA and CA19-9 identify inflammatory iCCA. Therapeutically, HSP90 inhibition synergizes with anti-PD1 in inflammatory iCCA, whereas combined anti-PD1 and anti-TIM3 suppresses neurodegenerative iCCA. Collectively, our study provides a robust molecular framework and actionable therapeutic strategies for iCCA.
PMID:41916296 | DOI:10.1016/j.xcrm.2026.102708