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cs.AI, q-bio.NC updates on arXiv.org
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Not All Tokens Are Created Equal: Query-Efficient Jailbreak Fuzzing for LLMs
arXiv:2603.23269v1 Announce Type: cross Abstract: Large Language Models(LLMs) are widely deployed, yet are vulnerable to jailbreak prompts that elicit policy-violating outputs. Although prior studies have uncovered these risks, they typically treat all tokens as equally important during prompt mutation, overlooking the varying contributions of individual tokens to triggering model refusals. Consequently, these attacks introduce substantial redundant searching under query-constrained scenarios,
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Spatial Omics in Gastrointestinal Oncology: Recent Advances, Therapeutic Insights, and Clinical Translation
J Cancer. 2026 Jan 30;17(3):515-523. doi: 10.7150/jca.127381. eCollection 2026.ABSTRACTGastrointestinal (GI) cancers remain a leading cause of cancer-related morbidity and mortality worldwide, largely due to their molecular heterogeneity, complex tumor microenvironment (TME), and variable treatment responses. In recent years, the emergence of spatially resolved omics technologies-encompassing spatial transcriptomics, proteomics, metabolomics, and epigenomics-has revolutionized the ability to int
Spatial Omics in Gastrointestinal Oncology: Recent Advances, Therapeutic Insights, and Clinical Translation
J Cancer. 2026 Jan 30;17(3):515-523. doi: 10.7150/jca.127381. eCollection 2026.
ABSTRACT
Gastrointestinal (GI) cancers remain a leading cause of cancer-related morbidity and mortality worldwide, largely due to their molecular heterogeneity, complex tumor microenvironment (TME), and variable treatment responses. In recent years, the emergence of spatially resolved omics technologies-encompassing spatial transcriptomics, proteomics, metabolomics, and epigenomics-has revolutionized the ability to interrogate tumor architecture with unprecedented resolution. These methods enable precise mapping of cellular and molecular interactions within intact tissue contexts, thereby uncovering spatially defined niches that influence tumor progression, immune evasion, and therapeutic resistance. In GI malignancies such as colorectal, gastric, and esophageal cancers, spatial omics have provided critical insights into cancer-stromal-immune crosstalk, identified predictive biomarkers for immunotherapy and targeted agents, and guided the development of novel therapeutic strategies. This review synthesizes the latest advances in spatial omics applied to GI oncology over the past five years, with an emphasis on their integration into early diagnosis, treatment stratification, and real-time monitoring of therapeutic efficacy. We also discuss current challenges, including standardization, data integration, and clinical validation, as well as future directions for incorporating spatial profiling into routine oncology practice. By bridging the gap between bench discoveries and bedside applications, spatial omics hold transformative potential for achieving truly personalized treatment in gastrointestinal cancers.
PMID:41869445 | PMC:PMC13003551 | DOI:10.7150/jca.127381
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cs.AI, q-bio.NC updates on arXiv.org
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ELLA: Generative AI-Powered Social Robots for Early Language Development at Home
arXiv:2603.12508v1 Announce Type: cross Abstract: Early language development shapes children's later literacy and learning, yet many families have limited access to scalable, high-quality support at home. Recent advances in generative AI make it possible for social robots to move beyond scripted interactions and engage children in adaptive, conversational activities, but it remains unclear how to design such systems for pre-schoolers and how children engage with them over time in the home. We p
ELLA: Generative AI-Powered Social Robots for Early Language Development at Home
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Multi-Omics Characterization of Lactate-Associated Molecular Subtypes in Lung Cancer Suggests a Role for DKK1 in Lactate-Linked Migration, Invasion, and Lactylation Programs
Cancers (Basel). 2026 Feb 25;18(5):735. doi: 10.3390/cancers18050735.ABSTRACTBACKGROUND: Lactate accumulation is increasingly recognized as a feature of tumor metabolic reprogramming that can coincide with immune dysregulation and aggressive phenotypes. The prognostic and immunologic relevance of lactate-associated heterogeneity in lung cancer remains to be clarified.METHODS: We curated lactate-related genes and identified prognostic candidates in lung cancer cohorts. Consensus clustering was ap
Multi-Omics Characterization of Lactate-Associated Molecular Subtypes in Lung Cancer Suggests a Role for DKK1 in Lactate-Linked Migration, Invasion, and Lactylation Programs
Cancers (Basel). 2026 Feb 25;18(5):735. doi: 10.3390/cancers18050735.
ABSTRACT
BACKGROUND: Lactate accumulation is increasingly recognized as a feature of tumor metabolic reprogramming that can coincide with immune dysregulation and aggressive phenotypes. The prognostic and immunologic relevance of lactate-associated heterogeneity in lung cancer remains to be clarified.
METHODS: We curated lactate-related genes and identified prognostic candidates in lung cancer cohorts. Consensus clustering was applied to define lactate-associated molecular subtypes, followed by characterization of survival and tumor microenvironment features. A LASSO-based gene signature was developed to generate an individual-level risk score and an integrated nomogram. Multi-omics analyses were used to evaluate concordance between transcriptomic and proteomic alterations. Single-cell transcriptomic data were analyzed to explore cellular heterogeneity in lactate-related programs. In vitro assays evaluated the response of candidate genes to lactate exposure and assessed cell migration and invasion under proliferation-inhibited conditions after genetic perturbation.
RESULTS: Two lactate-associated molecular subtypes were identified with distinct overall survival and divergent immune microenvironment features. Subtype 1 was associated with better outcomes and a more immune-inflamed profile, whereas Subtype 2 was associated with poorer outcomes and a myeloid-enriched, immunosuppressive contexture. Pathway analyses indicated subtype-associated differences in extracellular matrix-related processes and apoptosis-associated signaling. We developed an 11-gene prognostic signature and nomogram that stratified patients by risk across TCGA and GEO cohorts. Multi-omics integration highlighted ANLN, FGA, and DKK1 as consistently dysregulated at both transcript and protein levels. Among these candidates, DKK1 showed lactate-responsive induction in vitro. DKK1 perturbation altered lactate-enhanced migratory and invasive phenotypes and was accompanied by changes in intracellular lactate levels and global protein lactylation, supporting a potential feedforward relationship between lactate exposure, DKK1 expression, and lactylation.
CONCLUSIONS: This study characterizes lactate-associated molecular heterogeneity in lung cancer and provides a lactate-related subtype framework and prognostic risk model for patient stratification. The findings nominate DKK1 as a lactate-responsive candidate linked to migration/invasion phenotypes and lactate/lactylation changes in vitro.
PMID:41827671 | PMC:PMC12985219 | DOI:10.3390/cancers18050735
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Omics In Lung
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Multi-Omics Characterization of Lactate-Associated Molecular Subtypes in Lung Cancer Suggests a Role for DKK1 in Lactate-Linked Migration, Invasion, and Lactylation Programs
Cancers (Basel). 2026 Feb 25;18(5):735. doi: 10.3390/cancers18050735.ABSTRACTBACKGROUND: Lactate accumulation is increasingly recognized as a feature of tumor metabolic reprogramming that can coincide with immune dysregulation and aggressive phenotypes. The prognostic and immunologic relevance of lactate-associated heterogeneity in lung cancer remains to be clarified.METHODS: We curated lactate-related genes and identified prognostic candidates in lung cancer cohorts. Consensus clustering was ap
Multi-Omics Characterization of Lactate-Associated Molecular Subtypes in Lung Cancer Suggests a Role for DKK1 in Lactate-Linked Migration, Invasion, and Lactylation Programs
Cancers (Basel). 2026 Feb 25;18(5):735. doi: 10.3390/cancers18050735.
ABSTRACT
BACKGROUND: Lactate accumulation is increasingly recognized as a feature of tumor metabolic reprogramming that can coincide with immune dysregulation and aggressive phenotypes. The prognostic and immunologic relevance of lactate-associated heterogeneity in lung cancer remains to be clarified.
METHODS: We curated lactate-related genes and identified prognostic candidates in lung cancer cohorts. Consensus clustering was applied to define lactate-associated molecular subtypes, followed by characterization of survival and tumor microenvironment features. A LASSO-based gene signature was developed to generate an individual-level risk score and an integrated nomogram. Multi-omics analyses were used to evaluate concordance between transcriptomic and proteomic alterations. Single-cell transcriptomic data were analyzed to explore cellular heterogeneity in lactate-related programs. In vitro assays evaluated the response of candidate genes to lactate exposure and assessed cell migration and invasion under proliferation-inhibited conditions after genetic perturbation.
RESULTS: Two lactate-associated molecular subtypes were identified with distinct overall survival and divergent immune microenvironment features. Subtype 1 was associated with better outcomes and a more immune-inflamed profile, whereas Subtype 2 was associated with poorer outcomes and a myeloid-enriched, immunosuppressive contexture. Pathway analyses indicated subtype-associated differences in extracellular matrix-related processes and apoptosis-associated signaling. We developed an 11-gene prognostic signature and nomogram that stratified patients by risk across TCGA and GEO cohorts. Multi-omics integration highlighted ANLN, FGA, and DKK1 as consistently dysregulated at both transcript and protein levels. Among these candidates, DKK1 showed lactate-responsive induction in vitro. DKK1 perturbation altered lactate-enhanced migratory and invasive phenotypes and was accompanied by changes in intracellular lactate levels and global protein lactylation, supporting a potential feedforward relationship between lactate exposure, DKK1 expression, and lactylation.
CONCLUSIONS: This study characterizes lactate-associated molecular heterogeneity in lung cancer and provides a lactate-related subtype framework and prognostic risk model for patient stratification. The findings nominate DKK1 as a lactate-responsive candidate linked to migration/invasion phenotypes and lactate/lactylation changes in vitro.
PMID:41827671 | PMC:PMC12985219 | DOI:10.3390/cancers18050735