Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Hierarchical and Permutation-Invariant Feature Transformation Learning via Policy-Guided Embedding Search
arXiv:2609.10225v1 Announce Type: cross Abstract: Feature transformation improves predictive performance on tabular data by constructing informative abstractions from raw features. Recent generative approaches encode transformation knowledge into continuous embedding spaces for efficient exploration of candidate strategies, but face three key limitations: (1) overlooking hierarchical relationships between low-level features, operations, and high-level abstractions; (2) enforcing order-sensitive
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cs.AI, q-bio.NC updates on arXiv.org
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City Editing: Hierarchical Agentic Execution for Dependency-Aware Urban Geospatial Modification
arXiv:2602.19326v3 Announce Type: replace-cross Abstract: Urban renewal requires incremental modifications to existing geospatial plans, yet manually updating complex layouts under spatial constraints is labor-intensive and error-prone. To tackle this, we propose CEAE, a hierarchical agentic framework that formulates urban renewal as machine-executable GeoJSON editing from natural-language instructions. CEAE decomposes instructions into hierarchical geometric intents, executing edits from coars
City Editing: Hierarchical Agentic Execution for Dependency-Aware Urban Geospatial Modification
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Omics In Lung
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Early stage nonsmall cell lung cancer: Toward a risk-adaptive paradigm in the era of biologic precision
CA Cancer J Clin. 2026 Sep-Oct;76(5):e70100. doi: 10.3322/caac.70100.ABSTRACTThe clinical landscape of early stage nonsmall cell lung cancer is at transformative crossroads. Driven by the widespread adoption of low-dose computed tomography screening, the frequent detection of ground-glass opacities, and a rising incidence among never-smokers, the diagnostic center of gravity has shifted toward earlier, potentially curable disease. This shift has been accompanied by equally important therapeutic
Early stage nonsmall cell lung cancer: Toward a risk-adaptive paradigm in the era of biologic precision
CA Cancer J Clin. 2026 Sep-Oct;76(5):e70100. doi: 10.3322/caac.70100.
ABSTRACT
The clinical landscape of early stage nonsmall cell lung cancer is at transformative crossroads. Driven by the widespread adoption of low-dose computed tomography screening, the frequent detection of ground-glass opacities, and a rising incidence among never-smokers, the diagnostic center of gravity has shifted toward earlier, potentially curable disease. This shift has been accompanied by equally important therapeutic advances, including parenchyma-sparing surgical techniques, minimally invasive platforms enhanced by digital navigation, and the transformative integration of perioperative immunotherapy and targeted agents. Concurrently, noninvasive monitoring approaches, such as liquid biopsy, have emerged as powerful tools to guide precision management. Despite this progress, substantial barriers to achieving a universal cure persist. Clinicians continue to face uncertainty in the management of ground-glass opacities, the anatomy-based TNM staging system fails to capture the biologic heterogeneity of early tumors, and global disparities in access to innovation remain unresolved. To address these challenges, the authors propose a shift toward a risk-adaptive management paradigm that harnesses artificial intelligence-driven analytics and multi-omics profiling to tailor treatment intensity according to each patient's biologic risk. Such an approach would enable appropriate escalation for high-risk individuals while permitting safe de-escalation for those at low risk. This holistic, lifespan-oriented strategy must be embraced to deliver equitable and durable cures for patients with early stage nonsmall cell lung cancer.
PMID:42713910 | PMC:PMC13555834 | DOI:10.3322/caac.70100
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Early stage nonsmall cell lung cancer: Toward a risk-adaptive paradigm in the era of biologic precision
CA Cancer J Clin. 2026 Sep-Oct;76(5):e70100. doi: 10.3322/caac.70100.ABSTRACTThe clinical landscape of early stage nonsmall cell lung cancer is at transformative crossroads. Driven by the widespread adoption of low-dose computed tomography screening, the frequent detection of ground-glass opacities, and a rising incidence among never-smokers, the diagnostic center of gravity has shifted toward earlier, potentially curable disease. This shift has been accompanied by equally important therapeutic
Early stage nonsmall cell lung cancer: Toward a risk-adaptive paradigm in the era of biologic precision
CA Cancer J Clin. 2026 Sep-Oct;76(5):e70100. doi: 10.3322/caac.70100.
ABSTRACT
The clinical landscape of early stage nonsmall cell lung cancer is at transformative crossroads. Driven by the widespread adoption of low-dose computed tomography screening, the frequent detection of ground-glass opacities, and a rising incidence among never-smokers, the diagnostic center of gravity has shifted toward earlier, potentially curable disease. This shift has been accompanied by equally important therapeutic advances, including parenchyma-sparing surgical techniques, minimally invasive platforms enhanced by digital navigation, and the transformative integration of perioperative immunotherapy and targeted agents. Concurrently, noninvasive monitoring approaches, such as liquid biopsy, have emerged as powerful tools to guide precision management. Despite this progress, substantial barriers to achieving a universal cure persist. Clinicians continue to face uncertainty in the management of ground-glass opacities, the anatomy-based TNM staging system fails to capture the biologic heterogeneity of early tumors, and global disparities in access to innovation remain unresolved. To address these challenges, the authors propose a shift toward a risk-adaptive management paradigm that harnesses artificial intelligence-driven analytics and multi-omics profiling to tailor treatment intensity according to each patient's biologic risk. Such an approach would enable appropriate escalation for high-risk individuals while permitting safe de-escalation for those at low risk. This holistic, lifespan-oriented strategy must be embraced to deliver equitable and durable cures for patients with early stage nonsmall cell lung cancer.
PMID:42713910 | DOI:10.3322/caac.70100
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(Multiomics OR Omics) AND (Pancreatic)
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Multi-omics integration identifies APOE as a metabolic regulator of macrophage-fibroblast crosstalk in idiopathic pulmonary fibrosis
Front Immunol. 2026 Aug 18;17:1904638. doi: 10.3389/fimmu.2026.1904638. eCollection 2026.ABSTRACTBACKGROUND: Aberrant tissue repair and relentless fibroblast activation are hallmark features of idiopathic pulmonary fibrosis (IPF). Although IPF and Alzheimer's disease (AD) share underlying aging-related pathologies, including immune and metabolic dysregulation, the putative genetic mechanisms linking AD susceptibility to pathogenic macrophage remodeling in the fibrotic niche are not fully establi
Multi-omics integration identifies APOE as a metabolic regulator of macrophage-fibroblast crosstalk in idiopathic pulmonary fibrosis
Front Immunol. 2026 Aug 18;17:1904638. doi: 10.3389/fimmu.2026.1904638. eCollection 2026.
ABSTRACT
BACKGROUND: Aberrant tissue repair and relentless fibroblast activation are hallmark features of idiopathic pulmonary fibrosis (IPF). Although IPF and Alzheimer's disease (AD) share underlying aging-related pathologies, including immune and metabolic dysregulation, the putative genetic mechanisms linking AD susceptibility to pathogenic macrophage remodeling in the fibrotic niche are not fully established.
METHODS: We performed a two-sample Mendelian randomization (MR) analysis to assess the genetic association and potential causal relationship between AD and IPF. Shared hub genes were identified via protein interaction networks. To characterize macrophage heterogeneity and intercellular crosstalk within the IPF microenvironment, we interrogated scRNA-seq data (GSE122960) utilizing Monocle 3 and CellChat algorithms. The functional essentiality of APOE was evaluated bridging computational virtual knockout (scTenifoldKnk) with laboratory in vitro assays. Specifically, downstream transcriptomic shifts and fibroblast activation capacities were validated using APOE-silenced THP-1 macrophages and a Transwell co-culture model with MRC-5 cells.
RESULTS: MR estimates indicated that genetic liability to AD is associated with a lower risk of developing IPF. Integrated profiling identified the lipid-metabolism gene APOE as a central hub, specifically enriched in lung macrophages. Pseudotime modeling captured a pathogenic bifurcation in IPF, where macrophages evolve toward a terminal state marked by profound oxidative phosphorylation defects and massive SPP1 secretion. These SPP1+ macrophages primarily activate fibroblasts via CD44 and integrin signaling axes. Furthermore, both virtual simulations and in vitro THP-1 experiments demonstrated that loss of APOE function triggers the hyperactivation of complement (C1QA) and antigen-presentation (HLA-DR) pathways. Co-culture assays ultimately confirmed that APOE ablation in macrophages strongly exacerbates myofibroblast differentiation (elevated α-SMA and collagen I) in adjacent MRC-5 cells.
CONCLUSION: APOE functions as a vital metabolic barrier against pro-fibrotic macrophage polarization in the lung. Disruption of this specific lipid metabolic network is strongly associated with SPP1-driven fibroblast activation and local immune imbalance, providing a theoretical framework that strictly warrants future in vivo investigation to determine its clinical relevance.
PMID:42682427 | PMC:PMC13529525 | DOI:10.3389/fimmu.2026.1904638
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(Multiomics OR Omics) AND (Pancreatic)
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Nitrogen dioxide exposure promotes CD8(+)T cell infiltration and contributes to increased susceptibility to ulcerative colitis: An integrative multi-omics, artificial intelligence, and mouse model study
J Hazard Mater. 2026 Sep 15;516:143449. doi: 10.1016/j.jhazmat.2026.143449. Epub 2026 Aug 30.ABSTRACTThe global incidence of ulcerative colitis (UC) has significantly increased in rapidly industrializing nations, with numerous studies highlighting environmental exposures, particularly nitrogen dioxide (NO2), as potential contributors to disease susceptibility. However, the clinical implications and molecular mechanisms linking NO2 exposure to UC susceptibility remain poorly understood. This stud
Nitrogen dioxide exposure promotes CD8(+)T cell infiltration and contributes to increased susceptibility to ulcerative colitis: An integrative multi-omics, artificial intelligence, and mouse model study
J Hazard Mater. 2026 Sep 15;516:143449. doi: 10.1016/j.jhazmat.2026.143449. Epub 2026 Aug 30.
ABSTRACT
The global incidence of ulcerative colitis (UC) has significantly increased in rapidly industrializing nations, with numerous studies highlighting environmental exposures, particularly nitrogen dioxide (NO2), as potential contributors to disease susceptibility. However, the clinical implications and molecular mechanisms linking NO2 exposure to UC susceptibility remain poorly understood. This study investigated the associations between NO2 and UC by integrating multi-omics data. We identified a CD8+ T cell subpopulation with a distinct phenotype characterized by perforin production, which potentially exacerbated colonic inflammation related to NO2 exposure. To validate this hypothesis, we established mouse models exposed to NO2, confirming increased CD8+ T cell infiltration and elevated perforin secretion through immunofluorescent (IF) staining. Employing artificial intelligence techniques, we identified Cell Division Cycle 25B (CDC25B) as a gene of interest correlated with putative NO2-related UC signatures. Finally, through molecular docking (MD) and molecular dynamics simulations (MDS), we identified ozanimod as one of several computationally nominated compounds associated with the CDC25B‑related network; however, none of these computational predictions were experimentally validated in the present study. Collectively, these findings suggest a correlative link between perforin or CD8+ T cell-associated colonic inflammation and NO2-associated UC susceptibility, and nominate CDC25B as a candidate gene for further investigation.
PMID:42679583 | DOI:10.1016/j.jhazmat.2026.143449
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Cell Death Discovery nature.com science feeds
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Ibrutinib-triggered matriptase maintains extracellular CD19 and limits antigen escape in B-cell malignancy
Cell Death Discovery, Published online: 31 August 2026; doi:10.1038/s41420-026-03306-5Ibrutinib-triggered matriptase maintains extracellular CD19 and limits antigen escape in B-cell malignancy
Ibrutinib-triggered matriptase maintains extracellular CD19 and limits antigen escape in B-cell malignancy
Cell Death Discovery, Published online: 31 August 2026; doi:10.1038/s41420-026-03306-5
Ibrutinib-triggered matriptase maintains extracellular CD19 and limits antigen escape in B-cell malignancy-
Cell
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Skin-innervating glutamatergic neurons modulate aging
Within the skin, glutamatergic neurons expressing neurofilament heavy chain (Nefh) play a role in aging. Loss of Nefh during aging drives skin fibroblast senescence and collagen loss, whereas glutamate supplementation improves skin aging phenotypes.
Skin-innervating glutamatergic neurons modulate aging
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cs.AI, q-bio.NC updates on arXiv.org
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Disentangled Double Machine Learning for Accurate Causal Effect Estimation
arXiv:2605.24808v1 Announce Type: cross Abstract: Confounding bias is a key challenge in causal effect estimation from observational data. Double Machine Learning (DML) addresses this issue by estimating treatment and outcome nuisance functions, constructing treatment and outcome residuals, and estimating causal effects from the residuals. However, DML often produces biased and unstable estimates in highdimensional or finite-sample scenarios. One reason is that DML estimates nuisance functions
Disentangled Double Machine Learning for Accurate Causal Effect Estimation
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cs.AI, q-bio.NC updates on arXiv.org
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PageLLM: A Multi-Grained Reward Framework for Whole-Page Optimization with Large Language Models
arXiv:2506.09084v2 Announce Type: replace-cross Abstract: Whole-page optimization (WPO) decides how search and recommendation results are surfaced to users, and large language models (LLMs) open a new route to it by treating page generation as sequence generation. Adapting LLMs to web-scale WPO, however, remains bottlenecked by the need for costly human annotations and by the mismatched granularity between page-level coherence and item-level placement. In this work we show that these two challe
PageLLM: A Multi-Grained Reward Framework for Whole-Page Optimization with Large Language Models
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cs.AI, q-bio.NC updates on arXiv.org
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ChunkLLM: A Lightweight Pluggable Framework for Accelerating LLMs Inference
arXiv:2510.02361v2 Announce Type: replace-cross Abstract: Transformer-based large models excel in natural language processing and computer vision, but face severe computational inefficiencies due to the self-attention's quadratic complexity with input tokens. Recently, researchers have proposed a series of methods based on block selection and compression to alleviate this problem, but they either have issues with semantic incompleteness or poor training-inference efficiency. To comprehensively
ChunkLLM: A Lightweight Pluggable Framework for Accelerating LLMs Inference
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cs.AI, q-bio.NC updates on arXiv.org
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SSDAU: Structured Semantic Data Augmentation for Joint Entity and Relation Extraction
arXiv:2605.23440v2 Announce Type: replace-cross Abstract: Joint Entity and Relation Extraction (JERE) is highly susceptible to weak generalization due to low-quality training data. Data augmentation is a common strategy to enhance model generalization across different domains. However, existing data augmentation methods often overlook text relevance and may disrupt semantic structures and dependencies, making it difficult to generate effective augmented data for improving model generalization.
SSDAU: Structured Semantic Data Augmentation for Joint Entity and Relation Extraction
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Oncogene - Issue - nature.com science feeds
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circPARPBP promotes cancer stemness and chemoresistance in triple-negative breast cancer through recruiting SRCAP complex to activate CCL20 transcription
Oncogene, Published online: 21 May 2026; doi:10.1038/s41388-026-03819-4circPARPBP promotes cancer stemness and chemoresistance in triple-negative breast cancer through recruiting SRCAP complex to activate CCL20 transcription
circPARPBP promotes cancer stemness and chemoresistance in triple-negative breast cancer through recruiting SRCAP complex to activate CCL20 transcription
Oncogene, Published online: 21 May 2026; doi:10.1038/s41388-026-03819-4
circPARPBP promotes cancer stemness and chemoresistance in triple-negative breast cancer through recruiting SRCAP complex to activate CCL20 transcription-
Omics in Hepatocellular
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Integrative multi-omics and experimental validation reveal UBE2C as a central hub gene and prognostic biomarker in hepatocellular carcinoma
Int Immunopharmacol. 2026 May 19;183:116866. doi: 10.1016/j.intimp.2026.116866. Online ahead of print.ABSTRACTHepatocellular carcinoma (HCC) is a lethal malignancy with a high recurrence rate and limited treatment options. Ubiquitin-conjugating enzyme E2 C (UBE2C) is implicated in various cancers, yet its impact on the HCC immune landscape remains incompletely understood. Herein, hub genes in HCC were identified, by integrating co-expression networks and protein-protein interaction analyses, fro
Integrative multi-omics and experimental validation reveal UBE2C as a central hub gene and prognostic biomarker in hepatocellular carcinoma
Int Immunopharmacol. 2026 May 19;183:116866. doi: 10.1016/j.intimp.2026.116866. Online ahead of print.
ABSTRACT
Hepatocellular carcinoma (HCC) is a lethal malignancy with a high recurrence rate and limited treatment options. Ubiquitin-conjugating enzyme E2 C (UBE2C) is implicated in various cancers, yet its impact on the HCC immune landscape remains incompletely understood. Herein, hub genes in HCC were identified, by integrating co-expression networks and protein-protein interaction analyses, from the TCGA, GEO, and CPTAC databases. Their expression was analysed using a single-cell transcriptomic database and verified in HCC tissues and cell lines via quantitative reverse transcription-PCR and immunoblotting. Functional roles of UBE2C were assessed using in vitro knockdown experiments and an in vivo subcutaneous tumour model. The tumour immune microenvironment was profiled using spatial transcriptomics, RNA-seq data, and ssGSEA. A prognostic nomogram was constructed based on multivariate Cox regression. UBE2C was identified as a significantly upregulated hub gene in HCC. Single-cell RNA-seq revealed predominant expression of UBE2C in hepatocytes, with dynamic upregulation along differentiation trajectories. UBE2C knockdown suppressed proliferation, induced apoptosis, and inhibited tumour growth. Spatial transcriptomics highlighted UBE2C-high regions within proliferative niches exhibiting immunosuppressive traits-including TGFB1 enrichment, impaired CXCL9-CXCR3 signalling, and exclusion of cytotoxic T cells-which were reduced in immunotherapy responders. UBE2C expression correlated with immune checkpoint genes and specific immune cell subsets. A UBE2C-based nomogram integrating T stage and tumour stage robustly predicted patient survival, and miR-300 and miR-381-3p were identified as potential upstream regulators. These findings establish UBE2C as a key driver of HCC progression and a biomarker for prognosis and immunotherapy stratification.
PMID:42155390 | DOI:10.1016/j.intimp.2026.116866
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Cell
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An activated wheat CCG10-NLR immune receptor forms an octameric resistosome
An activated CCG10-NLR WAI3 plant immune receptor forms an octameric resistosome, which induces calcium influx and immune responses through a unique channel architecture.
An activated wheat CCG10-NLR immune receptor forms an octameric resistosome
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(Multiomics OR Omics) AND (Pancreatic)
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Unraveling RELA as a potential dioctyl terephthalate-related target regulates M2-like macrophages to induce an immunosuppressive microenvironment in colorectal cancer: a multi-omics data study by experimental validation
Mol Divers. 2026 Apr 12. doi: 10.1007/s11030-026-11545-y. Online ahead of print.NO ABSTRACTPMID:41966666 | DOI:10.1007/s11030-026-11545-y
Unraveling RELA as a potential dioctyl terephthalate-related target regulates M2-like macrophages to induce an immunosuppressive microenvironment in colorectal cancer: a multi-omics data study by experimental validation
Mol Divers. 2026 Apr 12. doi: 10.1007/s11030-026-11545-y. Online ahead of print.
NO ABSTRACT
PMID:41966666 | DOI:10.1007/s11030-026-11545-y
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Nature - Issue - nature.com science feeds
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Clinical application of base editing for treating β-thalassaemia
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10342-9A clinical phase 1 trial of a single infusion of CS-101, CD34+ cells modified using a transformer base editor to reactivate fetal haemoglobin production, led to early and enduring transfusion independence in patients with β-thalassaemia.
Clinical application of base editing for treating β-thalassaemia
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10342-9
A clinical phase 1 trial of a single infusion of CS-101, CD34+ cells modified using a transformer base editor to reactivate fetal haemoglobin production, led to early and enduring transfusion independence in patients with β-thalassaemia.-
Nature - Issue - nature.com science feeds
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Asymmetric selection of a rice immune module and rebuild of disease resistance
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10361-6Stacking XA48-mediated effector-triggered immunity with XA21-mediated pattern-triggered immunity in Oryza sativa japonica reconstitutes the broad-spectrum resistance from wild rice.
Asymmetric selection of a rice immune module and rebuild of disease resistance
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10361-6
Stacking XA48-mediated effector-triggered immunity with XA21-mediated pattern-triggered immunity in Oryza sativa japonica reconstitutes the broad-spectrum resistance from wild rice.-
cs.AI, q-bio.NC updates on arXiv.org
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Agile Deliberation: Concept Deliberation for Subjective Visual Classification
arXiv:2512.10821v2 Announce Type: replace Abstract: From content moderation to content curation, applications requiring vision classifiers for visual concepts are rapidly expanding. Existing human-in-the-loop approaches typically assume users begin with a clear, stable concept understanding to be able to provide high-quality supervision. In reality, users often start with a vague idea and must iteratively refine it through "concept deliberation", a practice we uncovered through structured inter
Agile Deliberation: Concept Deliberation for Subjective Visual Classification
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cs.AI, q-bio.NC updates on arXiv.org
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Efficient Reasoning with Balanced Thinking
arXiv:2603.12372v3 Announce Type: replace Abstract: Large Reasoning Models (LRMs) have shown remarkable reasoning capabilities, yet they often suffer from overthinking, expending redundant computational steps on simple problems, or underthinking, failing to explore sufficient reasoning paths despite inherent capabilities. These issues lead to inefficiencies and potential inaccuracies, limiting practical deployment in resource-constrained settings. Existing methods to mitigate overthinking, such