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A Sober Look at Agentic Misalignment in Automated Workflows
Divide-and-Conquer Inference for Large-Scale Visual Recognition with Multimodal Large Language Models
SEP-Attack: A Simple and Effective Paradigm for Transfer-Based Textual Adversarial Attack
Anatomy-Anchored Self-Supervision: Distilling Vision Foundation Models for Invariant Ultrasound Representation
SeqRoute: Global Budget-Aware Sequential LLM Routing via Offline Reinforcement Learning
MoBiQuant: Mixture-of-Bits Quantization for Token-Adaptive Any-Precision LLM
Design Conditions for Intra-Group Learning of Sequence-Level Rewards: Token Gradient Cancellation
Reducing Credit Assignment Variance via Counterfactual Reasoning Paths
How Few-Shot Examples Add Up: A Causal Decomposition of Function Vectors in In-Context Learning
The role of growth heterogeneity in solid nodular non-small cell lung cancer in clinical practice: a narrative review
J Thorac Dis. 2026 Apr 30;18(4):417. doi: 10.21037/jtd-2025-1-2697. Epub 2026 Mar 26.
ABSTRACT
BACKGROUND AND OBJECTIVE: Lung cancer remains the leading cause of cancer related mortality worldwide, and early detection and precise stratified management are crucial for improving patient outcomes. Tumor growth kinetics, as a characterization of its proliferation and malignant differentiation, is a key decision-making factor and research hotspot in clinical practice today. This study aimed to elucidate the growth kinetics of solid nodular non-small cell lung cancer (NSCLC) as a critical determinant of early diagnosis, prognostic evaluation, and treatment strategy selection, and to address the challenge that significant heterogeneity in tumor growth poses to risk stratification and clinical decision-making.
METHODS: We conducted a retrospective search of PubMed, Embase, Web of Science, and Scopus databases, focusing on the current research status of solid nodular NSCLC, particularly in terms of molecular mechanisms, prognosis, modeling prediction, and management strategies related to its growth heterogeneity, with the aim of exploring future research directions.
KEY CONTENT AND FINDINGS: Volume doubling time (VDT) serves as a key metric for evaluating nodule dynamics. While earlier studies suggested a generally rapid growth pattern (VDT <400 days) in solid nodular NSCLC, recent evidence reveals considerable heterogeneity, with some tumors demonstrating indolent growth pattern (VDT >40-600 days). The prognosis of rapidly growing nodules is usually poor, so nodule management recommendations should be personalized based on growth dynamics and patient characteristics. Traditional radiological features, and deep learning models show promise for growth risk stratification but require large-scale external validation and refinement. Molecular and pathological studies suggest that the tumor microenvironment and immune cell infiltration may contribute to growth heterogeneity, though direct mechanistic evidence remains limited. Artificial intelligence (AI) based approaches exhibit significant potential in predicting individual tumor growth behavior.
CONCLUSIONS: Growth heterogeneity in solid nodular NSCLC carries substantial clinical significance but remains insufficiently studied. Future research should prioritize imaging based modeling to predict individualized growth dynamics. Integrating multi-omics analyses may help elucidate the molecular factors underlying growth heterogeneity. AI driven risk stratification based on large-scale multi center sequence data can achieve truly personalized and growth oriented management strategies.
PMID:42182806 | PMC:PMC13190150 | DOI:10.21037/jtd-2025-1-2697
The role of growth heterogeneity in solid nodular non-small cell lung cancer in clinical practice: a narrative review
J Thorac Dis. 2026 Apr 30;18(4):417. doi: 10.21037/jtd-2025-1-2697. Epub 2026 Mar 26.
ABSTRACT
BACKGROUND AND OBJECTIVE: Lung cancer remains the leading cause of cancer related mortality worldwide, and early detection and precise stratified management are crucial for improving patient outcomes. Tumor growth kinetics, as a characterization of its proliferation and malignant differentiation, is a key decision-making factor and research hotspot in clinical practice today. This study aimed to elucidate the growth kinetics of solid nodular non-small cell lung cancer (NSCLC) as a critical determinant of early diagnosis, prognostic evaluation, and treatment strategy selection, and to address the challenge that significant heterogeneity in tumor growth poses to risk stratification and clinical decision-making.
METHODS: We conducted a retrospective search of PubMed, Embase, Web of Science, and Scopus databases, focusing on the current research status of solid nodular NSCLC, particularly in terms of molecular mechanisms, prognosis, modeling prediction, and management strategies related to its growth heterogeneity, with the aim of exploring future research directions.
KEY CONTENT AND FINDINGS: Volume doubling time (VDT) serves as a key metric for evaluating nodule dynamics. While earlier studies suggested a generally rapid growth pattern (VDT <400 days) in solid nodular NSCLC, recent evidence reveals considerable heterogeneity, with some tumors demonstrating indolent growth pattern (VDT >40-600 days). The prognosis of rapidly growing nodules is usually poor, so nodule management recommendations should be personalized based on growth dynamics and patient characteristics. Traditional radiological features, and deep learning models show promise for growth risk stratification but require large-scale external validation and refinement. Molecular and pathological studies suggest that the tumor microenvironment and immune cell infiltration may contribute to growth heterogeneity, though direct mechanistic evidence remains limited. Artificial intelligence (AI) based approaches exhibit significant potential in predicting individual tumor growth behavior.
CONCLUSIONS: Growth heterogeneity in solid nodular NSCLC carries substantial clinical significance but remains insufficiently studied. Future research should prioritize imaging based modeling to predict individualized growth dynamics. Integrating multi-omics analyses may help elucidate the molecular factors underlying growth heterogeneity. AI driven risk stratification based on large-scale multi center sequence data can achieve truly personalized and growth oriented management strategies.
PMID:42182806 | PMC:PMC13190150 | DOI:10.21037/jtd-2025-1-2697
The role of growth heterogeneity in solid nodular non-small cell lung cancer in clinical practice: a narrative review
J Thorac Dis. 2026 Apr 30;18(4):417. doi: 10.21037/jtd-2025-1-2697. Epub 2026 Mar 26.
ABSTRACT
BACKGROUND AND OBJECTIVE: Lung cancer remains the leading cause of cancer related mortality worldwide, and early detection and precise stratified management are crucial for improving patient outcomes. Tumor growth kinetics, as a characterization of its proliferation and malignant differentiation, is a key decision-making factor and research hotspot in clinical practice today. This study aimed to elucidate the growth kinetics of solid nodular non-small cell lung cancer (NSCLC) as a critical determinant of early diagnosis, prognostic evaluation, and treatment strategy selection, and to address the challenge that significant heterogeneity in tumor growth poses to risk stratification and clinical decision-making.
METHODS: We conducted a retrospective search of PubMed, Embase, Web of Science, and Scopus databases, focusing on the current research status of solid nodular NSCLC, particularly in terms of molecular mechanisms, prognosis, modeling prediction, and management strategies related to its growth heterogeneity, with the aim of exploring future research directions.
KEY CONTENT AND FINDINGS: Volume doubling time (VDT) serves as a key metric for evaluating nodule dynamics. While earlier studies suggested a generally rapid growth pattern (VDT <400 days) in solid nodular NSCLC, recent evidence reveals considerable heterogeneity, with some tumors demonstrating indolent growth pattern (VDT >40-600 days). The prognosis of rapidly growing nodules is usually poor, so nodule management recommendations should be personalized based on growth dynamics and patient characteristics. Traditional radiological features, and deep learning models show promise for growth risk stratification but require large-scale external validation and refinement. Molecular and pathological studies suggest that the tumor microenvironment and immune cell infiltration may contribute to growth heterogeneity, though direct mechanistic evidence remains limited. Artificial intelligence (AI) based approaches exhibit significant potential in predicting individual tumor growth behavior.
CONCLUSIONS: Growth heterogeneity in solid nodular NSCLC carries substantial clinical significance but remains insufficiently studied. Future research should prioritize imaging based modeling to predict individualized growth dynamics. Integrating multi-omics analyses may help elucidate the molecular factors underlying growth heterogeneity. AI driven risk stratification based on large-scale multi center sequence data can achieve truly personalized and growth oriented management strategies.
PMID:42182806 | PMC:PMC13190150 | DOI:10.21037/jtd-2025-1-2697
Author Correction: Inactivating <i>SnRK1β1A</i> promotes broad-spectrum disease resistance in rice
Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10659-5
Author Correction: Inactivating SnRK1β1A promotes broad-spectrum disease resistance in ricePulmonary-Intestinal Axis: Shared Genetic Basis and Mediating Factors Identified Through Multi-Omics Analysis
Int J Chron Obstruct Pulmon Dis. 2026 Apr 7;21:561645. doi: 10.2147/COPD.S561645. eCollection 2026.
ABSTRACT
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a systemic condition with comorbidities beyond the lung (eg, cardiovascular and metabolic disorders), and gastrointestinal (GI) disorders are also common. The shared genetic basis of COPD-GI comorbidity and its mediating factors remain unclear. We hypothesized that COPD and GI diseases share pleiotropic genetic architecture implicating lipid-metabolic pathways, with smoking mediating part of the association.
METHODS: We analyzed publicly available European-ancestry GWAS summary statistics for COPD (Global Biobank Meta-analysis Initiative), 15 GI diseases (FinnGen), and smoking phenotypes (UK Biobank). Genetic correlation was estimated using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Multi-trait analysis of GWAS (MTAG) boosted COPD discovery by leveraging genetically correlated GI traits. We integrated locus-to-gene mapping with multi-tissue expression quantitative trait loci (eQTL) and plasma protein quantitative trait loci (pQTL) evidence to prioritize shared loci, genes, and proteins. Bidirectional two-sample Mendelian randomization (MR) tested causal directions, and two-step mediation MR evaluated smoking.
RESULTS: COPD showed significant genetic correlation with nine GI diseases. We identified six comorbidity-associated loci (three with CADD > 12.37) and 13 unique candidate pleiotropic genes; APOE was supported by proteomic evidence. Enrichment analyses highlighted lipid-metabolism pathways. MR suggested COPD increases risk of gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), acute appendicitis, and gastric ulcer, while diverticular disease showed reverse causality toward COPD. Smoking partially mediated the COPD effect on GERD, acute appendicitis, and gastric ulcer.
CONCLUSION: COPD and multiple GI disorders share a distributed pleiotropic genetic basis within the broader systemic comorbidity spectrum of COPD. Multi-omics evidence supports a genomic pulmonary-intestinal axis in which lipid metabolism and smoking-related mechanisms contribute to COPD and GI comorbidity, providing targets for risk stratification and potential intervention.
PMID:41978582 | PMC:PMC13070119 | DOI:10.2147/COPD.S561645
Transplantation of encapsulated mitochondria alleviates dysfunction in mitochondrial and Parkinson’s disease models
Genetic mutation and dysfunction of AT2 cells drive B(a)P/LPS-induced inflammation-related lung tumorigenesis: evidence and mechanism of autophagy
Acta Biochim Biophys Sin (Shanghai). 2026 Mar 25. doi: 10.3724/abbs.2025238. Online ahead of print.
ABSTRACT
The environmental pollutant benzo(a)pyrene (B(a)P), a representative polycyclic aromatic hydrocarbon (PAH), is a recognized carcinogen, and chronic pulmonary inflammation is closely associated with lung carcinogenesis. Although alveolar type 2 (AT2) cells are the origin of lung adenocarcinoma, the genetic and functional changes in AT2 cells and the mechanisms involved in inflammation-related lung tumorigenesis have not been elucidated. Here, C57BL/6J mice are exposed to B(a)P and the inflammatory irritant lipopolysaccharide (LPS) to establish a model of inflammation-related lung tumorigenesis. Single-cell RNA sequencing is performed on lung tissues. DNA mutations in AT2 cells are analyzed via whole-exome sequencing. The protein expression of AT2 cells in lung cancer tissue is determined by immunofluorescence staining. The results reveal that LPS promotes B(a)P-induced lung tumorigenesis; in the whole lungs of B(a)P/LPS, a decreased proportion, altered differentiation trajectory, and increased gene mutation number in AT2 cells are observed. Additionally, in B(a)P/LPS-treated lung cancer tissue, the levels of γ-H2AX DNA damage and the proliferation marker Ki67 in AT2 cells are increased, whereas the levels of differentiation markers are decreased. Single-cell RNA transcriptomics reveals that the autophagy-related genes Foxo3 and Ppp2r5, which are enriched in the PI3K-Akt pathway, and the autophagy-related genes in AT2 cells in lung cancer are decreased in the B(a)P/LPS group. Thus, chronic inflammation promotes DNA damage, gene mutation and dysfunction in AT2 cells, and decreased autophagy in AT2 cells may be an important mechanism for inflammation-related lung tumorigenesis.
PMID:41952558 | DOI:10.3724/abbs.2025238
Autonomous Agents for Scientific Discovery: Orchestrating Scientists, Language, Code, and Physics
Multidimensional evaluation of large language models in radiology report readability
npj Digital Medicine, Published online: 01 April 2026; doi:10.1038/s41746-026-02589-3
Multidimensional evaluation of large language models in radiology report readability