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  • βœ‡Omics In Lung
  • Tumorigenesis and Tumor Microenvironment in Lung Cancer Puneet Dhillon Β· Moshe Carroll Β· Haiying Cheng
    Curr Issues Mol Biol. 2026 Feb 26;48(3):247. doi: 10.3390/cimb48030247.ABSTRACTLung cancer remains a leading cause of cancer mortality worldwide and continues to impose substantial clinical and economic burdens. Beyond tumor-intrinsic oncogenic drivers, disease progression and therapy response are shaped by the tumor microenvironment (TME), including immune cells, cancer-associated fibroblasts (CAFs), endothelial cells, extracellular matrix, inflammatory mediators, etc. In lung cancer, chronic i
     

Tumorigenesis and Tumor Microenvironment in Lung Cancer

28 March 2026 at 18:00

Curr Issues Mol Biol. 2026 Feb 26;48(3):247. doi: 10.3390/cimb48030247.

ABSTRACT

Lung cancer remains a leading cause of cancer mortality worldwide and continues to impose substantial clinical and economic burdens. Beyond tumor-intrinsic oncogenic drivers, disease progression and therapy response are shaped by the tumor microenvironment (TME), including immune cells, cancer-associated fibroblasts (CAFs), endothelial cells, extracellular matrix, inflammatory mediators, etc. In lung cancer, chronic injury from tobacco smoke, airway disease, and treatment itself remodels local tissue programs that can either support antitumor immunity or promote immune exclusion, fibrosis, and metastatic seeding. Here, we analyze recent evidence linking lung tumorigenesis to TME ecology across histologies, with emphasis on CAF heterogeneity, spatial organization of immune niches, and the distinct microenvironments that govern organ-specific metastasis (including brain metastasis). We also evaluate emerging therapeutic strategies that aim to target or reprogram the TME, including perioperative immune checkpoint blockade, combined immunotherapy-radiotherapy approaches, and pathways such as IL-6 and TGF-Ξ² that coordinate immune suppression and stromal remodeling. Finally, we outline key gaps and potential future directions, such as longitudinal and spatial multi-omics, better biomarkers of stromal state, and trial designs that account for dynamic microenvironmental adaptation.

PMID:41899399 | PMC:PMC13025777 | DOI:10.3390/cimb48030247

Making Slow Thinking Faster: Compressing LLM Chain-of-Thought via Step Entropy

arXiv:2508.03346v2 Announce Type: replace Abstract: Large Language Models (LLMs) using Chain-of-Thought (CoT) prompting excel at complex reasoning but generate verbose thought processes with considerable redundancy, leading to increased inference costs and reduced efficiency. We introduce a novel CoT compression framework based on step entropy, a metric that quantifies \emph{the informational contribution of individual reasoning steps} to identify redundancy. Through theoretical analysis and extensive empirical validation on mathematical reasoning benchmarks, we demonstrate that steps with low entropy are indeed highly redundant. Our experiments reveal that an astonishing 80\% of low-entropy intermediate steps can be pruned with minor degradation in the final answer accuracy across DeepSeek-R1-7B, 14B and Qwen3-8B. This finding sharply contrasts with random or high-entropy pruning, which severely impairs reasoning performance. Building on this, we propose a novel two-stage training strategy combining Supervised Fine-Tuning (SFT) and Group Relative Policy Optimization (GRPO) reinforcement learning. This approach enables LLMs to autonomously learn to generate compressed COTs during inference by strategically incorporating [SKIP] tokens. Our method significantly improves LLM inference efficiency while preserving accuracy, paving the way for more scalable LLM deployments and a better understanding of their internal reasoning. The code and data are released in https://github.com/staymylove/COT_Compresstion_via_Step_entropy.
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