中国肺癌杂志最新文献

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[Research Progress on the Regulatory Mechanism of Respiratory Microbiota in the 
Comorbidity of Chronic Obstructive Pulmonary Disease and Lung Cancer]. [呼吸道微生物群在
慢性阻塞性肺疾病和肺癌合并症中的调控机制研究进展]。
中国肺癌杂志 Pub Date : 2025-12-20 DOI: 10.3779/j.issn.1009-3419.2025.106.33
Yin Zhang, Tianming Zhang, Hong Wang
{"title":"[Research Progress on the Regulatory Mechanism of Respiratory Microbiota in the \u2029Comorbidity of Chronic Obstructive Pulmonary Disease and Lung Cancer].","authors":"Yin Zhang, Tianming Zhang, Hong Wang","doi":"10.3779/j.issn.1009-3419.2025.106.33","DOIUrl":"10.3779/j.issn.1009-3419.2025.106.33","url":null,"abstract":"<p><p>Both chronic obstructive pulmonary disease (COPD) and lung carcinoma (LC) are major public health challenges in China. With the continuous advancement of microbial detection methods, the role of the respiratory microbiome in the pathogenesis and progression of respiratory diseases has become increasingly prominent. This article systematically reviews the dynamic characteristics of the respiratory microbiome during the progression of COPD and LC, then explores its crucial bridging role in COPD-LC comorbidity through mechanisms such as persistently driving chronic inflammation, mediating genomic damage, and participating in immune regulation. The aim is to deepen the understanding of the respiratory microbiome, and to provide new perspectives for optimizing existing treatment strategies, exploring microbial biomarkers for early cancer screening, and improving the clinical management of chronic respiratory diseases.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 12","pages":"939-947"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Lung Cancer with Pulmonary Embolism:
Evidence-based Progress in Anticoagulation Assessment and Management]. [肺癌合并肺栓塞:
基于证据的抗凝评估和管理进展]。
中国肺癌杂志 Pub Date : 2025-12-20 DOI: 10.3779/j.issn.1009-3419.2025.101.25
Yiming Ma, Kun Liu, Changling Tu, Tongyao Xu, Bolin Liu
{"title":"[Lung Cancer with Pulmonary Embolism:\u2029Evidence-based Progress in Anticoagulation Assessment and Management].","authors":"Yiming Ma, Kun Liu, Changling Tu, Tongyao Xu, Bolin Liu","doi":"10.3779/j.issn.1009-3419.2025.101.25","DOIUrl":"10.3779/j.issn.1009-3419.2025.101.25","url":null,"abstract":"<p><p>Lung cancer is the malignant tumour with the highest incidence and mortality rates globally. Patients with lung cancer face a high risk of developing venous thromboembolism (VTE), particularly pulmonary embolism (PE). This not only prolongs hospital stays and increases inpatient costs but also severely impacts patient survival and quality of life. Current risk assessment models for PE and bleeding risk in lung cancer patients remain limited in efficacy, posing challenges for clinicians in selecting anticoagulation or preventing bleeding. Additionally, anticoagulation management involves complex issues such as drug interactions and managing special populations. Based on existing literature, this review summarizes the clinical risk assessment and management of anticoagulation and bleeding, the selection of anticoagulants, and secondary prevention strategies for lung cancer patients with PE, to provide a reference for individualized clinical diagnosis and treatment.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 12","pages":"931-938"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[China National Lung Cancer Screening Guideline with Low-dose Computed Tomography (2025 Version)]. [中国肺癌低剂量ct筛查指南(2025版)]。
中国肺癌杂志 Pub Date : 2025-12-20 Epub Date: 2026-01-22 DOI: 10.3779/j.issn.1009-3419.2025.102.43
{"title":"[China National Lung Cancer Screening Guideline with Low-dose Computed Tomography (2025 Version)].","authors":"","doi":"10.3779/j.issn.1009-3419.2025.102.43","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.43","url":null,"abstract":"<p><p>Lung cancer remains the leading cause of cancer-related deaths in China. Optimizing lung cancer screening strategies to improve screening efficiency and mitigate associated harms has become a key research focus and priority in current clinical practice. The purpose of this paper is to revise the China national lung cancer screening guideline with low-dose computed tomography (LDCT) (2023 version). The revision work for the 2025 version of this guideline was jointly undertaken by experts from the Chinese Expert Group on Early Diagnosis and Treatment of Lung Cancer and experts from the China Lung Oncology Group. Drawing on recent advances in LDCT lung cancer screening at home and abroad, combined with the epidemiological characteristics of lung cancer in China, the expert panel revised the guideline with the following key updates: (1) In the selection criteria of high-risk population, the exposure duration to occupational lung carcinogens is clearly specified; additionally, if an individual's physical condition cannot tolerate potential lung cancer resection surgery or the individual suffers from a life-threatening disease during annual screening, discontinuation of LDCT screening is recommended. (2) The method for measuring nodule size is updated, with mean diameter adopted as the metric for assessing nodule size. (3) In nodule management, the positive threshold for the mean diameter of solid nodules or the solid components of part-solid nodules in baseline screening is raised to 6 mm, and the follow-up interval for positive solid or part-solid nodules is adjusted from 6 months to 3-6 months. (4) It is recommended that informed consent and shared decision-making be integrated throughout the entire process, including high-risk group identification, screening interval determination, and nodule management. This revision further clarifies and optimizes the selection of high-risk groups and the management of screen-detected nodules. Based on a comprehensive balance between the benefits and potential harms of lung cancer screening, it emphasizes the critical importance of informed consent and shared decision-making. This revised guideline will be more aligned with China's national conditions and enhance the standardization and applicability of LDCT-based lung cancer screening across the country.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":" ","pages":"887-895"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146020008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Identification of SORD as A Key Gene Mediating Osimertinib Primary Resistance 
in EGFR-Mutant Lung Adenocarcinoma via Machine Learning and Methylomics]. [通过机器学习和甲基组学发现SORD是egfr突变肺腺癌中介导奥西替尼原发性耐药的关键基因
]。
中国肺癌杂志 Pub Date : 2025-12-20 DOI: 10.3779/j.issn.1009-3419.2025.102.46
Guowei Liang, Hongfeng Wu, Chaoyi Jia, Penghu Gao, Zhanrui Zhang, Chen Chen, Yongwen Li, Hongyu Liu, Jun Chen
{"title":"[Identification of SORD as A Key Gene Mediating Osimertinib Primary Resistance \u2029in EGFR-Mutant Lung Adenocarcinoma via Machine Learning and Methylomics].","authors":"Guowei Liang, Hongfeng Wu, Chaoyi Jia, Penghu Gao, Zhanrui Zhang, Chen Chen, Yongwen Li, Hongyu Liu, Jun Chen","doi":"10.3779/j.issn.1009-3419.2025.102.46","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.46","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC), and epidermal growth factor receptor (EGFR) mutation is its primary molecular driver event. Although the third-generation tyrosine kinase inhibitors (TKIs) Osimertinib has become the standard first-line therapy for such patients, the development of drug resistance severely limits long-term survival benefits. However, increasing evidence suggests that epigenetic remodeling is a crucial non-genetic mechanism contributing to resistance. Specifically, hypermethylation of DNA promoter regions can assist tumor cells in evading drug cytotoxicity by silencing key tumor suppressor genes or metabolic regulatory genes. This study aims to identify key genes regulating Osimertinib sensitivity through machine learning and high-throughput screening, and to dissect the role of methylation modifications in regulating primary resistance to Osimertinib.</p><p><strong>Methods: </strong>Based on The Cancer Genome Atlas (TCGA)-LUAD EGFR mutation cohort, the oncoPredict model was applied to predict Osimertinib half inhibitory concentration (IC50) values. Through multi-omics association analysis, differentially expressed genes in the transcriptome and methylome significantly associated with IC50 were screened, respectively. The intersection of the two omics datasets was identified based on the \"hypermethylation-low expression\" negative correlation pattern, and LASSO regression with Bootstrap validation was applied to screen for the most robust core genes. Finally, in EGFR-mutant LUAD cell lines, the effects of the core gene on Osimertinib resistance, cell proliferation, and apoptosis were validated via drug sensitivity assays, demethylation treatment, and gene overexpression/knockdown experiments.</p><p><strong>Results: </strong>Multi-omics analysis and machine learning algorithms identified SORD as the core candidate gene, with the methylation level of its key site (cg06424894) showing a significant negative correlation with mRNA expression. In vitro experiments revealed that the Osimertinib-resistant cell line H1650 was characterized by SORD hypermethylation and low expression, and demethylation treatment significantly restored its expression; whereas sensitive strains showed the opposite trend. Functional experiments confirmed that overexpression of SORD in H1650 resistant cells could reverse resistance, inhibit cell proliferation, and promote apoptosis. Conversely, knockdown of SORD in sensitive H1975 and PC9 cells significantly induced resistance, promoted proliferation, and inhibited apoptosis.</p><p><strong>Conclusions: </strong>The methylation status or expression level of SORD holds promise as a potential biomarker for predicting Osimertinib efficacy, and targeting SORD-related pathways may provide new strategies for overcoming Osimertinib resistance.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 12","pages":"916-923"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Ensartinib Combined with Radiotherapy for the Treatment of Advanced Primary 
Pulmonary Epithelioid Inflammatory Myofibroblastic Sarcoma Harboring 
TPM3-ALK Fusion: A Case Report]. [恩沙替尼联合放疗治疗晚期原发性
肺上皮样炎性肌成纤维肉瘤
TPM3-ALK融合1例]。
中国肺癌杂志 Pub Date : 2025-12-20 DOI: 10.3779/j.issn.1009-3419.2025.102.40
Ye Zhao, Shuangbing Xu
{"title":"[Ensartinib Combined with Radiotherapy for the Treatment of Advanced Primary \u2029Pulmonary Epithelioid Inflammatory Myofibroblastic Sarcoma Harboring \u2029TPM3-ALK Fusion: A Case Report].","authors":"Ye Zhao, Shuangbing Xu","doi":"10.3779/j.issn.1009-3419.2025.102.40","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.40","url":null,"abstract":"<p><p>Epithelioid inflammatory myofibroblastic sarcoma (EIMS) is a rare and highly aggressive mesenchymal neoplasm that is frequently associated with anaplastic lymphoma kinase (ALK) gene fusion. Surgical resection remains the cornerstone of treatment for patients with early- and intermediate-stage EIMS; however, a standardized therapeutic approach for advanced-stage EIMS has yet to be established. Primary pulmonary EIMS is exceedingly rare, with only a limited number of cases reported in the literature. While treatment with ALK-tyrosine kinase inhibitors (TKIs) is considered a viable therapeutic option, and clinical outcomes with monotherapy using ALK-TKIs have frequently been suboptimal. This study presents a case of advanced primary pulmonary EIMS with a TPM3-ALK fusion. The patient received first-line targeted therapy with the second-generation ALK-TKI Ensartinib, in conjunction with radiotherapy for residual and metastatic lesions. This treatment regimen resulted in significant tumor reduction and sustained disease control. The progression-free survival (PFS) exceeded 32 months, with no significant treatment-related adverse events observed. This study investigates the feasibility of combining targeted therapy with local radiotherapy, guided by genetic testing, to offer novel treatment strategies for patients with advanced primary pulmonary EIMS.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 12","pages":"956-960"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Research Advances on the Immune Evasion Mechanisms of Disseminated Tumor Cells and Their Roles in Cancer Metastasis]. 播散性肿瘤细胞免疫逃避机制及其在肿瘤转移中的作用研究进展
中国肺癌杂志 Pub Date : 2025-12-20 DOI: 10.3779/j.issn.1009-3419.2025.101.23
Zujun Que, Bin Luo, Jianhui Tian
{"title":"[Research Advances on the Immune Evasion Mechanisms of Disseminated Tumor Cells and Their Roles in Cancer Metastasis].","authors":"Zujun Que, Bin Luo, Jianhui Tian","doi":"10.3779/j.issn.1009-3419.2025.101.23","DOIUrl":"10.3779/j.issn.1009-3419.2025.101.23","url":null,"abstract":"<p><p>Tumor metastasis is the leading cause of cancer-related mortality. Disseminated tumor cells (DTCs), serving as the critical 'seeds' in the metastatic cascade, hold the key to determining the success or failure of metastasis. Following dissemination from the primary tumor and colonization of distant organs, DTCs often enter a prolonged state of dormancy. Their subsequent escape from immune surveillance through sophisticated mechanisms enables them to transition from this dormant state to a proliferative one, ultimately culminating in clinically detectable metastatic lesions. A profound understanding of DTCs immune evasion is therefore essential for unraveling the fundamental biology of metastasis and developing effective anti-metastatic strategies. This article systematically reviewed the latest advances in the mechanisms underlying DTCs immune evasion, focusing on three core aspects: defects in antigen presentation, formation of an immunosuppressive microenvironment, and metabolism reprogramming-mediated immunosuppression. Specifically, DTCs achieve 'immune invisibility' by downregulating major histocompatibility complex class-I (MHC-I) molecule expression; they actively construct a local 'protective shield' by recruiting immunosuppressive cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs); and they impair effector immune cell function at the energetic and metabolic levels by remodeling glucose, amino acid, and lipid metabolism. Building upon this, we innovatively integrate the traditional Chinese medicine (TCM) theories of 'hidden toxicity due to vital qi deficiency' and the 'metastatic state' to elucidate the dynamic pathogenic relationship between the body's systemic 'Zhengqi' (vital energy) status and the dormancy-awakening switch of DTCs, offering a novel holistic perspective for comprehending the metastatic process. Finally, we discussed the prospects of multi-target combination therapeutic strategies against DTCs immune evasion and highlight the potential of emerging technologies, such as single-cell sequencing and spatial transcriptomics, aiming to provide valuable insights for future in-depth research and clinical translation in the field of anti-metastasis therapy.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 12","pages":"948-955"},"PeriodicalIF":0.0,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12972579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147349641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Progress in the Immune Mechanism of Microwave Ablation Therapy for Lung Cancer]. 微波消融治疗肺癌的免疫机制研究进展
中国肺癌杂志 Pub Date : 2025-11-20 DOI: 10.3779/j.issn.1009-3419.2025.106.30
Zhenyu Yang, Xiaowen Chen, Junhong Jiang
{"title":"[Progress in the Immune Mechanism of Microwave Ablation Therapy for Lung Cancer].","authors":"Zhenyu Yang, Xiaowen Chen, Junhong Jiang","doi":"10.3779/j.issn.1009-3419.2025.106.30","DOIUrl":"10.3779/j.issn.1009-3419.2025.106.30","url":null,"abstract":"<p><p>Microwave ablation (MWA) is a minimally invasive thermal ablation treatment method and has been widely applied in the local treatment of lung cancer. MWA not only can effectively induce local tumor cell necrosis, but also can activate anti-tumor immune responses by regulating the tumor immune microenvironment (TIME) and inducing potential distant effects. In addition, the combination of MWA and anti-tumor immune drugs may exert a synergistic effect, which provides a new direction for the treatment of lung cancer patients. This article reviews the mechanisms of activation of anti-tumor immune responses during MWA treatment of lung cancer, aiming to provide a theoretical basis and practical guidance for future treatment strategies of lung cancer.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 11","pages":"875-881"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Mechanisms of Exosomes in Lung Cancer Bone Metastasis and Related Clinical Advances]. 外泌体在肺癌骨转移中的作用机制及相关临床进展
中国肺癌杂志 Pub Date : 2025-11-20 DOI: 10.3779/j.issn.1009-3419.2025.101.22
Yuan Yuan, Hao Tang
{"title":"[Mechanisms of Exosomes in Lung Cancer Bone Metastasis and Related Clinical Advances].","authors":"Yuan Yuan, Hao Tang","doi":"10.3779/j.issn.1009-3419.2025.101.22","DOIUrl":"10.3779/j.issn.1009-3419.2025.101.22","url":null,"abstract":"<p><p>Lung cancer is the malignant tumor with the highest morbidity and mortality, and it is usually diagnosed with advanced metastasis. Tumor metastasis is an important factor affecting treatment resistance and poor prognosis of lung cancer, among which bone metastasis is a common metastatic pattern of lung cancer and is associated with a particularly dismal prognosis. Meanwhile, bone metastasis frequently causes skeletal-related events such as bone pain, pathological fractures, nerve compression, and hypercalcemia. Exosomes are extracellular vesicles with a diameter of 40-160 nm that are released from the fusion of intracellular multivesicular bodies and the cell membrane. Carrying proteins, lipids, and nucleic acids, they mediate communication between tumor cells and their surrounding matrix, immune cells, and the bone microenvironment. So, it has attracted increasing attention from researchers. This paper aims to summarize and organize the latest research advances on exosomes promoting lung cancer bone metastasis, focusing on their key mechanisms and signaling pathways. These include promoting tumor cells proliferation, invasion and metastasis at the primary lesion, as well as participating in energy metabolism reprogramming, pre-metastatic niche remodeling, immune microenvironment regulation, and interactions with osteocytes, stromal cells, and other cells during distant bone metastasis colonization. In addition, this review analyzes the potential clinical translational value of exosomes in the early diagnosis, treatment, and prognosis of lung cancer bone metastasis.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 11","pages":"831-840"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Expression Characteristics and Prognostic Study of PPP1R13L in Brain Metastases 
of Lung Adenocarcinoma]. [PPP1R13L在肺腺癌脑转移瘤
中的表达特点及预后研究]。
中国肺癌杂志 Pub Date : 2025-11-20 DOI: 10.3779/j.issn.1009-3419.2025.106.32
Luyao Liu, Peiwen Fan, Cheng Chang, Ruozheng Wang
{"title":"[Expression Characteristics and Prognostic Study of PPP1R13L in Brain Metastases \u2029of Lung Adenocarcinoma].","authors":"Luyao Liu, Peiwen Fan, Cheng Chang, Ruozheng Wang","doi":"10.3779/j.issn.1009-3419.2025.106.32","DOIUrl":"10.3779/j.issn.1009-3419.2025.106.32","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma is prone to brain metastasis, and the prognosis of patients is extremely poor. The inhibitor of apoptosis-stimulating protein of p53 (iASPP) protein, encoded by the protein phosphatase 1 regulatory subunit 13-like (PPP1R13L) gene, is a key inhibitor of the p53 pathway and promotes carcinogenesis in various tumors, but its role in brain metastasis of lung adenocarcinoma is unknown. This study aims to analyze the tumor microenvironment characteristics of patients with brain metastasis of lung adenocarcinoma and explore the expression of PPP1R13L in brain metastasis tissues and its clinical significance by single-cell sequencing and clinical sample analysis.</p><p><strong>Methods: </strong>Brain tissues from 4 patients with lung adenocarcinoma brain metastasis and 2 patients with oligodendroglioma (ODG) were collected from the Affiliated Tumor Hospital of Xinjiang Medical University from January 2014 to December 2024 for single-cell sequencing. The tumor microenvironment was analyzed by combining single-cell sequencing data from 4 lung adenocarcinoma samples and 4 normal lung tissue samples from public databases. Additionally, clinical data and paraffin sections of 50 patients with lung adenocarcinoma brain metastasis in this hospital were collected, and immunohistochemistry was used to assess iASPP expression and its association with clinicopathologic features and patient outcome.</p><p><strong>Results: </strong>Compared with the ODG and lung adenocarcinoma groups, the specific epithelial cells in the lung adenocarcinoma brain metastasis group were mainly enriched in oxidative phosphorylation, apoptosis, hypoxia, and p53 pathways. PPP1R13L, as an upregulated differential gene, was highly expressed in the specific epithelial cell subpopulation of the brain metastasis group; the interaction between PPP1R13L-positive cells and fibroblasts was significant, activating cell-matrix adhesion related pathways, with the key ligand-receptor pair being collagen type I alpha 1 chain-cluster of differentiation 44 (COL1A1-CD44). Statistical evaluation revealed that smoking (HR=2.543, 95%CI: 1.159-5.583, P=0.020) and high expression of iASPP (HR=3.351, 95%CI: 1.310-8.575, P=0.012) were independent predictors of poor prognosis in lung adenocarcinoma patients with brain metastases.</p><p><strong>Conclusions: </strong>This study revealed the interaction between epithelial cells and fibroblasts in the microenvironment of lung adenocarcinoma brain metastasis and implicate PPP1R13L as a potential prognostic indicator and actionable target, offering rationale for precision therapy against lung adenocarcinoma brain metastases.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 11","pages":"818-830"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Combination of Radiotherapy and Immunotherapy for Unresectable Stage III 
Non-small Cell Lung Cancer: Clinical Progress Advances and Future Directions]. [放疗和免疫治疗联合治疗不可切除的III期
非小细胞肺癌:临床进展、进展和未来方向]。
中国肺癌杂志 Pub Date : 2025-11-20 DOI: 10.3779/j.issn.1009-3419.2025.102.42
Zuoyuan Tan, Yuling Zhong, Jingyi Wang, Lin Wu
{"title":"[Combination of Radiotherapy and Immunotherapy for Unresectable Stage III \u2029Non-small Cell Lung Cancer: Clinical Progress Advances and Future Directions].","authors":"Zuoyuan Tan, Yuling Zhong, Jingyi Wang, Lin Wu","doi":"10.3779/j.issn.1009-3419.2025.102.42","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.42","url":null,"abstract":"<p><p>Stage III non-small cell lung cancer (NSCLC) accounts for approximately 30% of newly diagnosed NSCLC cases, and the vast majority of these patients present with unresectable disease. Its unresectable nature makes definitive chemoradiotherapy the cornerstone of treatment. In recent years, with immune checkpoint inhibitors (ICIs) becoming a major research focus in lung cancer, increasing evidence demonstrates that the combination of radiotherapy and immunotherapy (iRT) can significantly enhance antitumor efficacy through synergistic mechanisms. The groundbreaking results of the landmark PACIFIC trial further established consolidation immunotherapy following concurrent chemoradiotherapy as the standard of care. However, controversies persist regarding optimal radiotherapy strategies, timing of immune intervention, management of adverse reactions, and exploration of biomarkers. This review aims to systematically elucidate the synergistic mechanisms of iRT, summarize clinical trial advances under different iRT treatment modalities (concurrent, consolidation and induction), and provide an in-depth analysis of key issues in current clinical practice along with future research directions.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 11","pages":"866-874"},"PeriodicalIF":0.0,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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