中国肺癌杂志最新文献

{"title":"[Immune Checkpoints Mediate Tumor Immune Regulation \u2029through Metabolic Pathways].","authors":"Weiguang Du, Xiyang Tang, Yulong Zhou, Mengchao Li, Ze Jin, Jiaqi Dou, Jinbo Zhao","doi":"10.3779/j.issn.1009-3419.2025.106.08","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.106.08","url":null,"abstract":"<p><p>Immune checkpoints include a series of receptor-ligand pairs that play a key role in the proliferation, activation, and immune regulatory responses of immune cells. Although immune checkpoint inhibitors (ICIs), such as programmed death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) have achieved good therapeutic effects in clinical practice, some patients still experience ineffective treatment and immune resistance. A large amount of evidence has shown that immune checkpoint proteins are related to cell metabolism during immune regulation. On the one hand, immune checkpoints connect to alter the metabolic reprogramming of tumor cells to compete for nutrients required by immune cells. On the other hand, immune checkpoints regulate the metabolic pathways of immune cells, such as phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) to affect the activation of immune cells. Based on a review of the literature, this article reviews the mechanisms by which PD-1, CTLA-4, T cell immunoreceptor with Ig and ITIM domains (TIGIT), T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3), cluster of differentiation 47 (CD47), and indoleamine 2,3-dioxygenase 1 (IDO1) regulate cell metabolic reprogramming, and looks forward to whether targeting the ligand-receptor pairs of immune checkpoints in a \"dual regulation\" manner and inhibiting metabolic pathways can effectively solve the problem of tumor immune resistance.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"213-220"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031716","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}

{"title":"[Comprehensive Analysis of the Expression, Prognosis and Function of TRAF Family Proteins \u2029in NSCLC].","authors":"Yixuan Wang, Qiang Chen, Yaguang Fan, Shuqi Tu, Yang Zhang, Xiuwen Zhang, Hongli Pan, Xuexia Zhou, Xuebing Li","doi":"10.3779/j.issn.1009-3419.2025.102.09","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.102.09","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Currently, lung cancer is one of the malignant tumors with a high morbidity and mortality all over the world. However, the exact mechanisms underlying lung cancer progression remain unclear. The tumor necrosis factor receptor associated factor (TRAF) family members are cytoplasmic adaptor proteins, which function as both adaptor proteins and ubiquitin ligases to regulate diverse receptor signalings, leading to the activation of nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK) and interferon regulatory factor (IRF) signaling. The aim of this study was to investigate the expression of TRAFs in different tissues and cancer types, as well as its mRNA expression, protein expression, prognostic significance and functional enrichment analysis in non-small cell lung cancer (NSCLC), in order to provide new strategies for the diagnosis and treatment of NSCLC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;RNA sequencing data from the The Genotype-Tissue Expression database was used to analyze the expression patterns of TRAF family members in different human tissues. RNA sequencing data from the Cancer Cell Line Encyclopedia database was used to analyze the expression patterns of TRAF family members in different types of cancer cell lines. RNA sequencing data from the The Cancer Genome Atlas (TCGA) database was used to analyze the mRNA levels of TRAF family members across different types of human cancers. Immunohistochemistry (IHC) analyses from HPA database were used to analyze the TRAF protein levels in NSCLC [lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC)]. Overall survival analysis was performed by Log-rank test using original data from Kaplan-Meier Plotter database to evaluate the correlation between TRAF expressions and prognosis. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed on the TRAF family-related genes using RNA sequencing data from the TCGA database for NSCLC. The correlation between the expression levels of TRAF family members and the tumor immune microenvironment was analyzed using the ESTIMATE algorithm based on RNA sequencing data from the TCGA database.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The TRAF family members exhibited significant tissue-specific expression heterogeneity. TRAF2, TRAF3, TRAF6 and TRAF7 were widely expressed in most tissues, while the expressions of TRAF1, TRAF4 and TRAF5 were restricted to specific tissues. The expressions of TRAF family members were highly specific among different types of cancer cell lines. In mRNA database of LUAD and LUSC, the expressions of TRAF2, TRAF4, TRAF5 and TRAF7 were significantly upregulated; while TRAF6 did the opposite; moveover, TRAF1 and TRAF3 only displayed a significant upregulation in LUAD and LUSC, respectively. Except for TRAF3, TRAF4 and TRAF7, other TRAF proteins displayed an obviously deeper IHC staining in LUAD and LUSC tissues compared with normal tissues. Additionally, pa","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"183-194"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144053968","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}

{"title":"[Erratum: Crizotinib Treatment for Lorlatinib-resistant MET-amplified EML4-ALK-fusion Positive Advanced Lung Adenocarcinoma: A Case Report].","authors":"","doi":"10.3779/j.issn.1009-3419.2025.103.01","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.103.01","url":null,"abstract":"<p><p>This corrects the article DOI: 10.3779/j.issn.1009-3419.2024.102.37.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"236"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039098","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}

{"title":"[ARID1B Gene Deletion Promotes the Proliferation, Migration and Invasion \u2029of NSCLC Cells].","authors":"Linlin Zhu, Xuchao Zhang","doi":"10.3779/j.issn.1009-3419.2025.101.04","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.101.04","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Abnormalities of the switch/sucrose nonfermentable (SWI/SNF) chromatin-remodeling complex are closely related to various cancers, and ARID1B (AT-rich interaction domain 1B) is one of the core subunits of the SWI/SNF complex. Mutations or copy number deletions of the ARID1B gene are associated with impaired DNA damage response and altered chromatin accessibility. However, whether ARID1B deficiency affects the proliferation, migration and invasion abilities of non-small cell lung cancer (NSCLC) cells and its molecular mechanisms remain poorly understood. This study aims to reveal the regulatory role of ARID1B gene deletion on the malignant phenotype of NSCLC cells and its molecular mechanism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Online databases were used to analyze the relationship between ARID1B and the prognosis of patients with lung cancer, and the expression levels of ARID1B in lung cancer tissues. The CRISPR/Cas9 (clustered regularly interspaced short palindromic repeat) technology was employed to construct stable ARID1B gene knockout (KO) cell lines. The plate colony formation assay was used to detect cell proliferation, and the Transwell cell migration and invasion assays were used to detect changes in cell migration ability. RNA-Seq was utilized for the expression and enrichment analysis of differentially expressed genes. Western blot (WB) was used to verify the knockout effect of the ARID1B gene and to detect the expression changes of epithelial-mesenchymal transition (EMT) markers and mitogen-activated protein kinases (MAPK) signaling pathway-related proteins. Nude mouse tumor models were constructed and the tumorigenic abilities of control and ARID1B-deficient cells were compared.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Patients with low ARID1B expression have poor overall survival. ARID1B is differentially expressed in lung cancer and normal tissues, and its expression level being lower in cancer cells. ARID1B-deficient cells had significantly enhanced in vitro proliferation, migration and invasion abilities. In animal experiments, the tumor formation speed of ARID1B gene deficient cells was significantly accelerated. Enrichment analysis of RNA-Seq results revealed that the differentially expressed genes were mainly enriched in MAPK, phosphoinositide 3-kinase-protein kinase B (PI3K/Akt) and other signaling pathways. WB experiments demonstrated that the expressions of E-cadherin, N-cadherin and Vimentin changed in ARID1B gene deficient cells, and the expressions of MAPK and p-MAPK was increased.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;The A549-ARID1B KO and PC9-ARID1B KO cell lines were successfully established. The ARID1B-deficient cell lines demonstrated high migration, invasion and proliferation potential at both in vitro and in vivo biological behavior levels and at the transcriptome sequencing level. The changes in the expression of EMT markers and the activation of the MAPK signaling pathway suggest possible metasta","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"165-175"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020340","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}

{"title":"[Research Progress of Neutrophil Extracellular Traps in Lung Cancer].","authors":"Xu Hao, Yilin Feng, Anqi Lu, Ying Sun, Jinchan Xia, Xue Mei, Long Feng, Min Jiang, Baiyan Wang, Huitong Yang","doi":"10.3779/j.issn.1009-3419.2025.106.06","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.106.06","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs), intricate reticular structures released by activated neutrophils, play a pivotal regulatory role in the pathogenesis of malignant tumors. Lung cancer is one of the most prevalent malignancies globally, with persistently high incidence and mortality rates. Recent studies have revealed that NETs dynamically modulate the tumor microenvironment through unique pathological mechanisms, exhibiting complex immunoregulatory characteristics during the progression of lung cancer, and this discovery has increasingly become a focal point in tumor immunology research. This paper provides a comprehensive review of the latest advancements in NETs research related to lung cancer, offering an in-depth analysis of their impact on lung cancer progression, their potential diagnostic value, and the current state of research on targeting NETs for lung cancer prevention and treatment. The aim is to propose novel strategies to enhance therapeutic outcomes and improve the prognosis for lung cancer patients.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"201-212"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050381","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}

{"title":"[A Case of Multiple Primary Pulmonary Neuroendocrine Carcinoma\u2029with EML4-ALK Fusion Gene Positive].","authors":"Yin Zhang, Yue Hou, Tianming Zhang, Hong Wang","doi":"10.3779/j.issn.1009-3419.2025.102.10","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.102.10","url":null,"abstract":"<p><p>Neuroendocrine carcinoma (NEC), a subtype of neuroendocrine tumors with high proliferative activity, is characterized by strong invasiveness and poor prognosis. This article reports a previously healthy female non-smoker who developed NEC occurring sequentially in different lobes of both lungs. The lesions were pathologically diagnosed by hematoxylin-eosin (HE) staining as large cell neuroendocrine carcinoma (LCNEC) and small cell lung cancer (SCLC), respectively. Next-generation sequencing (NGS) performed on both lesions revealed the presence of echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion mutations in both lesions. Notably, the patient achieved a significant therapeutic response to ALK-tyrosine kinase inhibitors (TKIs) targeted therapy.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"230-236"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003172","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}

{"title":"[Application Practice of AI Empowering Post-discharge Specialized Disease Management in Postoperative Rehabilitation of the Lung Cancer Patients Undergoing Surgery].","authors":"Mei Li, Hongbing Zhang, Chunqiu Xia, Yuqi Zhang, Huihui Ji, Yi Shi, Liran Duan, Lingyu Guo, Jinghao Liu, Xin Li, Ming Dong, Jun Chen","doi":"10.3779/j.issn.1009-3419.2025.102.11","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.102.11","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is the leading malignancy in China in terms of both incidence and mortality. With increased health awareness and the widespread use of low-dose computed tomography (CT), early diagnosis rates have been steadily improving. Surgical intervention remains the primary treatment option for early-stage lung cancer, and video-assisted thoracoscopic surgery (VATS) has become a common approach due to its minimal invasiveness and rapid recovery. However, post-discharge recovery remains incomplete, underscoring the importance of postoperative care. Traditional follow-up methods, lack standardization, consume significant medical resources, and increase the burden of the patients. Artificial intelligence (AI)-driven disease management platforms offer a novel solution to optimize postoperative follow-up. This study followed 463 lung cancer surgery patients using an AI-based platform, aiming to identify common postoperative issues, propose solutions, improve quality of life, reduce recurrence-related costs, and promote AI integration in healthcare.</p><p><strong>Methods: </strong>Using the AI disease management platform, this study integrated educational videos, collaboration between healthcare teams and AI assistants, daily health logs, health assessment forms, and personalized interventions to monitor postoperative recovery. The postoperative rehabilitation status of the patients was assessed by the Leicester Cough Questionnaire (LCQ-MC). Two independent t-test and one-way ANOVA were used to analyze the causes of postoperative cough in lung cancer.</p><p><strong>Results: </strong>Most issues occurred within 7 d post-discharge, significantly declined on 14 d post-discharge. Factors such as gender, smoking history, and surgical approaches were found to influence cough recovery. The incidence of cough on 7 d post-discharge in females was higher than that in males (P<0.01), while the incidence of cough on 14 d post-discharge in elderly patients was lower than that in young patients (P=0.03). The AI-based platform effectively addressed cough, pain, and sleep disturbances through phased interventions.</p><p><strong>Conclusions: </strong>The AI-based platform significantly enhanced postoperative management efficiency and the self-care capabilities of the patients, particularly in phased cough management. Future integration with wearable devices could enable more precise and personalized postoperative care, further advancing the application of AI technology across multidisciplinary healthcare domains.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"176-182"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001832","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}

{"title":"[Surgical Perspective on Lung Cancer in 2024: Innovation and Challenges].","authors":"Pengxu Kong, Xiaohan Chen, Wang Lv, Pinghui Xia, Luming Wang, Jian Hu","doi":"10.3779/j.issn.1009-3419.2025.106.07","DOIUrl":"https://doi.org/10.3779/j.issn.1009-3419.2025.106.07","url":null,"abstract":"<p><p>Lung cancer, a highly prevalent and deadly malignancy globally, poses a significant disease burden in China and is the leading cause of cancer death. Despite rapid advances in medicine, its incidence and mortality rates remain stubbornly high, making it a major challenge in public health. Against the backdrop of rapid progress in precision medicine, the paradigm of lung cancer treatment is shifting from single traditional therapy to multi-dimensional integration. This article comprehensively reviews the innovations and challenges in lung cancer surgery in 2024, aiming to explore the future development of surgical treatment with colleagues and to improve patients' quality of life and achieve the goal of \"cure\".\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 3","pages":"195-200"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11986690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019474","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}

{"title":"[Expert Consensus on Diagnosis and Treatment of NSCLC with MET Abnormalities \u2029(2025 Version)].","authors":"Jun Chen, Baohui Han, Yi Hu, Jian Hu","doi":"10.3779/j.issn.1009-3419.2025.102.01","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.01","url":null,"abstract":"<p><p>The mesenchymal-epithelial transition factor (MET) gene, located on human chromosome 7, plays a crucial role in the regulation of physiological processes such as cell proliferation, migration, invasion, and angiogenesis. The MET gene is one of the key drivers in non-small cell lung cancer (NSCLC), with various forms of abnormalities including MET exon 14 (METex14) skipping mutations, MET gene amplification, MET fusions, MET protein overexpression, MET activating mutations and etc. With an increasing understanding of the mechanisms underlying MET abnormalities, therapeutic strategies targeting these abnormalities have gained significant attention, and numerous studies have confirmed that NSCLC patients with MET abnormalities can derive substantial benefits from such treatments. Lung Cancer Specialty Committee of Chinese Elderly Health Care Association organized a panel of experts to provide professional recommendations on current clinical issues in the diagnosis and treatment of MET-aberrant NSCLC, combining clinical practice experiences and evidence-based medical evidences. The \"Expert Consensus on Diagnosis and Treatment of NSCLC with MET Abnormalities (2025 Version)\" has been formulated to provide standardized guidances for clinical practice in China, with the aim of optimizing the treatment outcomes.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 2","pages":"81-94"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671287","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}

{"title":"[Research Progress on Molecular Subtypes and Precision Therapy \u2029of Pulmonary Large Cell Neuroendocrine Carcinoma].","authors":"Yuchao Feng, Xiaohong Cao","doi":"10.3779/j.issn.1009-3419.2025.102.06","DOIUrl":"10.3779/j.issn.1009-3419.2025.102.06","url":null,"abstract":"<p><p>Pulmonary large cell neuroendocrine carcinoma (LCNEC) is a high-grade neuroendocrine tumor with unique characteristics, and its treatment regimens are primarily derived from those for small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). In recent years, the incidence rate has been on the rise, and the prognosis are affected by the interaction of multiple factors such as individual, clinical stage and treatment mode, and the heterogeneity is significant. In the study of molecular subtypes, multiple subgroups were divided according to key gene mutations such as RB1 and TP53, and genomic subtypes were associated with survival, chemotherapy response, and efficacy of precision therapy. Targeted therapy excavates multiple targets, and the efficacy of drugs is different. Immunotherapy has made remarkable progress, and immune checkpoint inhibitors (ICIs) have been effective in all stages of chemotherapy alone or in combination with chemotherapy or radiation therapy, but there is a risk of hyperprogressive diseases, and accurate prognostic markers need to be explored urgently. This review reviews the latest research progress in the study of molecular subtypes and precision therapies such as targeted therapy and immunotherapy of pulmonary LCNEC, and points out that pulmonary LCNEC treatment will develop in the direction of precision and individualization in the future.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"28 2","pages":"146-154"},"PeriodicalIF":0.0,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671369","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}