中国肺癌杂志最新文献

{"title":"[Ziyuglycoside II Inhibit the Progression of Non-small Cell Lung Cancer \u2029through the ITGB4/FAK Signaling Pathway].","authors":"Jiaxuan Ren, Yani Liu, Bo Wang, Jiayi Lv, Yunbo Di, Zhenwen Chen, Yirong Xu","doi":"10.3779/j.issn.1009-3419.2026.102.10","DOIUrl":"10.3779/j.issn.1009-3419.2026.102.10","url":null,"abstract":"<p><strong>Background: </strong>The incidence and mortality rates of non-small cell lung cancer (NSCLC) are generally on the rise, and the overall prognosis of patients remains poor. Current clinical treatment strategies have significant limitations. Notably, the bioactive components of traditional Chinese medicine possess unique advantages, including diverse targets of action and low toxicity. Ziyuglycoside II (ZGS II), a major active component of Sanguisorba officinalis L, has been shown to inhibit cancer cell proliferation, migration, and invasion. This property confers potential application value and developmental prospects for its use in cancer therapy. Nevertheless, the effects of ZGS II on NSCLC and the underlying mechanisms remain unclear. This study aimed to investigate the anti-tumor molecular mechanism of ZGS II in NSCLC and to explore the potential of being a novel therapeutic strategy for improving the prognosis of NSCLC patients.</p><p><strong>Methods: </strong>First, the cell counting kit-8 (CCK-8) and the colony formation assay were used to detect the changes in the viability and proliferation ability of NSCLC cells after treatment with ZGS II. Wound-healing and Transwell assays were used to evaluate the effects of ZGS II on migration and invasion abilities. Western blot, Lentiviral transfection, wound healing assay, and Transwell assay were used to study the effects of ZGS II on the integrin β4/focal adhesion kinase (ITGB4/FAK) signaling pathway. A rescue experiment was then performed using the FAK agonist ZINC40099027. A nude mouse xenograft model was used to evaluate the inhibitory effect of ZGS II on NSCLC metastasis in vivo.</p><p><strong>Results: </strong>ZGS II inhibited proliferation, migration, and invasion of NSCLC cells and suppressed the protein expression of ITGB4. This inhibitory effect was significantly enhanced upon ITGB4 knockdown. Meanwhile, total FAK expression remained nearly unchanged, but the protein expression level of phosphorylated focal adhesion kinase (p-FAK) was suppressed. Following the addition of an FAK activator, cell migration rate and the number of cells crossing the Transwell membrane increased, reversing the inhibitory effects of ZGS II on cell migration and invasion. Therefore, the anti-tumor effect of ZGS II depends on the reduced activation of the ITGB4/FAK signaling pathway. The nude mouse xenograft experiment results showed that ZGS II effectively inhibited tumor growth in nude mice.</p><p><strong>Conclusions: </strong>ZGS II inhibits proliferation, metastasis, and tumor growth in NSCLC by suppressing the ITGB4/FAK pathway. These findings highlight the potential of ZGS II as a promising drug for treating metastatic NSCLC and lay the foundation for its clinical research.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 4","pages":"251-262"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148253997","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":"[Effects of LINC00641 on the Malignant Progression and Chemotherapy Resistance \u2029of Non-small Cell Lung Cancer H1299 Cells by Regulating the miR-1306-5p/FGFR3 Axis].","authors":"Wurihan, Yuxin Du, Caixia Liu","doi":"10.3779/j.issn.1009-3419.2026.101.10","DOIUrl":"10.3779/j.issn.1009-3419.2026.101.10","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Non-small cell lung cancer (NSCLC) is one of the causes of cancer-related deaths worldwide. Although platinum-based chemotherapy is the main treatment method for advanced patients, acquired resistance often leads to treatment failure. Long non-coding RNAs (lncRNAs) play an important role in tumor occurrence and development, but the specific mechanism of their involvement in chemotherapy resistance in NSCLC is not yet fully understood. This study aims to explore the effect of LINC00641 on the microRNA-1306-5p (miR-1306-5p)/fibroblast growth factor receptor 3 (FGFR3) axis on the malignant progression and chemotherapy resistance of NSCLC cell line H1299.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The mRNA expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR); and the interaction was verified by the dual-luciferase reporter gene assay. H1299 cells were randomly divided into the following groups: CG group (normal culture), sh-NC group (transfected with sh-NC), sh-LINC00641 group (transfected with sh-LINC00641), sh-LINC00641+anti-NC group (transfected with sh-LINC00641 and anti-NC), sh-LINC00641+anti-miR-1306-5p group (transfected with sh-LINC00641 and anti-miR-1306-5p), mimic-NC group (transfected with mimic-NC), miR-1306-5p-mimics group (transfected with miR-1306-5p-mimics), miR-1306-5p-mimics+OE-NC group (transfected with miR-1306-5p-mimics and OE-NC), and miR-1306-5p-mimics+OE-FGFR3 group (transfected with miR-1306-5p-mimics and OE-FGFR3). Then cell proliferation, migration, and invasion were measured by plate colony formation assay, scratch assay, and Transwell assay, respectively. In addition, H1299/DDP cells were grouped as mentioned above. After that, the chemotherapy resistance of H1299/DDP cells was detected by the MTT method. And Western blot was implemented to detect the protein expressions of FGFR3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 13 (MMP-13), integrin β1 in H1299 cells, and the P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1) in H1299/DDP cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In NSCLC tissues or cells (H1299, H1299/DDP), LINC00641 and FGFR3 were highly expressed, while miR‑1306‑5p was lowly expressed, and the expression trends of these three factors changed more significantly in the drug‑resistant cell line H1299/DDP (P&lt;0.05). LINC00641 could negatively regulate miR‑1306‑5p in a targeted manner; and miR‑1306‑5p could negatively regulate FGFR3 in a targeted manner. Knockdown of LINC00641 (sh‑LINC00641) or overexpression of miR‑1306‑5p reduced the clone number, scratch healing rate, migration number, invasion number, and the expression of PCNA, MMP‑13, and integrin β1 proteins in H1299 cells (P&lt;0.05), and also suppressed the optical density (OD)540 value and the expression of P‑gp and MRP1 proteins in H1299/DDP cells (P&lt;0.05). In addition, inhibition of miR‑1306‑5p or overexpression of FGFR3 could reverse the inhibitory effects o","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 4","pages":"263-277"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148253933","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":"[Glycolytic Reprogramming in Lung Adenocarcinoma:\u2029Molecular Mechanisms, Metabolic Biomarkers and Targeted Therapeutic Strategies].","authors":"Caini Zhang, Yu Fu, Huiqin Feng, Yuqing Pan, Ya Li, Chenglu He","doi":"10.3779/j.issn.1009-3419.2026.102.07","DOIUrl":"10.3779/j.issn.1009-3419.2026.102.07","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is the most common and highly aggressive subtype of non-small cell lung cancer, characterized by metabolic reprogramming with enhanced glycolysis. Upregulation of key glycolytic enzymes [hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA)] and lactate accumulation not only support tumor energy production and biosynthesis but also promote tumor progression and immune evasion through lactate-mediated immunosuppression and epigenetic regulation such as histone lactylation. Oncogenic signaling pathways, including phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR), hypoxia-inducible factor-1α (HIF-1α), and MYC proto-oncogene (c-Myc), synergistically drive glycolytic activation, thereby reshaping the tumor immune microenvironment and influencing therapeutic responses. In recent years, glycolysis-related metabolic enzymes and imaging parameters have shown promising potential in the early diagnosis, prognostic evaluation, and treatment monitoring of LUAD, with multi-omics integration further facilitating their clinical translation. Collectively, glycolytic reprogramming is not only a hallmark metabolic feature of LUAD but also a critical nexus linking immunosuppression, therapeutic resistance, and precision medicine. This review summarizes the molecular mechanisms, associated biomarkers, and targeted strategies of glycolytic reprogramming, aiming to provide insights for early screening, risk stratification, and metabolism-targeted therapies in LUAD.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 4","pages":"278-285"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148254011","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":"[Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].","authors":"Mingzhu Liu, Chuanlin Wang, Jin Hu, Guangqiang Zhao, Yunchao Huang, Lan Zhou","doi":"10.3779/j.issn.1009-3419.2026.106.11","DOIUrl":"10.3779/j.issn.1009-3419.2026.106.11","url":null,"abstract":"<p><p>Lung cancer is the malignant tumor with the highest incidence and mortality rate worldwide. The current treatment methods have limited efficacy, and the prognosis of patients is poor. There is an urgent need to explore new therapeutic targets and strategies. Epigenetic modification disorders are closely related to the occurrence and development of tumors. Among them, histone deacetylase 1 (HDAC1), as a key epigenetic regulatory molecule, participates in the regulation of biological processes such as cell proliferation, differentiation, and apoptosis. HDAC1 is highly expressed in lung cancer, and its expression level is closely related to the malignancy degree, clinical stage, and poor prognosis of lung cancer. Abnormal activation of HDAC1 is also one of the core factors for the resistance of lung cancer to chemotherapy, targeted therapy, and immunotherapy. The development of HDAC1 inhibitors provides a new direction for the treatment of lung cancer, and the combination with chemotherapy, targeted therapy, and immunotherapy can significantly enhance the synergistic anti-tumor effect. This article systematically reviews the structural characteristics and physiological functions of HDAC1, deeply explores its regulatory mechanism in lung cancer, elaborates on its association with lung cancer resistance, and summarizes the research and development progress, clinical trial status, and challenges of HDAC1 inhibitors, with the aim of providing new ideas for the precise treatment of lung cancer.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 4","pages":"302-309"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148253945","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":"[Preliminary Analysis of Tumor Immune Microenvironment Characteristics\u2029in Lung Squamous Cell Carcinoma after Neoadjuvant Immunochemotherapy \u2029Based on Single-cell Transcriptomics].","authors":"Guannan Wang, Yanan Wang, Jinghao Liu, Minghui Liu, Xuanguang Li, Zihe Zhang, Hongbing Zhang, Yu Hua, Yongwen Li, Hongyu Liu, Jun Chen","doi":"10.3779/j.issn.1009-3419.2026.102.05","DOIUrl":"10.3779/j.issn.1009-3419.2026.102.05","url":null,"abstract":"<p><strong>Background: </strong>Neoadjuvant immunochemotherapy has emerged as an important treatment strategy for non-small cell lung cancer (NSCLC); however, substantial heterogeneity in therapeutic response persists among patients. Currently, treatment efficacy is primarily evaluated by imaging modalities, and there remains a lack of comprehensive studies investigating post-treatment alterations in the tumor microenvironment (TME) and their association with clinical response. This study applied single-cell RNA sequencing (scRNA-seq) to characterize TME remodeling in lung squamous cell carcinoma after neoadjuvant immunochemotherapy and to explore its potential association with differences in therapeutic response.</p><p><strong>Methods: </strong>Tumor specimens from two patients with lung squamous cell carcinoma who underwent surgical resection following neoadjuvant immunochemotherapy were subjected to scRNA-seq. An integrated analysis was performed to characterize the cellular composition, functional states, and intercellular communication patterns within the TME.</p><p><strong>Results: </strong>Preoperative imaging evaluation indicated partial response (PR) in patient 1 and stable disease (SD) in patient 2, whereas postoperative pathological evaluation showed major pathological response (MPR) and partial pathological response (PPR), respectively. ScRNA-seq identified nine major cell populations. The TME exhibited marked heterogeneity between the two patients: patient 1 was characterized by immune cell enrichment and inflammatory activation, whereas patient 2 showed remodeling dominated by myeloid and endothelial signals, together with more prominent immune regulatory and angiogenic features. Cell-cell communication analysis revealed that patient 1 was mainly characterized by inflammatory chemotactic interactions, whereas patient 2 showed enhanced C-X-C motif chemokine ligand (CXCL), secreted phosphoprotein 1 (SPP1), vascular endothelial growth factor (VEGF), macrophage migration inhibitory factor (MIF) and tumor necrosis factor (TNF) signaling, along with prominent immunosuppressive interaction axes. In addition, patient 2 showed a relative enrichment of macrophages and a more pronounced exhausted T-cell phenotype.</p><p><strong>Conclusions: </strong>After neoadjuvant immunochemotherapy, the TME in patients with lung squamous cell carcinoma exhibits marked heterogeneity in terms of cellular composition, functional states, and intercellular communication. The TME remodeling patterns revealed by scRNA-seq may provide insights into discrepancies in treatment response evaluation and help identify potential biomarkers.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"168-179"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934218","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":"[Value of CD4+/CD8+ Ratio Combined with nCD64 Index in Bronchoalveolar Lavage \u2029Fluid for Differential Diagnosis of Lung Cancer and Non-lung Cancer Diseases].","authors":"Xuexue Wu, Chan Yang, Lili Jiang","doi":"10.3779/j.issn.1009-3419.2026.106.08","DOIUrl":"10.3779/j.issn.1009-3419.2026.106.08","url":null,"abstract":"<p><strong>Background: </strong>Distinguishing lung cancer from pulmonary infection and interstitial lung disease (ILD) remains challenging. This study aimed to evaluate the diagnostic value of T lymphocyte subsets and neutrophil CD64 (nCD64) index in bronchoalveolar lavage fluid (BALF), alone and in combination, to address this challenge.</p><p><strong>Methods: </strong>BALF was collected between October 2021 and October 2022 from 70 patients admitted to West China Hospital, Sichuan University. Based on final diagnosis, the patients were divided into the lung cancer group (21 cases, including 14 with pure lung cancer and 7 with lung cancer and infection) and the non‑lung cancer group (49 cases, including 39 with pulmonary infection and 10 with ILD). Flow cytometry was used to detect T lymphocyte subsets and CD64 expression in BALF, and the CD4+/CD8+ ratio and nCD64 index were calculated. Receiver operating characteristic (ROC) curves were used to evaluate the performance of both indicators in differentiating lung cancer from pulmonary infection and from ILD, and the area under the curve (AUC) and 95% confidence interval (CI) were calculated. The diagnostic efficacy of combining the CD4+/CD8+ ratio and nCD64 index for differentiating lung cancer from pulmonary infection was further analyzed. Firth's logistic regression was performed to adjust for age and to assess the independent differential diagnosis value of the two indicators between lung cancer and pulmonary infection.</p><p><strong>Results: </strong>Compared with the non-lung cancer group, the lung cancer group showed significantly lower CD4+ T cell proportion, CD4+/CD8+ ratio, and nCD64 index (all P<0.05). Further analysis revealed that the lung cancer group also had significantly lower values of the above indicators compared with the pulmonary infection group (P<0.05), but no significant differences were observed compared with the ILD group (P>0.05). ROC curve analysis showed that the CD4+/CD8+ ratio had an AUC of 0.712 (95%CI: 0.575‑0.849, P=0.008) for differentiating lung cancer from pulmonary infection, with a sensitivity of 56.76% and a specificity of 85.00%; the nCD64 index had an AUC of 0.677 (95%CI: 0.539‑0.814, P=0.026), with a sensitivity of 44.74% and a specificity of 95.24%. When the two indicators were combined, the parallel test increased the sensitivity to 78.38%, while the serial test achieved 100.00% specificity and positive predictive value. After adjusting for age, Firth's logistic regression demonstrated that both the CD4+/CD8+ ratio and nCD64 index retained independent differential diagnosis value for differentiating lung cancer from pulmonary infection (both P<0.05).</p><p><strong>Conclusions: </strong>The combined detection of the CD4+/CD8+ ratio and nCD64 index in BALF improves the diagnostic efficacy for differentiating lung cancer from pulmonary infection.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"159-167"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934262","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 Advances in Obstructive Sleep Apnea and Lung Cancer Comorbidity].","authors":"He Cao, Shanshan Yang, Wenjia Sun, Jianya Zhou","doi":"10.3779/j.issn.1009-3419.2026.101.06","DOIUrl":"10.3779/j.issn.1009-3419.2026.101.06","url":null,"abstract":"<p><p>Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder characterized by recurrent upper airway collapse and apnea during sleep, resulting in intermittent hypoxia, oxidative stress, and systemic inflammation, and is closely associated with multisystem dysfunction, including cardiovascular disease, cognitive impairment, and metabolic abnormalities. Lung cancer remains one of the leading causes of cancer-related mortality worldwide and represents a major threat to human health. Recent studies suggest that OSA and lung cancer share several common risk factors, including smoking, older age, and obesity, and exhibit overlapping pathophysiological mechanisms, indicating that OSA may be involved in the initiation and progression of lung cancer. However, the epidemiological evidence regarding the association between OSA and lung cancer remains inconsistent, and the underlying molecular mechanisms as well as the clinical value of potential interventions have yet to be systematically elucidated. This review therefore summarizes the epidemiological characteristics, potential pathophysiological mechanisms, and therapeutic strategies related to the coexistence of OSA and lung cancer, with the aim of providing a theoretical basis for clinical decision-making and future mechanistic studies.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"221-228"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934233","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":"[Heterogeneity of Response to PD-1/PD-L1 Inhibitors in Elderly Patients with Advanced NSCLC under the Background of Immunosenescence and Intervention Strategies].","authors":"Yurong Huang, Yuan Wang, Aojiao Wei, Yulu Xiong, Mingzhi Duan, Tongyao Xu, Wenjie He","doi":"10.3779/j.issn.1009-3419.2026.101.05","DOIUrl":"10.3779/j.issn.1009-3419.2026.101.05","url":null,"abstract":"<p><p>The proportion of elderly patients with advanced non-small cell lung cancer (NSCLC) is on the rise. While programmed death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) inhibitors have revolutionized the management of advanced NSCLC and improved patient survival, but the elderly display prominent immunosenescence features. Age-associated thymic involution, diminished T-cell repertoire diversity, and chronic inflammation directly compromise the efficacy of immunotherapy. Furthermore, the underrepresentation of elderly patients in clinical trials and the paucity of high-quality evidence-based data jointly contribute to significant heterogeneity in their therapeutic responses to PD-1/PD-L1 inhibitors. While patients aged 65-74 years maintain significant survival benefits from immunotherapy - whether as monotherapy or combined regimens - those aged ≥75 years exhibit attenuated efficacy and heightened susceptibility to immune-related adverse events. To address these challenges, Comprehensive Geriatric Assessment (CGA) enables risk-adapted therapeutic strategies, guiding interventions such as adjusted-dose immunotherapy, selective combination therapies, and emerging approaches targeting senescence-associated immune dysfunction. Closing current evidence gaps, particularly for underrepresented octogenarians, remains imperative, as does advancing precision immunotherapy models founded on biological aging metrics rather than chronological age alone. Bridging these knowledge gaps will permit tailored treatment algorithms to optimize outcomes in this clinically complex population.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"190-199"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934101","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":"[Trastuzumab Deruxtecan for EGFR-mutant Lung Adenocarcinoma\u2029with Acquired High-level HER2 Amplification: A Case Report].","authors":"Xiaoxiao Ge, Hefeng Chen, Shaohua Cui","doi":"10.3779/j.issn.1009-3419.2026.104.01","DOIUrl":"10.3779/j.issn.1009-3419.2026.104.01","url":null,"abstract":"<p><p>Trastuzumab deruxtecan is a newly developed antibody-drug conjugate (ADC) designed to overcome human epidermal growth factor receptor 2 (HER2) aberrations. Studies have confirmed that Trastuzumab deruxtecan yields promising efficacy with a manageable safety profile in previously treated non-small cell lung cancer (NSCLC) patients harboring HER2 mutations. However, data on efficacy of Trastuzumab deruxtecan for acquired HER2-amplified NSCLC are limited. Here, we report a case of a patient with metastatic lung adenocarcinoma who developed acquired high-level HER2 amplification (20 copies) after 2nd-line Osimertinib. A partial response (PR) was achieved with reduced-dose Trastuzumab deruxtecan. Plasma next-generation sequencing (NGS) further confirmed successful inhibition of HER2 amplification. \u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"221-232"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934214","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":"[Role of Gut Mycobiome in Lung Cancer Immunotherapy: \u2029Mechanisms, Challenges and Translational Prospects].","authors":"Xinyi Wang, Yu Sun, Min Liu, Zixuan He, Wenjiao Cao, Weiying Liu","doi":"10.3779/j.issn.1009-3419.2026.101.07","DOIUrl":"10.3779/j.issn.1009-3419.2026.101.07","url":null,"abstract":"<p><p>Lung cancer is one of the most common malignancies with the highest morbidity and mortality worldwide. Immune checkpoint inhibitors (ICIs) have significantly improved the prognosis of patients with advanced lung cancer, but more than half of patients derive limited benefit. The gut microbiota can regulate tumor immunity and ICIs efficacy via the gut-lung axis. Although accounting for a small proportion, the gut mycobiome exerts key immunomodulatory effects, yet relevant research lags far behind that of bacteria. This review systematically summarizes the clinical association between the gut mycobiome and lung cancer, clarifies the potential mechanisms by which the mycobiome and its metabolites influence ICIs efficacy through immune regulation, metabolic modulation, and cross-kingdom interactions, and summarizes potential strategies including dietary intervention, fecal microbiota transplantation, and fungal targeting. It provides theoretical support for establishing mycobiome-based predictive models, developing precise interventions, and improving the efficacy of ICIs.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"29 3","pages":"200-207"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934231","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}