Immune checkpoint inhibitors (ICIs) have significantly improved the prognosis of patients with lung cancer. However, checkpoint inhibitor-related pneumonitis (CIP), as one of the most severe immune-related adverse events, lacks well-defined diagnostic criteria and reliable risk stratification tools. Radiomics enables high-throughput feature extraction from computed tomography images and provides a non-invasive technical approach for the early identification and risk stratification of CIP. This article systematically reviews the recent advances in the application of radiomics to risk prediction, diagnosis and differential diagnosis, and prognostic evaluation of CIP in lung cancer immunotherapy. Furthermore, it explores the value of integrating radiomics with multi-omics data in elucidating the pathogenesis of CIP, as well as the role of explainable artificial intelligence (XAI) in enhancing the clinical trustworthiness of models. .
Lung cancer is one of the malignancies with the highest incidence and mortality rates worldwide, with non-small cell lung cancer (NSCLC) accounting for the vast majority. Patients with postoperative central nervous system (CNS) metastasis have a dismal prognosis, highlighting the urgent need for more precise molecular biomarkers. Although circulating tumor DNA (ctDNA)-based molecular residual disease (MRD) testing can predict postoperative recurrence, its utility in detecting CNS metastasis remains debated. This review examines the association between MRD status and CNS recurrence risk, synthesizes evidence linking MRD status to overall survival (OS), and explores mechanisms underlying false-negative results of peripheral blood MRD in CNS metastasis detection alongside potential clinical strategies. Current evidence indicates that MRD positivity correlates with increased overall recurrence risk and shortened OS; some studies suggest a potential increase in CNS recurrence, yet direct evidence specifically targeting intracranial recurrence-free survival (iRFS) remains insufficient. MRD-negative patients generally have favorable prognosis; however, a subset of high-risk patients - those with epidermal growth factor receptor (EGFR) mutations, stage III disease, or adenocarcinoma - may still develop isolated CNS metastases, primarily due to the blood-brain barrier limiting ctDNA release. Adjuvant Osimertinib reduces CNS recurrence risk, though recurrence remains high within the first year after treatment discontinuation. MRD status serves as an important prognostic stratification tool after NSCLC resection, but negative peripheral blood MRD does not completely exclude CNS recurrence risk. Comprehensive assessment integrating imaging, risk factors, and cerebrospinal fluid testing is therefore warranted. .
Extensive-stage small cell lung cancer (ES-SCLC) is characterized by rapid progression, a high risk of recurrence, and poor prognosis, and remains a major therapeutic challenge in lung cancer. In recent years, immune checkpoint inhibitors combined with Platinum-Etoposide chemotherapy have become the standard first-line treatment for ES-SCLC, driving a shift from conventional chemotherapy toward multimodal combination strategies and precision-guided patient stratification, while creating both new opportunities and challenges for further therapeutic improvement. Following the clinical treatment pathway, this review summarizes advances in multidisciplinary combination treatment for ES-SCLC, including chemotherapy, immunotherapy, targeted therapy, radiotherapy, and traditional Chinese medicine, with emphasis on standard regimens, maintenance therapy, clinical limitations, and emerging research directions. This review aimed to provide a reference for individualized treatment and comprehensive disease management of ES-SCLC in the era of precision medicine. .
Brain metastasis in non-small cell lung cancer (NSCLC) is shaped by continuous interactions between tumor cells and the brain-specific microenvironment. Vascular, glial and immune components contribute to intracranial colonization, immune escape and therapeutic resistance, while single-cell and spatial omics reveal heterogeneity in cellular states, communication networks and spatial niches. This review summarizes NSCLC brain metastasis and intracranial colonization, the brain metastatic microenvironment and tumor-microenvironment interactions, and discusses the heterogeneity revealed by single-cell and spatial omics and its potential relevance to therapeutic response and patient stratification. .
Immune checkpoint inhibitors combined with Platinum-based Etopositde chemotherapy have become the first-line standard treatment for extensive-stage small cell lung cancer (ES-SCLC). However, treatment benefit varies substantially among patients, and the proportion of long-term survivors remains limited. In recent years, the molecular classification framework comprising SCLC-A, SCLC-N, SCLC-P and SCLC-I, based on the expression patterns of ASCL1, NEUROD1 and POU2F3 as well as immune-inflammatory status, has provided a new basis for understanding the heterogeneity of immunotherapy response and for developing precision stratified treatment in ES-SCLC. To standardize the clinical translation of molecular subtyping in ES-SCLC immunotherapy, this consensus was developed by multidisciplinary experts from respiratory medicine, oncology, pathology, radiation oncology, and basic medical sciences. Based on domestic and international evidence and clinical experience, the consensus provides recommendations on key issues, including first-line immunotherapy for ES-SCLC, molecular subtyping systems and immune microenvironment characteristics, testing and implementation pathways, immunotherapy-related biomarkers, subtype-informed treatment strategies, and dynamic monitoring. This consensus emphasizes that molecular subtyping should currently be positioned as a tool for biological and clinical research stratification based on standard treatment, and should not be used as an independent basis for treatment decisions. Immunohistochemistry can serve as an important method for qualified centers to conduct subtyping exploration and translational research. The SCLC-I subtype may provide a useful reference for biomarker-based stratification and immunotherapy benefit prediction. For different subtypes, delta-like ligand 3 (DLL3)-targeted therapy, epigenetic regulation, the MYC/AURKA axis, and poly (ADP-ribose) polymerase (PARP) inhibitors can be important choices for subsequent treatment optimization. This consensus aims to standardize pathological testing and clinical application of molecular subtyping in ES-SCLC, facilitate stratified management and individualized treatment optimization based on molecular subtypes, and provide a foundation for building a precision immunotherapy system. .
Chest drainage management is an essential component of perioperative care after pulmonary resection, aiming to evacuate intrapleural air and fluid and promote lung re-expansion. However, conventional chest drainage systems mainly rely on manual observation, making continuous and quantitative assessment of air leakage difficult and resulting in subjective decision-making regarding the timing of chest tube removal. In recent years, digital drainage systems (DDS) have been increasingly applied in clinical practice. By using integrated sensors, DDS enables continuous monitoring of pleural pressure, air flow, and fluid drainage, and provides dynamic trend curves, thereby offering objective evidence for chest tube management. DDS may improve the accuracy of drainage assessment and optimize chest tube management strategies; however, its widespread adoption remains influenced by factors such as cost, clinical experience, and healthcare system differences. This review summarizes the current application status, advantages, and challenges of DDS in postoperative chest drainage management after pulmonary resection. .
BACKGROUND:Next-generation sequencing (NGS)-based driver gene testing has become a routine component of molecular subtyping and precision therapy for non-small cell lung cancer (NSCLC). Dynamic genomic monitoring facilitates early detection of resistance-related molecular alterations and informs timely therapeutic adjustments. However, standardized criteria for evaluating the stability of serial NGS testing are currently lacking, and the applicability of NGS using formalin-fixed paraffin-embedded (FFPE) specimens for dynamic monitoring remains poorly defined. This study aims to establish a stability grading system for driver gene status alterations based on repeated NGS testing, and to provide evidence-based support for clinical repeat biopsy strategies. METHODS:Data from 1232 patients with NSCLC who underwent two or more NGS tests on FFPE tissue specimens at Beijing Chest Hospital between June 2019 and April 2026 were collected retrospectively. Patients with an interval of ≥4 months between the initial and last tests were included to ensure the representativeness of temporal analysis, resulting in a main analysis cohort of 942 patients. The Kappa consistency test was used to evaluate the state stability of nine core driver genes [epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1), mesenchymal‑epithelial transition factor (MET), rearranged during transfection (RET), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), erb‑b2 receptor tyrosine kinase 2 (ERBB2), and phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit alpha (PIK3CA)] and to construct a five‑level grading system. Paired variant allele frequency (VAF) differences were compared using the Wilcoxon signed‑rank test. Independent influencing factors for mutation accumulation were identified by binary Logistic regression. RESULTS:The state stability of the nine genes was classified into five levels: EGFR showed high stability (Kappa=0.838), ROS1/ALK/KRAS good stability, BRAF/PIK3CA/RET moderate stability, and ERBB2 low stability, and MET showed high instability. MET exhibited the highest rate of state change (9.3%) with a raw observed agreement of 90.7%. Its Kappa value (0.172) was influenced by the low prevalence (3.7%) compression effect and should therefore be interpreted alongside the observed agreement (90.7%) and the prevalence-adjusted and bias-adjusted Kappa (PABAK). The VAF of PIK3CA increased significantly (P=0.005). T790M positivity increased from 5.8% to 10.8%, and 30 new C797S mutations were detected at the last test (13 with T790M, 17 without). The overall rate of new driver gene variants in the main cohort was 18.0%. Binary Logistic regression showed that a lower number of initial mutated genes was the only independent predictor of new variants [odds ratio (OR)=0.399, P<0.001], while sex and detection interval showed no independent association. CONCLUSIONS:A five level stability grading system for state changes of driver genes in NSCLC based on repeated NGS testing has been established. MET showed the most frequent state changes, which should be interpreted in conjunction with the prevalence effect. The VAF increase of PIK3CA is an observational finding, and its clinical significance requires further prospective validation. A lower initial mutation burden may reflect tumor clonal complexity and was associated with a higher likelihood of subsequent acquisition of new variants. FFPE based NGS is applicable for repeated testing at clinical treatment decision nodes.
Circulating tumor DNA (ctDNA) enables minimally invasive, repeatable assessment of tumor burden and molecular evolution and is an important candidate biomarker for precision management of non-small cell lung cancer (NSCLC). This review summarizes current evidence on assay strategies, perioperative dynamics, molecular residual disease (MRD) after curative-intent treatment, relapse surveillance, and applications in unresectable stage III disease. The most consistent evidence shows that detectable ctDNA after definitive treatment is associated with a substantially increased risk of recurrence, whereas longitudinally undetectable MRD identifies lower-risk populations more reliably than a single negative result. ctDNA clearance during neoadjuvant therapy is associated with pathological response and long-term outcomes but cannot replace pathology or imaging. In oncogene-driven disease, epidermal growth factor receptor (EGFR)-mutated NSCLC has MRD evidence from samples collected in a randomized trial; a small prospective postoperative study has provided direct MRD evidence in early-stage anaplastic lymphoma kinase (ALK)- or ROS proto-oncogene 1, receptor tyrosine kinase (ROS1)-fusion-positive disease, although the evidence base remains limited; Kirsten rat sarcoma viral oncogene homolog (KRAS), GTPase specific postoperative MRD studies remain insufficient. When pathology, imaging, and ctDNA are discordant, assay validity should first be confirmed and lesion-directed imaging or tissue confirmation pursued according to the suspected relapse pattern; ctDNA alone should not trigger deviation from standard therapy. ctDNA has substantial clinical validity, but routine treatment decisions still require standardized analytical performance, cross-platform reproducibility, and prospective evidence of clinical utility. .
Hoarseness after lung cancer surgery is a common but often underestimated perioperative functional complication. Beyond impairing voice quality, it may involve swallowing dysfunction and compromised airway protection, thereby increasing the risk of aspiration, pulmonary infection, and delayed recovery. Iatrogenic recurrent laryngeal nerve injury is the major cause, closely associated with mediastinal lymph node dissection, with the left lower paratracheal lymph node station as typical high-risk anatomical areas. Nerve injury results from both direct mechanical trauma and indirect mechanisms such as traction and thermal spread. In addition, intubation-related laryngeal trauma can also present as postoperative hoarseness and should be differentiated from neurogenic causes. This review summarizes the etiology and risk factors, outlines postoperative evaluation and preventive strategies, and discusses the role of meticulous dissection, minimized thermal injury, and appropriate intraoperative neuromonitoring. Future prospective studies are needed to standardize outcomes and clarify the optimal timing and target populations for interventions, ultimately improving comprehensive perioperative management and patients' quality of life. .
BACKGROUND:SMARCA4-deficient pulmonary neoplasms have emerged as a major focus of lung cancer research in recent years. This subtype is characterized by aggressive behavior and poor prognosis. However, radiotherapy-related studies in this population remain scarce, and evidence is lacking regarding the optimal selection of radiotherapy parameters and the sequencing of combination with immunotherapy. The present study aimed to evaluate the efficacy of radiotherapy in these tumors and to explore the prognostic value of radiotherapy parameters. METHODS:Clinical data of 88 patients with SMARCA4-deficient pulmonary neoplasms were retrospectively analyzed. Patients were divided into a radiotherapy group (n=20) and a non-radiotherapy group (n=68). Overall survival (OS) was compared between groups using the Kaplan-Meier method. Subgroup analyses were performed for radiotherapy site, biological equivalent dose (BED), fractionation mode, and the timing of radiotherapy combined with immunotherapy. RESULTS:The radiotherapy group had a lower proportion of patients aged ≥60 years (25.0% vs 66.2%, P<0.001) and a higher proportion receiving immunotherapy (65.0% vs 33.8%, P=0.013) compared with the non-radiotherapy group. The median OS was not reached in the radiotherapy group, which was significantly superior to that in the non-radiotherapy group (22.9 mon, P=0.048). Among patients receiving radiotherapy, those who also received immunotherapy had a significantly longer median OS than those receiving radiotherapy alone. No statistically significant differences in OS were observed among subgroups stratified by radiotherapy site, BED, fractionation schedule or timing. CONCLUSIONS:Radiotherapy effectively improves OS in SMARCA4-deficient lung tumors, with synergistic potential when combined with immunotherapy. The lack of prognostic impact of radiotherapy parameters supports regimen simplification, while the timing of combined therapy needs refinement. These exploratory results lay a critical foundation for future large‑sample confirmatory studies.
Backgroud and objective Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer (NSCLC). Due to the lack of obvious symptoms and signs in the early stages, most patients are already in the middle or late stages at diagnosis. This makes treatment difficult and prognosis poor. Therefore, the identification of effective and specific biomarkers for lung cancer remains a focal area of research. So this study aimed to investigate the expression and clinical significance of S100 calcium-binding protein P (S100P) in LUAD. Methods Tissue samples of LUAD (n=50), adjacent normal lung tissue (n=50), and benign inflammatory lesions (n=50) were collected from The Affiliated Cancer Hospital, Guangzhou Medical University, used as the LUAD group, normal group and benign group. Immunohistochemistry (SP method) was employed to detect the expression of S100P, C-C chemokine ligand 4 (CCL4), and cluster of differentiation 8 (CD8) proteins. Correlation analyses were carried out. Results Database analysis (UALCAN, GEPIA2) identified S100P as an mRNA with high expression in LUAD. Immunohistochemistry demonstrated that the protein levels of S100P and CCL4 were significantly higher in lung tissues of the LUAD group compared to those in the normal group and benign group (all P<0.05). The area under the curve (AUC) of S100P for differentiating LUAD was 0.943. The expression of S100P showed no significant correlation with age, sex, tumor size, or degree of differentiation (all P>0.05). Correlation analysis revealed that S100P expression was moderately positively correlated with CCL4 (r=0.611, P<0.001), and positively correlated with CD8+ lymphocyte infiltration (r=0.461, P<0.001). CCL4 expression was also positively correlated with CD8+ infiltration (r=0.400, P<0.001). Conclusion Database analysis indicates that S100P is highly expressed in LUAD and associated with a poor prognosis, making it a potential biomarker for the prognosis of LUAD. Clinical tissue analysis further shows that S100P expression is correlated with CD8+ lymphocyte infiltration in LUAD, suggesting that S100P can serve as a biomarker of lymphocyte infiltration and a potential predictor of the response to immune checkpoint inhibitors.
Background and objective C-ROS proto-oncogene 1 receptor tyrosine kinase (ROS1) gene fusion-positive non-small cell lung cancer (NSCLC) is a high-risk subtype of lung cancer, and the accurate identification of this specific subtype is critically important. This study systematically analyzes the concordance between the results of next-generation sequencing (NGS), immunohistochemistry (IHC), and fluorescence in situ hybridization (FISH) to validate the clinical value of IHC as an initial screening tool for ROS1 fusions. Methods Patients with NSCLC diagnosed at Cancer Hospital, Chinese Academy of Medical Sciences between November 1, 2020 and November 30, 2022 were enrolled. All cases were tested for ROS1 gene fusion via NGS, re-examined with hematoxylin-eosin (HE) staining, and ROS1 protein expression and gene breakage were detected using IHC and FISH. The results of the three detection methods and their correlation with clinicopathological characteristics were compared. Results 22 were detected as ROS1 fusion-positive among 770 NSCLC cases. Histologically, all were lung adenocarcinoma, predominantly poorly differentiated. The main growth patterns included solid, acinar, and papillary types. IHC detection showed positive expression of ROS1 protein in all 22 cases, including 14 cases (63.6%) with strong diffuse positivity, resulting in a positive concordance rate of 100.0%. FISH detection revealed a typical isolated signal pattern in 16 cases, with a positive concordance rate of 72.7%. The overall concordance rate among NGS, IHC, and FISH was 72.7%. Conclusion ROS1 fusion-positive NSCLC exhibits characteristic clinicopathological features. In ROS1 fusion-positive cases confirmed by NGS, IHC serves as a highly sensitive tool with 100.0% sensitivity, suggesting its potential as an initial screening method, but its specificity still needs further verification. NGS testing is recommended as a priority in cases with strong ROS1 IHC positivity. When strong IHC positivity is observed alongside atypical FISH signals, NGS becomes a key technique for confirmation and precise identification of fusion partners and breakpoints. An integrated diagnostic strategy combining histomorphological evaluation, IHC preliminary screening, and NGS validation facilitates accurate diagnosis of ROS1-positive lung cancer, thereby guiding clinical targeted therapy implementation.
Interstitial lung disease (ILD) is characterized by varying degrees of inflammation and fibrosis of the pulmonary interstitium, posing a significant threat to human health. Patients with ILD have a significantly higher risk of developing lung cancer compared to the general population, which has led to growing clinical attention to the condition of ILD combined with lung cancer (ILD-LC). Nowadays, surgical intervention remains the primary treatment option for patients with ILD-LC. However, how to formulate individualized surgical strategies for this patient population represents a critical challenge in clinical practice. Additionally, patients with ILD-LC are prone to postoperative acute exacerbation of ILD (AE-ILD), which is often challenging to detect at an early stage and severely compromises prognosis. Against this background, this article systematically reviews key aspects of ILD-LC, including differential diagnosis, surgical strategies, and perioperative management, with particular emphasis on the recognition and management of postoperative AE-ILD. It aims to provide a reference for the surgical treatment of ILD-LC and to outline directions for future research.
The mesenchymal-epithelial transition factor (MET) gene, located on human chromosome 7, exerts critical regulatory roles in cellular processes including proliferation, migration, invasion, and angiogenesis. As a key driver gene in non-small cell lung cancer (NSCLC), MET abnormalities encompass MET exon 14 (METex14) skipping mutations, gene amplification, protein overexpression, gene fusions, and activating mutations. This consensus, developed by the Lung Cancer Specialty Committee of the Chinese Elderly Health Care Association, updates the 2025 version with several key modifications: elevating the recommendation level for MET amplification and protein overexpression testing, advocating routine testing for all newly diagnosed NSCLC patients and those with acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs); standardizing targeted therapy approaches for MET amplification in driver gene-negative settings and following EGFR-TKIs resistance; and subdividing MET protein overexpression-related management into post-EGFR-TKIs resistance and driver gene-negative categories with corresponding treatment protocols, thereby offering more actionable guidance for precise clinical decision-making.
Well-differentiated papillary mesothelial tumor (WDPMT) is a rare neoplasm characterized by a distinct papillary architecture, bland cytological features, and a propensity for superficial spread without stromal invasion. We herein report the diagnosis and management of a patient with pleural WDPMT presenting predominantly with recurrent spontaneous pneumothorax and pleural effusion, along with a review of the current literature on this entity. The patient was a 58-year-old female who presented with a two-week history of chest tightness and dyspnea on a background of recurrent spontaneous pneumothorax and pleural effusion over the preceding seven years. She had experienced four episodes of recurrence during that period and denied any history of asbestos exposure. Thoracoscopic exploration revealed pulmonary bullae, pleural effusion and pneumothorax, pleural thickening, and scattered grayish-white nodules on both the visceral and parietal pleura. Histopathological examination of the pleural nodule biopsy confirmed the diagnosis of WDPMT. Based on the features of this case and a review of the literature, clinicians should be aware that WDPMT may present with the atypical manifestation of recurrent spontaneous pneumothorax accompanied by pleural effusion.
Lung cancer ranks among malignant neoplasms with the highest incidence and mortality, and its diagnosis and treatment are complicated, requiring multidisciplinary participation. Multidisciplinary team (MDT) consultation is the core model for modern lung cancer management. By pooling the expertise of specialists from diverse disciplines, MDT develops optimal individualized treatment regimens for patients and markedly improves diagnostic and therapeutic quality as well as patient prognosis. This article systematically summarizes the organizational framework, standardized procedures and clinical value of lung cancer MDT, alongside key problems in its popularization including obstacles in data integration, inconsistent decision-making efficiency and imbalanced resource allocation. It elaborates on the innovative effect of new technologies represented by artificial intelligence large language models on conventional MDT modes, and analyzes their application value in high-efficiency integration of multimodal medical data, real-time evidence-based decision-making support, optimization of consultation procedures and resources, as well as precise individualized treatment, so as to furnish theoretical basis and development ideas for establishing a new-generation intelligent, efficient and precise lung cancer MDT platform.
With the wide application of low-dose spiral computed tomography and the advancement of imaging technology, the detection rate of pulmonary nodules has significantly increased. However, the traditional "one-size-fits-all" management strategy has been unable to meet the needs of precise diagnosis and treatment. This expert consensus was initiated by Professor Chunxia SU’s team and Professor Chang CHEN’s team from Shanghai Pulmonary Hospital and jointly formulated by experts from multiple disciplines including oncology, respiratory medicine, thoracic surgery, interventional medicine, radiology, and pathology. The aim is to provide scientific and practical decision-making references for clinical controversies that are less addressed or have differences in existing guidelines. The consensus uses the GRADE method for evidence assessment and forms 18 recommendations through two rounds of Delphi questionnaire surveys, focusing on differentiated screening for special populations, artificial intelligence assisted diagnosis, robot-assisted puncture, application of molecular markers, active monitoring of low-risk nodules, timing of invasive intervention, termination conditions of follow-up, management strategies for multiple nodules, and selection of individualized lymph node dissection range and surgical methods for early-stage lung cancer. This consensus would provides supplementary guidance for the entire process of precise management of pulmonary nodules from screening to treatment, with expectation of improving the long-term survival rate of lung cancer patients while minimizing unnecessary medical interventions and enhancing the quality of life of patients.
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.
Epidermal growth factor receptor (EGFR) gene mutations are the most common driver mutations in non-small cell lung cancer (NSCLC). This article reports a case of a patient with EGFR-sensitive mutant lung adenocarcinoma who developed secondary transformation to small cell lung cancer (SCLC) and anaplastic lymphoma kinase (ALK) gene fusion following first-line Osimertinib therapy. This paper reported a case of concurrent SCLC transformation and ALK fusion occurring after Osimertinib treatment, suggesting that the two can coexist as dual drug resistance mechanisms. Re-biopsy combined with genetic testing is essential for identifying drug resistance mechanisms and guiding individualized therapy.
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.
