中国肺癌杂志最新文献

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.
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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.
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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.

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

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.
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Lung cancer, one of the leading causes of cancer-related deaths worldwide, severely influences patients' quality of life and prognosis due to its complication of brain metastasis (primarily involving the brain parenchyma). While traditional treatments such as surgery, radiotherapy, and chemotherapy have demonstrated efficacy in clinical practice, their application remains limited due to toxicity and patient tolerance issues. Emerging targeted therapies and immunotherapies, which exhibit significant efficacy with fewer side effects, still face challenges including partial drug resistance and genetic mutations. In recent years, research on the association between gut microbiota and lung cancer brain metastasis has gained prominence. Its mechanism of action may influence the progression of brain metastasis through multidimensional interactions via the brain-gut axis, involving neuroendocrine and immune pathways. This review examines specific mechanisms by which gut microbiota modulate lung cancer brain metastasis through immune regulation, endocrine-metabolic regulation, and neurotransmitter control via the brain-gut axis, as well as therapeutic and traditional medicine research on regulating gut microbiota in lung cancer brain metastasis. It aims to provide theoretical support and identify potential clinical therapeutic targets for the prevention and treatment of lung cancer brain metastasis.
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As lung cancer treatment continues to advance, mainstream approaches such as surgery, radiotherapy, chemotherapy, neoadjuvant therapy, targeted therapy and immunotherapy have become widely adopted in clinical practice. However, the efficacy of these methods is still limited and they are associated with significant side effects. In recent years, the pivotal role of the gut microbiota in tumor immune regulation has become increasingly recognized, with its potential impact on tumor immunotherapy emerging as a novel therapeutic focus in lung cancer management. Against this backdrop, fecal microbiota transplantation (FMT) has been proposed as a potential immunomodulatory strategy. It enhances host immune responses and improves the tumor immune microenvironment by regulating the gut microbiota. This paper provides a systematic review of the latest research advances in FMT for lung cancer treatment. Focusing on the relationship between gut microbiota and lung cancer, the therapeutic mechanisms of FMT and clinical application studies, it provides a comprehensive exploration of the challenges and prospects for the use of FMT in lung cancer therapy.
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Pulmonary enteric adenocarcinoma (PEAC) is a distinct subtype of non-small cell lung cancer (NSCLC) whose histomorphology and immunophenotype closely resemble those of metastatic colorectal adenocarcinoma; its pathogenesis and standard treatment strategies have yet to be clearly established. Here, we reported a case of PEAC harboring epidermal growth factor receptor (EGFR) exon 19 deletion mutation with high programmed cell death ligand 1 (PD-L1) expression. The patient showed no meaningful response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including the first-generation (Icotinib), the second-generation (Afatinib) and the third-generation (Aumolertinib). Trophoblast cell surface antigen 2-antibody-drug conjugate (TROP2-ADC) and immune checkpoint inhibitors (ICIs) combined with Bevacizumab also resulted in limited efficacy. Based on the clinical features and treatment response of this case, we reviewed the published literature about the pathological characteristics, mutational landscape, and current therapeutic approaches for PEAC, with a particular focus on the therapeutic challenges and future research directions for EGFR-mutant PEAC, aiming to provide insights for clinical practice and further studies.
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In recent years, immune checkpoint inhibitors (ICIs), as a revolutionary therapeutic approach in oncology, have demonstrated remarkable clinical efficacy across various malignant tumors. With the widespread clinical application of ICIs, their associated toxicities have emerged as a critical issue that urgently requires resolution in the field of cancer immunotherapy. ICIs-associated pneumonitis (CIP) specifically refers to immune-related adverse events (irAEs) of the lung induced by ICIs therapy, the underlying pathogenesis of which remains incompletely elucidated. As a rare yet severe complication of ICIs treatment, and CIP is characterized by insidious onset, rapid progression, poor prognosis, and high mortality rate, with highly heterogeneous clinical manifestations and radiological features. Due to the lack of specific biomarkers and objective diagnostic indicators, the early identification and diagnosis of CIP present significant clinical challenges. By reviewing previous literature and studies, this paper summarizes recent advances in understanding the clinical manifestations, risk factors, potential molecular mechanisms, biomarkers, and early warning systems of CIP in patients receiving immunotherapy for lung cancer. The aim of this article is to provide a reference for the clinical management of CIP and offer a theoretical basis for establishing an early screening and precision diagnosis and treatment system for this condition.
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Background: The low response rate to immunotherapy can be partially attributed to tumor immune escape mechanisms arising from the heterogeneous tumor microenvironment. This study aims to determine the impact of inflammatory non-small cell lung cancer (NSCLC) on the efficacy of neoadjuvant immunotherapy combined with chemotherapy at the histological level, and to investigate the predictive value of specific CD8+ and CD4+ T cell numbers, as well as spatial interactions, in treatment response.

Methods: A retrospective study included 43 patients with NSCLC who underwent neoadjuvant immunotherapy combined with chemotherapy at Shandong Cancer Hospital from January 2021 to June 2023. Preoperative biopsy specimens were collected and subjected to multiplex immunofluorescence staining [CD8/programmed cell death protein 1 (PD-1)/T cell immunoglobulin and mucin-domain containing protein 3 (TIM-3)/CD4/ forkhead box protein 3 (FoxP3)/cytokeratin (CK)/4',6-diamidino-2-phenylindole (DAPI)]. InForm software was used to perform tissue segmentation (epithelial and stromal regions) and quantify the density and spatial proximity of tumor cells, CD8+ T cells and their subsets (cytotoxic, pre-exhausted and exhausted), as well as CD4+ T cells and their subsets (conventional and regulatory). NSCLC was classified into three subtypes based on the relative infiltration levels of CD8+ T cells in both the epithelial and stromal compartments: inflamed (both compartments>10/1000), excluded (epithelial compartment<10/1000 and stromal compartment>10/1000), and desert (both compartments<10/1000). The Kolmogorov-Smirnov test, Fisher's exact test, Mann-Whitney U test and Logistic regression were used to identify factors associated with major pathological response (MPR).

Results: Inflamed, excluded, and desert NSCLC accounted for 65.1%, 27.9% and 7.0%, respectively. Compared with patients with non-inflamed NSCLC, those with inflamed NSCLC exhibit a higher MPR rate (71.4% vs 33.3%, P=0.016). Both univariate and multivariate Logistic regression analyses confirmed that the inflamed subtype is an independent protective factor against the acquisition of MPR in NSCLC patients (OR=0.20, 95%CI: 0.05-0.74, P=0.020; adjusted OR=0.17, 95%CI: 0.03-0.80, P=0.030). Analysis of the spatial distance between CD8+ and CD4+ T cells within the epithelial regions of inflamed NSCLC revealed that the effective density of cytotoxic CD8+ T cells within a 30 μm radius of regulatory CD4+ T cells was lower in the MPR group than in the non-MPR group (0.00 vs 0.33, P=0.037).

Conclusions: Patients with inflamed NSCLC demonstrate superior efficacy when receiving neoadjuvant immunotherapy combined with chemotherapy. This may be due to reduced proximity between regulatory CD4+ T cells and cytotoxic CD8+ T cells.