The Chinese Society of Clinical Oncology Non-small Cell Lung Cancer(CSCO NSCLC)guidelines were first published in 2016,ranking among the earliest-released guidelines within the CSCO series.In 2020 the CSCO published s...The Chinese Society of Clinical Oncology Non-small Cell Lung Cancer(CSCO NSCLC)guidelines were first published in 2016,ranking among the earliest-released guidelines within the CSCO series.In 2020 the CSCO published separate guidelines for NSCLC and small cell lung cancer(SCLC)for the first time to improve clinical usability.展开更多
Background:Lung cancer is a life-threatening disease that occurs worldwide,but is especially common in China.The crucial role of the tumour microenvironment(TME)in non-small cell lung cancer(NSCLC)has attracted recent...Background:Lung cancer is a life-threatening disease that occurs worldwide,but is especially common in China.The crucial role of the tumour microenvironment(TME)in non-small cell lung cancer(NSCLC)has attracted recent attention.Cancer-associated fibroblasts(CAFs)are the main factors that contribute to the TME function,and CAF exosomes are closely linked to NSCLC.Methods:The expression levels of miR-3124-5p and Toll-interacting protein(TOLLIP)were analysed by bioinformatics prediction combined with RT-qPCR/Western Blot detection.Fibroblasts were isolated and identified from clinical NSCLC tissues.Transmission electron microscopy and Western Blot were used to identify exosomes from these cells.Changes in proliferation(CCK-8 and clone formation),migration(wound healing),and invasion(transwell)of NSCLC cells were measured.The Luciferase reporter test was applied to clarify the binding of miR-3124-5p to TOLLIP.The TOLLIP/TLR4/MyD88/NF-κB pathway proteins were determined using Western blot analysis.Results:MiR-3124-5p is overexpressed in clinical tissues and cells of NSCLC.MiR-3124-5p was dramatically enriched in CAF-derived exosomes.Cellular experiments revealed that CAFs delivered miR-3124-5p into NSCLC cells via exosomes,stimulating cancer cell progression.MiR-3124-5p acted as a sponge to negatively regulate TOLLIP expression,which activated the TLR4/MyD88/NF-κB axis to promote the occurrence and development of NSCLC.Functional salvage tests were performed to determine whether CAF-exosome-derived miR-3124-5p plays a pro-cancer role in NSCLC by affecting the TOLLIP signalling pathway.Conclusions:These results provide an interesting direction for the diagnosis and therapy of NSCLC.展开更多
Objectives:Non-small cell lung cancer(NSCLC)represents a formidable malignancy characterized by its marked metastatic potential and intrinsic resistance to therapeutic interventions.The identification of potential bio...Objectives:Non-small cell lung cancer(NSCLC)represents a formidable malignancy characterized by its marked metastatic potential and intrinsic resistance to therapeutic interventions.The identification of potential biomarkers delineating the progression and metastatic cascade of NSCLC assumes paramount importance in fostering advancements toward enhanced patient outcomes and prognostic stratification.Methods:The expression level of the actin-related protein 2/3 complex;subunit 1A(ARPC1A)in NSCLC was evaluated using The Cancer Genome Atlas(TCGA)and Gene Expression Profiling Interactive Analysis(GEPIA)databases;along with the LinkedOmics database for co-expression genes.Further verification of ARPC1A expression in normal lung cells and NSCLC cells;as well as in normal tissues and lung cancer tissues;was performed using quantitative real-time reverse transcription PCR(RTqPCR)and Western blotting.The function of ARPC1A was explored through Gene Set Enrichment Analysis(GSEA)and immune infiltration analysis;followed by functional experiments for validation.Results:ARPC1A is upregulated in NSCLC and is associated with unfavorable clinical prognoses.Additionally,the Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis highlights a potential link between the ARPC1A gene and the cell cycle and p53 signaling pathways.ARPC1A also promotes cell proliferation and resistance to chemotherapeutic drugs,thereby enhancing the oncogenic potential of NSCLC.Relevant cell-based experiments confirm that targeted inhibition of ARPC1A effectively suppresses cellular migratory and invasive capabilities.The immune infiltration analysis showed a close association between ARPC1A expression and various immune components,suggesting ARPC1A may interact with the tumor microenvironment.Mechanistically,ARPC1A promotes cell migration by stimulating the epithelialto-mesenchymal transition(EMT).Conclusion:The study results revealed the potential of ARPC1A as a valuable prognostic biomarker for NSCLC.Additionally,the associated mechanisms provide insights that may pave the way for therapeutic interventions for NSCLC patients.展开更多
Objective:Osimertinib(OSI)therapy,a cornerstone in treating non-small cell lung cancer(NSCLC),has been severely limited by rapidly developing acquired resistance.Inhibition of bypass activation using a combination str...Objective:Osimertinib(OSI)therapy,a cornerstone in treating non-small cell lung cancer(NSCLC),has been severely limited by rapidly developing acquired resistance.Inhibition of bypass activation using a combination strategy holds promise in overcoming this resistance.Biguanides,with excellent anti-tumor effects,have recently attracted much attention for this potential.The current study investigated whether novel biguanide compounds developed by our team could overcome OSI resistance and the underlying mechanisms were explored.Methods:A comprehensive screening assay using OSI-resistant cells identified the optimal combination of biguanide compounds with OSI.Proteomics,co-immunoprecipitation mass spectrometry,RNA sequencing,and homologous recombination assays were used to elucidate the molecular mechanisms underlying combination therapy.NSCLC tumor tissues,especially OSI-resistant tissues,obtained from our clinic were used to assess the correlations between key proteins and OSI resistance.Results:SMK-010,a highly potent biguanide compound,effectively overcame OSI resistance in vitro and in vivo.Mechanistical studies showed that BMI1/FGFR1 pathway activation is responsible for OSI resistance.Specifically,silencing BMI1 promoted NEDD4-mediated FGFR1 ubiquitination and proteasomal degradation,whereas SMK-010 treatment induced FGFR1 lysosomal degradation.This reduction in FGFR1 levels impaired homologous recombination,increased DNA damage,and surmounted OSI resistance.Analysis of clinical samples revealed overexpression of BMI1 and FGFR1 in NSCLC tissues and represented potential biomarkers for OSI resistance.Conclusions:These findings highlight the crucial role of the BMI1/FGFR1 axis in OSI resistance and provide a rational basis for the future clinical application of the biguanide,SMK-010,in combination with OSI.展开更多
最新流行病学数据显示,肺癌已超越乳腺癌再次跃居全球恶性肿瘤发病首位。在可切除非小细胞肺癌的临床实践中,术后复发难题始终困扰着医患双方。统计数据显示,仅接受手术治疗的早期患者中,6%~11%会出现局部复发,23%~30%面临远处转移风险...最新流行病学数据显示,肺癌已超越乳腺癌再次跃居全球恶性肿瘤发病首位。在可切除非小细胞肺癌的临床实践中,术后复发难题始终困扰着医患双方。统计数据显示,仅接受手术治疗的早期患者中,6%~11%会出现局部复发,23%~30%面临远处转移风险。当病情进展至III期时,术后五年复发率更是攀升至60%左右,这一严峻现状凸显了传统治疗模式的局限性。近年来兴起的围手术期全程免疫疗法为破解这一困境提供了新思路,该方案通过术前阶段调节机体免疫微环境,促进免疫系统精准识别并清除肿瘤细胞,术后持续巩固免疫应答,有效清除潜在残留病灶,从而显著降低复发概率并延长患者生存期。值得注意的是,这种新型治疗策略的出现为改善患者预后开辟了新路径,其作用机制涉及肿瘤免疫循环的重建与维持,这对优化现有治疗体系具有深远影响。随着相关临床研究的深入,围术期免疫治疗的时序安排、用药方案及疗效预测等关键问题正逐步明晰,这些突破性进展不仅为个体化治疗提供了理论支撑,更为重要的是将推动肺癌治疗模式从单一外科干预向多学科协作的精准医疗转型。深入探讨这种治疗模式的最新研究进展,不仅能为临床决策提供循证依据,更有助于推动肺癌诊疗体系的优化升级,最终使更多患者获得生存获益。The latest epidemiological data show that lung cancer has surpassed breast cancer to become the most commonly diagnosed malignant tumor globally. In the clinical practice of resectable non-small cell lung cancer, postoperative recurrence remains a persistent challenge for both physicians and patients. Statistics indicate that among early-stage patients treated with surgery alone, 6%~11% experience local recurrence, and 23%~30% face the risk of distant metastasis. When the disease progresses to stage III, the five-year postoperative recurrence rate soars to approximately 60%. This grim reality highlights the limitations of traditional treatment modalities. In recent years, the emerging comprehensive perioperative immunotherapy has provided a new solution to this dilemma. This approach involves modulating the immune microenvironment before surgery to enhance the immune system’s ability to accurately identify and eliminate tumor cells, and then consolidating the immune response after surgery to effectively clear any residual disease. This significantly reduces the recurrence rate and extends patient survival. Notably, the emergence of this novel treatment strategy has opened up a new path for improving patient prognosis, with its mechanism involving the reconstruction and maintenance of the tumor immune cycle. This has far-reaching implications for optimizing the existing treatment system. As relevant clinical research progresses, key issues such as the timing of perioperative immunotherapy, drug regimens, and efficacy prediction are becoming clearer. These breakthroughs not only provide theoretical support for personalized treatment but more importantly, they will drive the transformation of lung cancer treatment from a single surgical intervention to a multidisciplinary collaborative precision medicine model. Delving into the latest research progress of this treatment model not only provides evidence-based support for clinical decision-making but also helps to optimize and upgrade the lung cancer diagnosis and treatment system, ultimately benefiting more patients.展开更多
Our previous research demonstrated that the Wenxia Changfu Formula(WCF),as a neoadjuvant therapy,inhibits M2 macrophage infiltration in the tumor microenvironment and prevents lung cancer metastasis.Given tumor-associ...Our previous research demonstrated that the Wenxia Changfu Formula(WCF),as a neoadjuvant therapy,inhibits M2 macrophage infiltration in the tumor microenvironment and prevents lung cancer metastasis.Given tumor-associated macrophages(TAMs)in epithelial-mesenchymal transition(EMT),this study investigated whether WCF impedes lung cancer metastasis by attenuating TAM-induced EMT in non-small cell lung cancer(NSCLC)cells.Utilizing a co-culture model treated with or without WCF,we observed that WCF downregulated cluster of differentiation 163(CD163)expression in macrophages,reduced CCL18 levels in the conditioned medium,and inhibited the growth,invasion,and EMT of NSCLC cells induced by macrophage co-culture.Manipulation of CCL18 levels and Src overexpression in NSCLC cells revealed that WCF’s effects are mediated through CCL18 and Src signaling.In vivo,WCF inhibited recombinant CCL18(rCCL18)-induced tumor metastasis in nude mice by blocking Src signaling.These findings indicate that WCF inhibits NSCLC metastasis by impeding TAM-induced EMT via antagonistic modulation of CCL18,providing evidence for its potential development and clinical application in NSCLC patients.展开更多
目的:探讨甲基化转移酶3(methyltransferase-like 3,METTL3)联合程序死亡配体1(programmed death ligand 1,PD-L1检测在非小细胞肺癌(non-small cell lung cancer,NSCLC)患者程序性细胞死亡蛋白1(programmed death cell protein 1,PD-1...目的:探讨甲基化转移酶3(methyltransferase-like 3,METTL3)联合程序死亡配体1(programmed death ligand 1,PD-L1检测在非小细胞肺癌(non-small cell lung cancer,NSCLC)患者程序性细胞死亡蛋白1(programmed death cell protein 1,PD-1)抑制剂治疗效果和预后预测中的价值。方法:收集NSCLC患者原发病灶组织蜡块标本,免疫组织化学检测PD-L1、METTL3的蛋白表达情况,并分析其与NSCLC患者PD-1抑制剂治疗效果和预后间的联系。结果:符合入组标准的患者共228例;其中,METTL3蛋白的表达情况与病理类型、美国东部肿瘤合作组织(Eastern American Oncology Collaborative Group,ECOG)评分、治疗方案、治疗效果以及实体瘤疗效评价标准(response evaluation criteria in solid tumors,RECIST)等因素有关;METTL3蛋白高表达患者的中位无进展生存期(progression-free-survival,PFS)为12.33个月,METTL3蛋白低或无表达患者的中位PFS为6.50个月;在接受PD-1抑制剂治疗的NSCLC患者中,METTL3蛋白高表达患者有较长的PFS;METTL3蛋白高表达患者的中位总体生存期(overall-survival,OS)为23.54个月,METTL3蛋白低或无表达患者的中位OS为20.93个月,METTL3蛋白高表达与较长的OS相关。结论:METTL3蛋白可能为预测NSCLC PD-1抑制剂免疫治疗效果的标志物。展开更多
文摘The Chinese Society of Clinical Oncology Non-small Cell Lung Cancer(CSCO NSCLC)guidelines were first published in 2016,ranking among the earliest-released guidelines within the CSCO series.In 2020 the CSCO published separate guidelines for NSCLC and small cell lung cancer(SCLC)for the first time to improve clinical usability.
文摘Background:Lung cancer is a life-threatening disease that occurs worldwide,but is especially common in China.The crucial role of the tumour microenvironment(TME)in non-small cell lung cancer(NSCLC)has attracted recent attention.Cancer-associated fibroblasts(CAFs)are the main factors that contribute to the TME function,and CAF exosomes are closely linked to NSCLC.Methods:The expression levels of miR-3124-5p and Toll-interacting protein(TOLLIP)were analysed by bioinformatics prediction combined with RT-qPCR/Western Blot detection.Fibroblasts were isolated and identified from clinical NSCLC tissues.Transmission electron microscopy and Western Blot were used to identify exosomes from these cells.Changes in proliferation(CCK-8 and clone formation),migration(wound healing),and invasion(transwell)of NSCLC cells were measured.The Luciferase reporter test was applied to clarify the binding of miR-3124-5p to TOLLIP.The TOLLIP/TLR4/MyD88/NF-κB pathway proteins were determined using Western blot analysis.Results:MiR-3124-5p is overexpressed in clinical tissues and cells of NSCLC.MiR-3124-5p was dramatically enriched in CAF-derived exosomes.Cellular experiments revealed that CAFs delivered miR-3124-5p into NSCLC cells via exosomes,stimulating cancer cell progression.MiR-3124-5p acted as a sponge to negatively regulate TOLLIP expression,which activated the TLR4/MyD88/NF-κB axis to promote the occurrence and development of NSCLC.Functional salvage tests were performed to determine whether CAF-exosome-derived miR-3124-5p plays a pro-cancer role in NSCLC by affecting the TOLLIP signalling pathway.Conclusions:These results provide an interesting direction for the diagnosis and therapy of NSCLC.
基金supported by the Natural Science Foundation of Anhui Province(ML 2308085MC80)the Anhui Medical University Research and Innovation Talent Team(KZ).
文摘Objectives:Non-small cell lung cancer(NSCLC)represents a formidable malignancy characterized by its marked metastatic potential and intrinsic resistance to therapeutic interventions.The identification of potential biomarkers delineating the progression and metastatic cascade of NSCLC assumes paramount importance in fostering advancements toward enhanced patient outcomes and prognostic stratification.Methods:The expression level of the actin-related protein 2/3 complex;subunit 1A(ARPC1A)in NSCLC was evaluated using The Cancer Genome Atlas(TCGA)and Gene Expression Profiling Interactive Analysis(GEPIA)databases;along with the LinkedOmics database for co-expression genes.Further verification of ARPC1A expression in normal lung cells and NSCLC cells;as well as in normal tissues and lung cancer tissues;was performed using quantitative real-time reverse transcription PCR(RTqPCR)and Western blotting.The function of ARPC1A was explored through Gene Set Enrichment Analysis(GSEA)and immune infiltration analysis;followed by functional experiments for validation.Results:ARPC1A is upregulated in NSCLC and is associated with unfavorable clinical prognoses.Additionally,the Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis highlights a potential link between the ARPC1A gene and the cell cycle and p53 signaling pathways.ARPC1A also promotes cell proliferation and resistance to chemotherapeutic drugs,thereby enhancing the oncogenic potential of NSCLC.Relevant cell-based experiments confirm that targeted inhibition of ARPC1A effectively suppresses cellular migratory and invasive capabilities.The immune infiltration analysis showed a close association between ARPC1A expression and various immune components,suggesting ARPC1A may interact with the tumor microenvironment.Mechanistically,ARPC1A promotes cell migration by stimulating the epithelialto-mesenchymal transition(EMT).Conclusion:The study results revealed the potential of ARPC1A as a valuable prognostic biomarker for NSCLC.Additionally,the associated mechanisms provide insights that may pave the way for therapeutic interventions for NSCLC patients.
基金supported by grants from the National Natural Science Foundation of China(Grant Nos.82172653 and 82472728)the Key Project of Developmental Biology and Breeding from Hunan Province(Grant No.2022XKQ0205)+1 种基金the Research Team for Reproduction Health and Translational Medicine of Hunan Normal University(Grant No.2023JC101)the Natural Science Foundation of Hunan Province(Grant No.2025JJ80150).
文摘Objective:Osimertinib(OSI)therapy,a cornerstone in treating non-small cell lung cancer(NSCLC),has been severely limited by rapidly developing acquired resistance.Inhibition of bypass activation using a combination strategy holds promise in overcoming this resistance.Biguanides,with excellent anti-tumor effects,have recently attracted much attention for this potential.The current study investigated whether novel biguanide compounds developed by our team could overcome OSI resistance and the underlying mechanisms were explored.Methods:A comprehensive screening assay using OSI-resistant cells identified the optimal combination of biguanide compounds with OSI.Proteomics,co-immunoprecipitation mass spectrometry,RNA sequencing,and homologous recombination assays were used to elucidate the molecular mechanisms underlying combination therapy.NSCLC tumor tissues,especially OSI-resistant tissues,obtained from our clinic were used to assess the correlations between key proteins and OSI resistance.Results:SMK-010,a highly potent biguanide compound,effectively overcame OSI resistance in vitro and in vivo.Mechanistical studies showed that BMI1/FGFR1 pathway activation is responsible for OSI resistance.Specifically,silencing BMI1 promoted NEDD4-mediated FGFR1 ubiquitination and proteasomal degradation,whereas SMK-010 treatment induced FGFR1 lysosomal degradation.This reduction in FGFR1 levels impaired homologous recombination,increased DNA damage,and surmounted OSI resistance.Analysis of clinical samples revealed overexpression of BMI1 and FGFR1 in NSCLC tissues and represented potential biomarkers for OSI resistance.Conclusions:These findings highlight the crucial role of the BMI1/FGFR1 axis in OSI resistance and provide a rational basis for the future clinical application of the biguanide,SMK-010,in combination with OSI.
文摘最新流行病学数据显示,肺癌已超越乳腺癌再次跃居全球恶性肿瘤发病首位。在可切除非小细胞肺癌的临床实践中,术后复发难题始终困扰着医患双方。统计数据显示,仅接受手术治疗的早期患者中,6%~11%会出现局部复发,23%~30%面临远处转移风险。当病情进展至III期时,术后五年复发率更是攀升至60%左右,这一严峻现状凸显了传统治疗模式的局限性。近年来兴起的围手术期全程免疫疗法为破解这一困境提供了新思路,该方案通过术前阶段调节机体免疫微环境,促进免疫系统精准识别并清除肿瘤细胞,术后持续巩固免疫应答,有效清除潜在残留病灶,从而显著降低复发概率并延长患者生存期。值得注意的是,这种新型治疗策略的出现为改善患者预后开辟了新路径,其作用机制涉及肿瘤免疫循环的重建与维持,这对优化现有治疗体系具有深远影响。随着相关临床研究的深入,围术期免疫治疗的时序安排、用药方案及疗效预测等关键问题正逐步明晰,这些突破性进展不仅为个体化治疗提供了理论支撑,更为重要的是将推动肺癌治疗模式从单一外科干预向多学科协作的精准医疗转型。深入探讨这种治疗模式的最新研究进展,不仅能为临床决策提供循证依据,更有助于推动肺癌诊疗体系的优化升级,最终使更多患者获得生存获益。The latest epidemiological data show that lung cancer has surpassed breast cancer to become the most commonly diagnosed malignant tumor globally. In the clinical practice of resectable non-small cell lung cancer, postoperative recurrence remains a persistent challenge for both physicians and patients. Statistics indicate that among early-stage patients treated with surgery alone, 6%~11% experience local recurrence, and 23%~30% face the risk of distant metastasis. When the disease progresses to stage III, the five-year postoperative recurrence rate soars to approximately 60%. This grim reality highlights the limitations of traditional treatment modalities. In recent years, the emerging comprehensive perioperative immunotherapy has provided a new solution to this dilemma. This approach involves modulating the immune microenvironment before surgery to enhance the immune system’s ability to accurately identify and eliminate tumor cells, and then consolidating the immune response after surgery to effectively clear any residual disease. This significantly reduces the recurrence rate and extends patient survival. Notably, the emergence of this novel treatment strategy has opened up a new path for improving patient prognosis, with its mechanism involving the reconstruction and maintenance of the tumor immune cycle. This has far-reaching implications for optimizing the existing treatment system. As relevant clinical research progresses, key issues such as the timing of perioperative immunotherapy, drug regimens, and efficacy prediction are becoming clearer. These breakthroughs not only provide theoretical support for personalized treatment but more importantly, they will drive the transformation of lung cancer treatment from a single surgical intervention to a multidisciplinary collaborative precision medicine model. Delving into the latest research progress of this treatment model not only provides evidence-based support for clinical decision-making but also helps to optimize and upgrade the lung cancer diagnosis and treatment system, ultimately benefiting more patients.
基金supported by the National Natural Science Foundation of China(No.82274406,81774198)Zhejiang Provincial Natural Science Foundation of China(No.LZ24H270001)the Postgraduate Scientific Research Fund of Zhejiang Chinese Medical University(No.2022YKJ14).
文摘Our previous research demonstrated that the Wenxia Changfu Formula(WCF),as a neoadjuvant therapy,inhibits M2 macrophage infiltration in the tumor microenvironment and prevents lung cancer metastasis.Given tumor-associated macrophages(TAMs)in epithelial-mesenchymal transition(EMT),this study investigated whether WCF impedes lung cancer metastasis by attenuating TAM-induced EMT in non-small cell lung cancer(NSCLC)cells.Utilizing a co-culture model treated with or without WCF,we observed that WCF downregulated cluster of differentiation 163(CD163)expression in macrophages,reduced CCL18 levels in the conditioned medium,and inhibited the growth,invasion,and EMT of NSCLC cells induced by macrophage co-culture.Manipulation of CCL18 levels and Src overexpression in NSCLC cells revealed that WCF’s effects are mediated through CCL18 and Src signaling.In vivo,WCF inhibited recombinant CCL18(rCCL18)-induced tumor metastasis in nude mice by blocking Src signaling.These findings indicate that WCF inhibits NSCLC metastasis by impeding TAM-induced EMT via antagonistic modulation of CCL18,providing evidence for its potential development and clinical application in NSCLC patients.
文摘目的系统评价埃克替尼治疗非小细胞肺癌(non-small cell lung cancer,NSCLC)的不同组织病理学类型与ECOG评分差异的临床有效性。方法收集国内外埃克替尼治疗NSCLC的临床治疗性试验研究数据,用Revman5.2进行meta分析。结果腺癌vs鳞癌纳入了8篇研究,固定效应M-H分析合并效应优势比OR=2.46,P=0.0005;ECOG评分:0~1 vs 2~4和0~2 vs 3~4 2个亚组分别纳入研究6篇和3篇,均存在异质性,随机效应M-H分析合并效应分别是RR=1.20,P=0.15和RR=1.77,P=0.09。结论埃克替尼治疗NSCLC的有效性腺癌比鳞癌更敏感;ECOG评分高低不影响治疗的有效性,但仍可扩大研究样本进行分析。
文摘目的:探讨甲基化转移酶3(methyltransferase-like 3,METTL3)联合程序死亡配体1(programmed death ligand 1,PD-L1检测在非小细胞肺癌(non-small cell lung cancer,NSCLC)患者程序性细胞死亡蛋白1(programmed death cell protein 1,PD-1)抑制剂治疗效果和预后预测中的价值。方法:收集NSCLC患者原发病灶组织蜡块标本,免疫组织化学检测PD-L1、METTL3的蛋白表达情况,并分析其与NSCLC患者PD-1抑制剂治疗效果和预后间的联系。结果:符合入组标准的患者共228例;其中,METTL3蛋白的表达情况与病理类型、美国东部肿瘤合作组织(Eastern American Oncology Collaborative Group,ECOG)评分、治疗方案、治疗效果以及实体瘤疗效评价标准(response evaluation criteria in solid tumors,RECIST)等因素有关;METTL3蛋白高表达患者的中位无进展生存期(progression-free-survival,PFS)为12.33个月,METTL3蛋白低或无表达患者的中位PFS为6.50个月;在接受PD-1抑制剂治疗的NSCLC患者中,METTL3蛋白高表达患者有较长的PFS;METTL3蛋白高表达患者的中位总体生存期(overall-survival,OS)为23.54个月,METTL3蛋白低或无表达患者的中位OS为20.93个月,METTL3蛋白高表达与较长的OS相关。结论:METTL3蛋白可能为预测NSCLC PD-1抑制剂免疫治疗效果的标志物。
