Translational lung cancer research最新文献

{"title":"Squamous-cell carcinoma of the recipient's explanted lung.","authors":"Yuan Zeng, Guilin Peng, Chao Yang, Mengyang Liu, Weixue Cui, Jinzhu Mao, Jianxing He, Xin Xu","doi":"10.21037/tlcr-24-329","DOIUrl":"10.21037/tlcr-24-329","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in the prescription of immune checkpoint inhibitors for non-small cell lung cancer in the Netherlands from 2016 to 2020, a national cancer registry analysis.","authors":"Erick Suazo-Zepeda, Willemijn J Maas, Petra C Vinke, T Jeroen N Hiltermann, Mieke J Aarts, Geertruida Hendrika de Bock, Marjolein A Heuvelmans","doi":"10.21037/tlcr-24-264","DOIUrl":"10.21037/tlcr-24-264","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is the leading cause of cancer mortality globally, with a 5-year survival rate of 10-20%. In recent years, immune checkpoint inhibitors (ICIs) have significantly improved overall survival (OS) in patients with lung cancer. The approval of nivolumab in 2015 marked a milestone in non-small cell lung cancer (NSCLC) treatment, leading to ongoing trials and approvals of new ICI drugs that have reshaped treatment strategies and clinical outcomes for patients with lung cancer. This study aims to describe ICIs prescription trends for NSCLC in the Netherlands and their association with survival. We compared our results with data from randomized controlled trials (RCTs).</p><p><strong>Methods: </strong>We analyzed ICIs prescription trends and their relationship with survival using national-level data from the Netherlands Cancer Registry (NCR) for first-line treatments from 2016-2020. Additionally, we performed a secondary analysis using data from the Oncological Life Study (OncoLifeS) for any-line treatments. Descriptive statistics and annual percentage change (APC) assessed trends in patient and treatment characteristics. OS analyses were performed.</p><p><strong>Results: </strong>In the Netherlands (2016-2020), the proportion of first-line ICI-treated NSCLC patients significantly increased from 1.1% to 54.9% (APC =14.5%, P=0.002), replacing chemotherapy monotherapy. Stage III ICI-treated patients' proportion increased (APC =3.5%, P=0.034), while the proportion of ICI-treated patients with ≥50% programmed death-ligand 1 (PD-L1) expression decreased (APC =-13.82%, P=0.04). Two-year OS was 25.9%. Median OS remained stable, increasing from 2016 to 2018 (16.6 to 19.4 months) and declining slightly in 2019 and 2020 (17.3 and 16.6 months, respectively). In the secondary analysis, median OS varied by treatment line, being 18.8, 9.4 and 7.5 months for first-, second- and third-line treated patients respectively.</p><p><strong>Conclusions: </strong>Using real-world data, we determined that ICI-based therapies replaced chemotherapy-only schemes as first-line treatment for NSCLC. Our survival data are comparable with data from RCTs on first-line ICI-treated NSCLC. Median OS of ICI treated patients has remained stable, with small decreases in recent years possibly attributed to the proportional decrease of individuals with high PD-L1 expressions in treatment regimens. Further-line treatments are associated with lower survival.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histopathologic pattern and molecular risk stratification are associated with prognosis in patients with stage IB lung adenocarcinoma.","authors":"Weiran Liu, Chen Chen, Qiang Zhang, Jiping Xie, Xinyi Wu, Zhenfa Zhang, Lin Shao, Haiwei Du, Songan Chen, Hirokazu Iso, Kakeru Hisakane, Dongsheng Yue, Bin Zhang","doi":"10.21037/tlcr-24-506","DOIUrl":"10.21037/tlcr-24-506","url":null,"abstract":"<p><strong>Background: </strong>The benefit of adjuvant therapy remains controversial in completely resected (R0) stage IB non-small cell lung cancer (NCLSC) patients. In this study, we aimed to explore potential prognostic factors in stage IB NSCLC patients.</p><p><strong>Methods: </strong>This study included 215 patients with R0 stage IB lung adenocarcinoma (LUAD) (tumor size: 3-4 cm). DNA sequencing was performed with surgical samples of 126 patients using a panel of 9 driver genes. The molecular risk stratification was assessed by a 14-gene quantitative polymerase chain reaction assay.</p><p><strong>Results: </strong>Among the 215 patients, 67.9% had micropapillary/solid (MIP/SOL)-predominant tumors. Epidermal growth factor receptor (<i>EGFR</i>) mutations were detected in 75 of 126 patients (59.5%). MIP/SOL tumors harbored less common <i>EGFR</i> mutations than the other histologic patterns (50.6% <i>vs.</i> 79.5%, P=0.003). Molecular risk stratification was successfully assessed in 99 patients, of whom 37.4%, 26.3%, and 36.4% were high, intermediate, and low risk, respectively. The MIP/SOL pattern was associated with shorter disease-free survival (DFS) [hazard ratio (HR) =2.16, 95% confidence interval: 1.28-3.67; P=0.01]. The molecular high-risk patients had shorter DFS than the low- (HR =2.93, P=0.01) and intermediate-risk patients (HR =2.35, P=0.06). The prognostic value of molecular risk stratification was also significant in the MIP/SOL subset (median DFS high-risk: 45 months, low and intermediate risk: not reached; P=0.03).</p><p><strong>Conclusions: </strong>Our study showed that both the MIP/SOL pattern and molecular high-risk category were adverse prognostic factors in stage IB NSCLC patients. Our results suggest that combining histologic classification and molecular risk stratification may help to identify the subset of patients with poor prognosis.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>TFAP2A</i>-activated <i>ITGB4</i> promotes lung adenocarcinoma progression and inhibits CD4⁺/CD8⁺ T-cell infiltrations by targeting <i>NF-κB</i> signaling pathway.","authors":"Cheng Pan, Zhibo Wang, Qi Wang, Hongshun Wang, Xiaheng Deng, Liang Chen, Zhihua Li","doi":"10.21037/tlcr-24-50","DOIUrl":"10.21037/tlcr-24-50","url":null,"abstract":"<p><strong>Background: </strong>Immune-associated genes play vital roles in the tumorigenesis, progression and immunotherapy responses of malignant tumors. This study aimed to comprehensively evaluate the role and mechanism of novel immune-associated gene integrin β4 (<i>ITGB4</i>) in the progression and immune microenvironment of lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>There were 770 immune-associated genes curated from NanoString PanCancer Immune Profiling Panel. Differentially expressed immune-related genes were initially screened using transcriptome data from 57 paired LUAD samples in The Cancer Genome Atlas (TCGA) and 15 paired LUAD samples in GSE31210, and were further validated in 19 paired LUAD samples from our institution. Log-rank test was adopted to identify LUAD prognosis associated genes. Among the identified differentially expressed genes, <i>ITGB4</i> was ultimately chosen for further analysis. Subsequently, the functionality and mechanisms of <i>ITGB4</i> were investigated in two LUAD cell lines, A549 and PC9, which exhibited relatively high expression levels of <i>ITGB4</i>. Following this, the impact of <i>ITGB4</i> on the proliferation and metastasis of LUAD <i>in vivo</i> was evaluated using nude mice. Additionally, its effect on T cell infiltration was studied using immunocompetent C57BL/6J mice.</p><p><strong>Results: </strong><i>ITGB4</i> was found to be significantly up-regulated in LUAD and associated with an unfavorable prognosis. Functionally, <i>ITGB4</i> could promote LUAD cell proliferation, migration and invasion. Consistently, <i>in vivo</i> experiments demonstrated that <i>ITGB4</i> knockdown suppressed LUAD tumor growth and metastasis. Additionally, <i>ITGB4</i> could suppress CD4⁺ and CD8⁺ T-cell infiltrations in LUAD cells. Mechanistically, <i>ITGB4</i> could activate the <i>NF-κB</i> signaling pathway by interacting with <i>IκBα</i>. Furthermore, <i>TFAP2A</i> could directly bind to the <i>ITGB4</i> promoter and transcriptionally activate <i>ITGB4</i> in LUAD cells. In addition, <i>laminin-5</i>, a ligand of <i>ITGB4</i>, was found to promote LUAD progression by activating the <i>ITGB4</i> signaling.</p><p><strong>Conclusions: </strong><i>ITGB4</i> was transcriptionally activated by <i>TFAP2A</i>, and could promote LUAD progression and inhibit CD4⁺/CD8⁺ T-cell infiltrations by activating the <i>NF-κB</i> signaling pathway. <i>ITGB4</i> may serve as a potential immunotherapeutic target of LUAD.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of a survival predictive model for patients with two synchronous multiple primary lung cancers: a multicenter cohort analysis.","authors":"Ying Ji, Qing Zhao, Yi Liu, Bin Qiu, Guangyu Bai, Siyuan Ai, Wei Feng, Ligong Yuan, Xin Wang, Lulu Rong, Hua Fu, Huihui Xie, Linlin Qi, Ye Tao, Longyu Jin, Jing Zhou, Bin Hu, Shugeng Gao","doi":"10.21037/tlcr-24-252","DOIUrl":"10.21037/tlcr-24-252","url":null,"abstract":"<p><strong>Background: </strong>The prognostic predictors of the synchronous multiple primary lung cancer (SMPLC) still remain unclear, and there is a lack of studies on the prognosis of SMPLC patients excluding those with multifocal ground-glass/lepidic (GG/L) nodules. The aim of this study is to develop an effective model for predicting survival of SMPLC patients.</p><p><strong>Methods: </strong>In this multicenter cohort study, a total of 831 SMPLC patients presenting for lung cancer resection from January 2004 to January 2018 at five institutions were included for developing and validating a nomogram model. Specifically, 499 patients from the Cancer Hospital, Chinese Academy of Medical Sciences, and Beijing Chao-Yang Hospital, Capital Medical University were served as the training cohort. A total of 332 patients from The Third Xiangya Hospital of Central South University, the First Affiliated Hospital of University of Science and Technology of China, and Beijing Liangxiang Hospital were served as the external validation cohort. The nomogram model was compared with the Tumor Node Metastasis (TNM) system for the overall survival. The C-index, net reclassification improvement (NRI), and integrated discrimination improvement (IDI) were used to evaluate the model performance. A user-friendly website for SMPLC survival probability calculation was also provided for a better understanding of prognosis of patients with resected SMPLC.</p><p><strong>Results: </strong>A total of seven independent risk factors were selected by conducting a multivariate analysis on the training set. Further, a nomogram model was developed with these factors. Both the internal and external validations exhibited good discrimination (C-index: internal, 0.827; external, 0.784). The NRI and IDI of this model were 0.33 and 0.21, respectively. The survival rates for 1-year, 3-year, and 5-year were consistent with the actual observed values. A set of cutoff values were determined by grouping the patients into three different groups. For each group, we should expect a significant distinction between survival curves.</p><p><strong>Conclusions: </strong>The novel nomogram model enables accurate survival risk stratification of patients with resected SMPLC and may assist in decision-making that is conducive to patients with SMPLC at high risk.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Double immune checkpoint inhibitor therapy for unresectable pleural mesothelioma rarely induces hyperprogressive disease: a case report.","authors":"Gaspard Naulleau, Isabelle Monnet, Gaëlle Rousseau-Bussac, Florent Vinas, Gilles Mangiapan, Laurence Jabot, Amel Boudjemaa, Christos Chouaïd, Jean-Bernard Auliac, Jean-Baptiste Assié","doi":"10.21037/tlcr-24-382","DOIUrl":"10.21037/tlcr-24-382","url":null,"abstract":"<p><strong>Background: </strong>Use of immune checkpoint inhibitors (ICIs) is associated with new response types, such as hyperprogressive disease (HPD), whose definition is still being discussed. Some authors use dynamic indexes to define HPD. However, since the Checkmate-743 study, ICIs have been a first-line therapy for pleural mesothelioma (PM), thereby making use of dynamic indexes less appropriate. The aim of this study is to describe two cases of HPD and then discuss its definitions and implications.</p><p><strong>Case description: </strong>Herein, we report two cases of PM HPD on first-line ICI therapy. A 67-year-old man with right unresectable epithelioid PM, without <i>BAP1</i> or <i>CDKN2A</i> losses, high neutrophil/lymphocyte ratio and rapid-onset pulmonary and mediastinal HPD after two ICI cycles, died of respiratory failure 1 month after starting treatment. A 40-year-old woman with left unresectable epithelioid PM had HPD at first assessment after 4 ICI infusions with jugular thrombosis, liver metastases and more dismal biological parameters. There are multiple different ways to describe HPD, some not applicable to PM. Suspected mechanisms include macrophage reprogramming to M2 cells. There are no known predictive factors of HPD, and future works should focus on identifying them.</p><p><strong>Conclusions: </strong>HPD is a mode of progression for ICI-treated PM patients. Further investigation is needed to better define and anticipate HPD in these patients.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lymph nodes rather than pleural metabolic activity in ¹⁸F-FDG PET/CT correlates with malignant pleural effusion recurrence in advanced non-small cell lung cancer.","authors":"Yuxin Jiang, Tao Liu, Ke Xu, Qinpei Cheng, Wanjun Lu, Jingyuan Xie, Mo Chen, Yu Li, Yanjun Du, Shuo Liang, Yong Song, Jiang Wu, Tangfeng Lv, Ping Zhan","doi":"10.21037/tlcr-24-291","DOIUrl":"10.21037/tlcr-24-291","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Frequently recurrent malignant pleural effusion (MPE) significantly hampers the life quality of advanced non-small cell lung cancer (NSCLC) patients. We aimed to explore the effects of progression patterns and local intervention on MPE recurrence and apply fluorodeoxyglucose positron emission tomography/computed tomography (&lt;sup&gt;18&lt;/sup&gt;F-FDG PET/CT) to establish a predictive model for MPE recurrence in NSCLC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We retrospectively recruited two cohorts of patients including treatment-naïve NSCLC diagnosed with MPE at the onset and receiving PET/CT scanning, as well as those with MPE and undergoing first-line epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) treatment. Pleural maximum standardized uptake value (SUV&lt;sub&gt;max&lt;/sub&gt;), metabolic tumor burden (MTV), total lesion glycolysis (TLG), and uptake patterns as well as SUV&lt;sub&gt;max&lt;/sub&gt; of lymph nodes (LN) were extracted. The primary outcome was MPE recurrence defined as re-accumulation of cytologically proven ipsilateral MPE. Step-wise multivariate Cox regression was used to identify candidate variables. Cox regression analysis and random survival forest were applied to establish models.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;A total of 148 treatment-naïve patients with EGFR-TKI treatment and MPE were recruited during the median follow-up period of 683 days, with 69 (46.6%) and 35 (23.6%) witnessing MPE recurrence at least once and twice. Intrapleural perfusion therapy at first recurrence was a protective factor for the second MPE recurrence (P=0.006), while intrapleural perfusion therapy at baseline could not benefit the first MPE recurrence (P=0.14). Conversely, prior systemic progression indicative of the change of systemic treatment was a protective factor for time to the first MPE recurrence (P&lt;0.001); instead, the change of systemic treatment at the first MPE recurrence was not associated with second MPE recurrence (P=0.53). In another cohort with treatment-naïve NSCLC patients with MPE and PET/CT scanning, 103 patients regardless of the actionable mutation status were recruited during the median follow-up period of 304 days. Multivariate analysis suggested that the LN SUV&lt;sub&gt;max&lt;/sub&gt; &gt;4.50 g/mL [hazard ratio (HR), 2.54; P=0.01], female gender (HR, 0.40; P=0.01), bone metastases (HR, 3.16; P=0.001), and systemic treatment (targeted therapy &lt;i&gt;vs.&lt;/i&gt; chemotherapy: HR, 0.32; P=0.002; immunotherapy therapy &lt;i&gt;vs.&lt;/i&gt; chemotherapy: HR, 0.99; P=0.97) could collectively indicate MPE recurrence with an optimal 300-day area under the curve (AUC) of 0.83. For patients with actionable mutation, LN SUV&lt;sub&gt;max&lt;/sub&gt; &gt;4.50 g/mL (P=0.02) could forecast MPE recurrence independently.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;In summary, LN rather than pleural metabolic activity or uptake patterns could predict MPE recurrence for patients with or without targeted therapy. We should re-consider the application of intrapleural perfus","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-level investigation of the genetic relationship between gastroesophageal reflux disease and lung cancer.","authors":"Dongsheng Wu, Jian Zhou, Lujia Song, Quan Zheng, Tengyong Wang, Zhizhen Ren, Yuchen Huang, Shuqiao Liu, Lunxu Liu","doi":"10.21037/tlcr-24-345","DOIUrl":"10.21037/tlcr-24-345","url":null,"abstract":"<p><strong>Background: </strong>Observational studies have revealed a potential association between gastroesophageal reflux disease (GERD) and lung cancer (LC), but the genetic role in their comorbidity have not been fully elucidated. This study aimed to comprehensively dissect the genetic link underlying GERD and LC.</p><p><strong>Methods: </strong>Using large-scale genome-wide association study (GWAS) data, we investigated shared genetic architecture between GERD and LC. Our analyses encompassed genetic correlation, cross-trait meta-analysis, transcriptome-wide association studies (TWASs), and the evaluation of the causality though a bidirectional Mendelian randomization (MR) analysis with sufficient sensitivities.</p><p><strong>Results: </strong>We identified a significant genome-wide genetic correlation between GERD and overall LC (<i>r_g</i> =0.33, P=1.58×10^-14), as well as across other subtype-specific LC (<i>r_g</i> ranging from 0.19 to 0.39). After separating the whole genome into approximately 2,353 independent regions, 5 specific regions demonstrated significant local genetic correlation, with most significant region located at 9q33.3. Cross-trait meta-analysis revealed 22 pleiotropic loci between GERD and LC, including 3 novel loci (rs537160, rs10156445, and rs17391694). TWASs discovered a total of 49 genes shared in multiple tissues, such as lung tissues, esophagus muscularis, esophagus mucosa, and esophagus gastroesophageal junction. MR analysis suggested a significantly causal relationship between GERD and overall LC [odds ratio (OR) =1.34, 95% confidence interval (CI): 1.19-1.51], as well as other subtype-specific LC (OR ranging from 1.25 to 1.76). No evidence supports a significant causal effect of LC on GERD.</p><p><strong>Conclusions: </strong>Our findings suggest intrinsic genetic correlation underlying GERD and LC, which provides valuable insights for screening and management of LC in individuals with GERD.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484728/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>EGFR</i> mutations in patients with lung adenocarcinoma and malignant pleural effusion: a propensity score-matched analysis of a single-center database.","authors":"Qiwei Yang, Ziyi Wang, Qiang Fu, Xiaohai Hu, Liang Chen, Weiyang Chen, Ling Lv, Zhenghua Liu, Wanfu Men, Danni Li, Wenya Li","doi":"10.21037/tlcr-24-757","DOIUrl":"10.21037/tlcr-24-757","url":null,"abstract":"<p><strong>Background: </strong>Malignant pleural effusion (MPE) is associated with poor prognosis in patients with advanced lung adenocarcinoma (LUAD), and abnormal activation of epidermal growth factor receptor (EGFR) plays a crucial role in the development of LUAD. This study aimed to investigate the correlation between <i>EGFR</i> mutations and the occurrence of MPE in patients with LUAD and evaluate the effect of <i>EGFR</i> mutations on the prognosis of patients with LUAD with MPE.</p><p><strong>Methods: </strong>A case-control study design was adopted that included patients pathologically diagnosed with LUAD. Clinical data were collected, and patients were divided into the MPE group and the non-MPE (N-MPE) group based on the presence of MPE. Propensity score matching (PSM) was used to control for confounding factors. The correlation between <i>EGFR</i> mutations and the occurrence of MPE in LUAD was initially examined. Additionally, various factors affecting the overall survival (OS) of patients with LUAD and MPE were evaluated.</p><p><strong>Results: </strong>A total of 849 patients were included in the study. After 1:2 PSM, there were 180 patients in the MPE group and 360 in the N-MPE group. The <i>EGFR</i> mutation rate was significantly higher in the MPE group compared to the N-MPE group [62.7% <i>vs.</i> 50.2%; odds ratio (OR) =1.668; P=0.006]. This difference was primarily attributed to the T790M mutation (8.3% <i>vs.</i> 1.3%; OR =8.015; P<0.001), but no significant differences observed in other mutation sites between the groups. Further evaluation of factors affecting OS in patients with LUAD and MPE revealed that <i>EGFR</i> mutation was an independent protective factor for OS [hazard ratio (HR) 0.662, 95% CI: 0.456-0.962; P=0.03]. For patients with LUAD, MPE, and <i>EGFR</i> mutations, treatment with third-generation <i>EGFR</i>-tyrosine kinase inhibitors (TKIs) alone (HR 0.466, 95% CI: 0.233-0.930; P=0.03) or sequential first- and third-generation <i>EGFR</i>-TKIs (HR 0.385, 95% CI: 0.219-0.676; P=0.001) was associated with better median OS compared to first-generation <i>EGFR</i>-TKIs alone (first-generation <i>EGFR</i>-TKIs: 35 months, 95% CI: 28.4-41.6; third-generation <i>EGFR</i>-TKIs: 50 months, 95% CI: 37.3-62.7; sequential first- and third-generation <i>EGFR</i>-TKIs: 51 months, 95% CI: 45.6-56.4; P<0.001).</p><p><strong>Conclusions: </strong>This study found there to be a positive correlation between <i>EGFR</i> mutations, particularly the T790M mutation, and MPE in patients with LUAD. <i>EGFR</i> mutation was associated with improved OS in patients with LUAD and MPE. For patients with LUAD, MPE, and <i>EGFR</i> mutations, sequential treatment with first- and third-generation <i>EGFR</i>-TKIs or third-generation <i>EGFR</i>-TKIs alone is recommended, as these regimens provide significant benefit to OS.</p>","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating tumor DNA (ctDNA)-the next generation biomarker in non-small cell lung cancer patients treated with immunotherapy?","authors":"Per Hydbring","doi":"10.21037/tlcr-24-308","DOIUrl":"10.21037/tlcr-24-308","url":null,"abstract":"","PeriodicalId":23271,"journal":{"name":"Translational lung cancer research","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142475664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}