Clinical lung cancer最新文献

{"title":"Efficacy of First-Line Nivolumab Plus Ipilimumab in Unresectable Pleural Mesothelioma: A Multicenter Real-World Study (ImmunoMeso LATAM)","authors":"Diego Enrico ,&nbsp;Juan Elias Gomez ,&nbsp;Danilo Aguirre ,&nbsp;Natalia Soledad Tissera ,&nbsp;Florencia Tsou ,&nbsp;Carmen Pupareli ,&nbsp;Delfina Peralta Tanco ,&nbsp;Federico Waisberg ,&nbsp;Andrés Rodríguez ,&nbsp;Manglio Rizzo ,&nbsp;Nicolás Minatta ,&nbsp;Picon Rafael ,&nbsp;Luis Basbus ,&nbsp;Lorena Lupinacci ,&nbsp;Diego Kaen ,&nbsp;Mauro Ramos ,&nbsp;Virginia Bluthgen ,&nbsp;Nicolas Castagneris ,&nbsp;María Pía Coppola ,&nbsp;Alejandra Scocimarro ,&nbsp;Claudio Martín","doi":"10.1016/j.cllc.2024.09.005","DOIUrl":"10.1016/j.cllc.2024.09.005","url":null,"abstract":"<div><h3>Background</h3><div>The phase 3 CheckMate-743 trial demonstrated a prolonged overall survival (OS) benefit with nivolumab plus ipilimumab over chemotherapy as first-line treatment in patients with unresectable pleural mesothelioma (PM). However, given that Latin American (LATAM) patients were notably underrepresented in this trial, we retrospectively assessed the effectiveness and safety of this regimen in this population.</div></div><div><h3>Methods</h3><div>This retrospective study included patients from 15 centers in LATAM with unresectable or metastatic PM treated with first-line nivolumab plus ipilimumab in a real-world data (RWD) scenario. Demographic, clinicopathological characteristics, and safety data were collected from medical charts. Progression-free survival (PFS), and OS were calculated using the Kaplan-Meier method.</div></div><div><h3>Results</h3><div>From June 2017, and January 2024 96 patients were included: epithelioid 78% (n = 75), 81% were ECOG 0-1 (n = 78). With a median follow-up of 24.1 months, median PFS and OS were 8 months (95% CI, 6.6-9.4), and 22 months (95% CI, 18.9-25), respectively. No statistical difference in OS was observed between epithelioid versus nonepithelioid histology (median 23 months vs. 19 months, respectively; <em>P =</em> .29). Treatment efficacy was also consistent among different clinical subgroups. Any and grade 3-4 adverse events were found in 43.1% (n = 28), and 18.5% (n = 12) of patients, respectively. Remarkably, no OS impact was observed in patients who had dose delay or treatment discontinuation due to immune-related adverse events, and those who experienced any adverse event.</div></div><div><h3>Conclusions</h3><div>This multicenter RWD study demonstrated the clinically meaningful benefit of first-line ipilimumab and nivolumab in LATAM patients with unresectable or metastatic PM, and data is consistent with previous trial findings.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages 723-731.e2"},"PeriodicalIF":3.3,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FLAIR: A Phase II, Open Label, Randomized Study of Osimertinib Plus Bevacizumab Versus Osimertinib in Recurrent or Metastatic Treatment-Naïve NSCLC Patients Harboring EGFR 21L858R Mutation","authors":"Qing Zhou ,&nbsp;Jie Li ,&nbsp;Shun-Dong Cang ,&nbsp;Jia-Xin Lin ,&nbsp;Hai-Yan Tu ,&nbsp;Yingying Du ,&nbsp;Jian-Wen Qin ,&nbsp;Xiao-Hua Liang ,&nbsp;Yan Yu ,&nbsp;Hai-Tao Lan ,&nbsp;Hua-Qiu Shi ,&nbsp;Dong Hua ,&nbsp;Si-Yang Maggie Liu ,&nbsp;Yi-Long Wu","doi":"10.1016/j.cllc.2024.09.002","DOIUrl":"10.1016/j.cllc.2024.09.002","url":null,"abstract":"<div><h3>Introduction</h3><div>Osimertinib, the 3rd generation EGFR-TKI, has emerged as standard first-line treatment for patients with advanced <em>EGFR</em> mutated nonsmall cell lung cancer (NSCLC). Patients with exon 21 L858R mutation showed lower efficacy with EGFR-TKIs than those with 19Del mutation, even with osimertinib, it remains an unmet medical need to further improve the efficacy in L858R population. We present the rationale and design for FLAIR (NCT04988607), which will investigate the efficacy and safety of osimertinib plus bevacizumab versus osimertinib monotherapy in treatment-naïve recurrent or metastatic NSCLC patients harboring <em>EGFR</em> exon 21 L858R mutation.</div></div><div><h3>Materials and Methods</h3><div>FLAIR is a prospective, multicenter, randomized, open label study, which is initiated by Chinese Thoracic Oncology Group (CTONG2002). Patients age ≥18 years with primary recurrent or metastatic nonsquamous NSCLC who are treatment-naïve with documented <em>EGFR</em> exon 21 L858R mutation is eligible. Patients will be randomized 1:1 to receive osimertinib 80 mg once daily plus bevacizumab 15mg/kg every 3 weeks or osimertinib monotherapy 80 mg once daily until progression or another discontinuation criterion is met. The primary endpoint is investigator-assessed progression free survival (PFS). Secondary endpoints include: overall survival rate at 24 months, time to treatment failure (TTF), overall response rate (ORR), disease control rate (DCR), duration of response (DoR), central nervous system (CNS) PFS, CNS ORR and safety.</div></div><div><h3>Results</h3><div>FLAIR has completed the enrollment, and results are expected in the fourth quarter of 2025 (depending on the actual event rate).</div></div><div><h3>Conclusions</h3><div>This study will offer better perspectives on the efficacy and safety of osimertinib plus bevacizumab combination therapy in treatment-naïve recurrent or metastatic NSCLC patients harboring EGFR exon 21 L858R mutation, providing valuable guidance for clinical practice.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"26 2","pages":"Pages 152-157.e1"},"PeriodicalIF":3.3,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Phase II Study of Neoadjuvant Opnurasib KRAS G12C Inhibitor in Patients With Surgically Resectable Non-Small Cell Lung Cancer (CCTG IND.242A): A Substudy of the IND.242 Platform Master Protocol","authors":"J. Spicer ,&nbsp;N. Blais ,&nbsp;S. Owen ,&nbsp;A.G. Robinson ,&nbsp;Q. Chu ,&nbsp;C. Labbe ,&nbsp;B. Shieh ,&nbsp;P. Brown-Walker ,&nbsp;J. Sederias ,&nbsp;K. Jensen ,&nbsp;A.F. Farago ,&nbsp;M.-S. Tsao ,&nbsp;T.R. Cottrell ,&nbsp;B. Kidane ,&nbsp;S. Laurie ,&nbsp;R. Juergens ,&nbsp;P.A. Bradbury ,&nbsp;W. Tu ,&nbsp;P.-O. Gaudreau","doi":"10.1016/j.cllc.2024.09.003","DOIUrl":"10.1016/j.cllc.2024.09.003","url":null,"abstract":"<div><div>Molecularly targeted agents are increasingly being studied in the treatment of early-stage non-small cell lung cancer (NSCLC) to try and improve cure. However, phase 3 data on neoadjuvant therapy have largely been conducted in a biomarker agnostic manner with inconsistent exclusion of <em>EGFR</em> and <em>ALK</em> alterations. Our objective was to develop IND.242 as a large-scale neoadjuvant platform trial to introduce novel agents into the preoperative window for molecularly-defined NSCLC patient populations. Given that <em>KRAS</em> G12C mutations are common in the overall NSCLC patient population, ranging from 9.4% to 13% of cases across different cohorts, and may be associated to worse prognosis, the initial IND.242A Substudy was designed to test neoadjuvant JDQ443 (opnurasib), a selective KRAS G12C inhibitor. This current trial report describes the multicenter, Canadian Cancer Trials Group (CCTG)-led IND.242 neoadjuvant phase 2 platform master protocol and its first Substudy (IND.242A) of neoadjuvant opnurasib KRAS G12C inhibitor for patients with surgically resectable NSCLC (AJCC 8th edition stage IA2 to IIIA). In IND.242A, a maximum of 27 patients will be accrued in participating Canadian sites. The primary objective is the rate of major pathological response (MPR) following neoadjuvant opnurasib. Secondary objectives include safety and tolerability of the treatment regimen, objective response rate (ORR) by RECIST 1.1 for the neoadjuvant treatment period, pathological complete response (pCR) rate, event-free survival (EFS) at 2 years, and surgical outcomes. Exploratory objectives are to explore patient related outcomes (PROs) and identify potential predictive biomarkers of response and mechanisms of resistance on tissue and peripheral blood samples.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"26 2","pages":"Pages 146-151"},"PeriodicalIF":3.3,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of Oncogene Overlap by Tissue-Based Next-Generation Sequencing to Explore the Mutational Landscape and Survival Impact of HER2, KRAS and MET Copy-Number Gain in Nonsmall Cell Lung Cancer","authors":"Alexander S. Watson ,&nbsp;Harris B. Krause ,&nbsp;Andrew Elliott ,&nbsp;Alex Farrell ,&nbsp;Stephen V. Liu ,&nbsp;Patrick C. Ma ,&nbsp;Ari VanderWalde ,&nbsp;George W. Sledge ,&nbsp;David Spetzler ,&nbsp;Erin L. Schenk ,&nbsp;D. Ross Camidge","doi":"10.1016/j.cllc.2024.09.001","DOIUrl":"10.1016/j.cllc.2024.09.001","url":null,"abstract":"<div><h3>Background</h3><div>Gene copy number gain (CNG) is a continuous variable. The relevant cutpoint for <em>HER2, KRAS</em> and <em>MET</em> CNG in non-mall cell lung cancer remains uncertain. As de novo driver oncogenes are largely mutually exclusive, oncogene overlap analysis can be used to explore CNG thresholds.</div></div><div><h3>Patient and Methods</h3><div>We retrospectively analysed NGS of DNA/RNA in 13,702 NSCLC adenocarcinoma samples. Alternate and same-gene driver oncogene co-occurrence with <em>HER2, KRAS</em> and <em>MET</em> CNG was examined. Overall survival (OS) from time of biopsy collection was correlated with CNG and pathogenic mutations in driver oncogenes (Driver+).</div></div><div><h3>Results</h3><div>The frequency of Driver+ tumors decreased with increasing CNG. Setting CNG thresholds by oncogene overlap and dataset size (CNA ≥ 6 for <em>HER2, KRAS</em> and ≥ 4 for <em>MET</em>), tumors considered relevantly amplified (Amp) for <em>MET, HER2</em> and <em>KRAS</em> were significantly less likely to be Driver+ (<em>P</em> &lt; .001). When Driver+ did overlap with Amp status, same-gene alterations (mutation and CNG) were significantly enriched for all 3 genes (<em>HER2, KRAS</em> and <em>MET</em>), while <em>BRAF</em> and <em>EGFR</em> mutations were more common in <em>MET</em>-Amp than in <em>HER2</em>- or <em>KRAS</em>-Amp tumors. A negative OS association with Amp status was independent of Driver+ status for <em>HER2</em> and <em>MET</em>, however not <em>KRAS</em>.</div></div><div><h3>Conclusion</h3><div>Tissue NGS-based <em>HER2, KRAS</em> and <em>MET</em> CNG thresholds set by oncogene overlap identified potentially clinically relevant “Amp” subgroups with altered genetic profiles and decreased survival. Prospective research into targeted therapy benefit in these groups is encouraged.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages 712-722.e1"},"PeriodicalIF":3.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Smoking and the Risk of Second Primary Lung Cancer Among Breast Cancer Survivors from the Population-Based UK Biobank Study","authors":"Anna Graber-Naidich ,&nbsp;Eunji Choi ,&nbsp;Julie T. Wu ,&nbsp;Timothy J. Ellis-Caleo ,&nbsp;Joel Neal ,&nbsp;Heather A. Wakelee ,&nbsp;Allison W. Kurian ,&nbsp;Summer S. Han","doi":"10.1016/j.cllc.2024.08.017","DOIUrl":"10.1016/j.cllc.2024.08.017","url":null,"abstract":"<div><h3>Objective</h3><div>Long-term breast cancer (BC) survivors are known to develop second malignancies, with second primary lung cancer (SPLC) one common type. Smoking was identified as a main risk factor for SPLC among BC survivors. These findings were limited to the U.S. and focused on smoking status, not incorporating cumulative smoking exposures (eg, pack-years). We examine SPLC incidence and evaluate the associations between SPLC risk and cumulative cigarette smoking exposures and other potential factors among BC survivors in a prospective European cohort.</div></div><div><h3>Methods</h3><div>Of 502,505 participants enrolled in the UK Biobank in 2006 to 2010, we identified 8429 patients diagnosed with BC between 2006 and 2016 and followed for second malignancies through 2016. Smoking information was collected at enrollment, and treatment data were collected using electronic health records. Multivariable cause-specific Cox regression (CSC) evaluated the association between each factor and SPLC risk.</div></div><div><h3>Results</h3><div>Of 8429 BC patients, 40 (0.47%) developed SPLC over 45,376 person-years. The 10-year cumulative SPLC incidence was 0.48% (95% CI = 0.33%-0.62%). The CSC analysis confirmed the association between SPLC and ever-smoking status (adjusted hazard-ratio (aHR) = 3.46 (<em>P</em> &lt; .001). The analysis showed a 24% increment in SPLC risk per 10 smoking pack-years among BC survivors (aHR = 1.24 per-10 pack-years, <em>P</em> = .01). The associations between SPLC and other variables remained statistically insignificant. We applied the USPSTF lung cancer screening eligibility criteria and found that 80% of the 40 BC survivors who developed SPLC would have been ineligible for lung cancer screening.</div></div><div><h3>Conclusion</h3><div>In a large, European cohort, cumulative smoking exposure is significantly associated with SPLC risk among BC survivors.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages 705-711.e7"},"PeriodicalIF":3.3,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brief Report: Targeted Therapies and Pancreatitis in Patients With Advanced Nonsmall Cell Lung Cancer","authors":"May-Lucie Meyer ,&nbsp;Louis Gros ,&nbsp;Natalie Décosterd ,&nbsp;Marco Tagliamento ,&nbsp;Arianna Marinello ,&nbsp;David Planchard ,&nbsp;David Combarel ,&nbsp;Fabrice Barlesi ,&nbsp;Jordi Remon ,&nbsp;Benjamin Besse ,&nbsp;Mihaela Aldea","doi":"10.1016/j.cllc.2024.08.016","DOIUrl":"10.1016/j.cllc.2024.08.016","url":null,"abstract":"<div><div><ul><li><span></span><span><div>Targeted treatments are commonly used to treat lung cancer but can induce elevations in pancreatic enzyme levels in up to 24% of patients. While these drugs are recognized as potential triggers for pancreatitis, the clinical significance of monitoring pancreatic enzymes and the incidence of clinical acute pancreatitis remains uncertain. In our study of 1207 targeted treatments in 725 patients with advanced lung cancer, we observed that, although elevations in pancreatic enzymes were frequent (37%), instances of clinical acute pancreatitis were scarce (0.08%). Based on our findings and in line with the current recommendations of drug-induced pancreatitis, we suggest that routine monitoring for pancreatitis is not necessary in asymptomatic patients.</div></span></li></ul></div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages e482-e486.e3"},"PeriodicalIF":3.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Phase I Open-Label Study of Cediranib Plus Etoposide and Cisplatin as First-Line Therapy for Patients With Extensive-Stage Small-Cell Lung Cancer or Metastatic Neuroendocrine Non–Small-Cell Lung Cancer","authors":"Kyle F. Concannon ,&nbsp;Bonnie S. Glisson ,&nbsp;Robert C. Doebele ,&nbsp;Chao Huang ,&nbsp;Marcelo Marotti ,&nbsp;D. Ross Camidge ,&nbsp;John V. Heymach","doi":"10.1016/j.cllc.2024.08.015","DOIUrl":"10.1016/j.cllc.2024.08.015","url":null,"abstract":"<div><h3>Introduction</h3><div>Small cell lung cancer (SCLC) is known to express high levels of the proangiogenic factor vascular endothelial growth factor (VEGF). We assessed the safety and tolerability of cediranib, an oral inhibitor of VEGF receptor tyrosine kinases, in combination with etoposide and cisplatin as first-line therapy for extensive-stage (ES) SCLC or metastatic lung neuroendocrine cancer (NEC).</div></div><div><h3>Methods</h3><div>Patients received up to six 21-day cycles of etoposide (100 mg/m², days 1-3) and cisplatin (80 mg/m², day 1) with once-daily cediranib until disease progression or unacceptable toxicity. Cediranib dosing started at 30 mg with de-escalation cohorts planned based on cycle 1 dose-limiting toxicities (DLTs). An expansion cohort of 12 patients was enrolled at the recommended phase II dose.</div></div><div><h3>Results</h3><div>Twenty-two patients (18 with ES SCLC, 4 with NEC) received treatment. Only 4 patients were enrolled at the 30 mg cediranib dose before other studies established 20 mg/day as the recommended dose with chemotherapy. Among the 18 patients enrolled at the 20-mg dose, common adverse events included nausea/vomiting, neutropenia, and diarrhea; 8 patients (44%) had grade 1 or 2 hypertension, and 2 (11%) had grade 3 hemoptysis. For all 18 patients, the objective response rate and median progression-free survival duration were 67% and 7.9 months. Plasma levels of VEGF were significantly higher, and those of soluble VEGFR2 were significantly lower, on day 22 than at baseline but were not correlated with tumor shrinkage.</div></div><div><h3>Conclusions</h3><div>Cediranib (20 mg) plus etoposide and cisplatin is well tolerated and has promising clinical activity.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 7","pages":"Pages 601-611"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to Editor: Commentary on “Influence of Tumor Cavitation on Assessing the Clinical Benefit of Anti-PD1 or PD-L1 Inhibitors in Advanced Lung Squamous Cell Carcinoma”","authors":"Qin Chen ,&nbsp;Xinyue Wang ,&nbsp;Richeng Jiang","doi":"10.1016/j.cllc.2024.08.013","DOIUrl":"10.1016/j.cllc.2024.08.013","url":null,"abstract":"","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages e479-e481"},"PeriodicalIF":3.3,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Treatment of Lung Cancer Oncogenic Drivers in a Diverse Safety Net Setting","authors":"Kalyani Narra ,&nbsp;Bassam Ghabach ,&nbsp;Vivek Athipatla ,&nbsp;James-Michael Blackwell ,&nbsp;Kari J. Teigen ,&nbsp;Jolonda C. Bullock ,&nbsp;Anna Diaz ,&nbsp;David E. Gerber ,&nbsp;Mitchell S. von Itzstein","doi":"10.1016/j.cllc.2024.08.014","DOIUrl":"10.1016/j.cllc.2024.08.014","url":null,"abstract":"<div><h3>Introduction</h3><div>Advances in the testing and treatment of patients with non-small cell lung cancer (NSCLC) harboring oncogenic drivers have improved outcomes. Little is known about testing and treatment patterns in diverse patient populations.</div></div><div><h3>Methods</h3><div>We conducted a retrospective study in a diverse cohort of patients treated in the John Peter Smith safety net healthcare system. We determined patterns of blood- and tissue-based testing and treatment of patients with <em>EGFR</em> and <em>ALK</em> alterations. Cox proportional-hazards regression models were used to assess the impact of <em>EGFR</em> and <em>ALK</em> testing.</div></div><div><h3>Results</h3><div>A total of 220 patients were included, 97 (44%) were non-Hispanic White, 72 (33%) were Black, 28 (13%) were Hispanic, and 23 (10%) were Asian. <em>EGFR</em> and <em>ALK</em> testing increased over time from 55% and 52%, respectively, in 2017 to 87% and 82%, respectively, in 2021. Frequency of <em>EGFR</em> alterations were highest in Asian patients (45%) and comparable among other groups (6-13%). Frequency of <em>ALK</em> alterations were highest in Hispanic (13%), and Asian (11%) patients, and were 2% for both Black and non-Hispanic White patients. In a multivariate model, lack of testing was associated with worse survival (aHR 1.6; <em>P</em> = .003) and testing positive for <em>EGFR</em> (aHR 0.43; <em>P</em> = .01) or <em>ALK</em> (aHR 0.28; <em>P</em> = .04) was associated with improved survival. Race and ethnicity were not associated with survival differences.</div></div><div><h3>Conclusion</h3><div>As molecular testing for oncogenic mutations in NSCLC increases, druggable alterations such as <em>ALK</em> and <em>EGFR</em> can be identified in all race-ethnicity groups and are associated with improved outcomes.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"26 2","pages":"Pages 83-92"},"PeriodicalIF":3.3,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Social Risk Factors That Avert Equitable Lung Cancer Care","authors":"Christopher M. Kapp ,&nbsp;Chelsi Green ,&nbsp;Jeffrey Thiboutot ,&nbsp;Jeremy Kim ,&nbsp;Mary M. Pasquinelli ,&nbsp;Benjamin Aronson ,&nbsp;A. Christine Argento","doi":"10.1016/j.cllc.2024.08.011","DOIUrl":"10.1016/j.cllc.2024.08.011","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer remains the leading cause of cancer death in the United States. There is an association between certain social determinants of health (SDOH) and adverse cancer outcomes. These include Black race and low-income, which are associated with poorer adherence to lung cancer screening and presentation at a later stage of disease.</div></div><div><h3>Methods</h3><div>We conducted a retrospective review of all patients with a diagnosis of lung cancer at a single urban, academic center from 2015 to 2021. Demographic data including race and clinical data including time taken to progress through various checkpoints (ie, concerning CT scan to diagnosis, diagnosis to treatment) were collected. Income data was approximated based on population medians at patient's home address zip code.</div></div><div><h3>Results</h3><div>A total of 550 patients were included in the final analysis. The study population was 57.4% Black and 61.2% of patients presenting with a household income of $40,000 US Dollars or lower based on approximated median household income. The time from CT scan to first treatment for the entire cohort was 121.3 days with no statistically significant variance by race. However, among patients presenting at stage IV, 72.7% were black and 76.0% resided in a zip code with a median income &lt; $40,000.</div></div><div><h3>Conclusions</h3><div>This study demonstrated no significant delays in progressing through checkpoints of lung cancer diagnosis and treatment on the basis of race or income approximation. Black patients and patients in low-income households were diagnosed with lung cancer at a more advanced stage. Efforts to close the gap in lung cancer disparities should be focused on targeting screening and early identification toward social groups that may be at highest risk of late presentation. Institutional focus on patient navigation through these stages should be paramount.</div></div><div><h3>Tweetable Abstract</h3><div>There were no delays in progression to lung cancer diagnostic and therapeutic milestones based on race or income approximation. Black race and residing in a low-income area are predictors for presenting at stage IV.</div></div>","PeriodicalId":10490,"journal":{"name":"Clinical lung cancer","volume":"25 8","pages":"Pages 699-704"},"PeriodicalIF":3.3,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}