Journal of Thoracic Oncology最新文献

{"title":"Rapid Intracranial Response With Tarlatamab in Patients With Untreated Brain Metastases From SCLC-A Real-World Case Series: Case Report.","authors":"Bingnan Zhang, Komal B Shah, Mitchell Parma, Kaiwen Wang, Eric K Singhi, Whitney Lewis, Melvin Rivera, Mehmet Altan, Jenny Pozadzides, Xiuning Le, Natalie Vokes, Frank Fossella, Barbara O'Brien, Chenyang Wang, Martin C Tom, Thomas Beckham, Todd Swanson, Julianna Bronk, Steven H Lin, Maria Franco Vega, Joshua Jacome, Alexa Halliday, Marcelo Negrao, Jianjun Zhang, Don L Gibbons, John V Heymach, Lauren A Byers, Carl M Gay","doi":"10.1016/j.jtho.2025.02.023","DOIUrl":"https://doi.org/10.1016/j.jtho.2025.02.023","url":null,"abstract":"<p><p>SCLC has the highest propensity for brain metastases among all malignancies. Systemic treatment for SCLC, particularly in the setting of brain metastases, is very limited. Tarlatamab, the CD3/delta-like ligand 3 bispecific T-cell engager, has changed the treatment landscape of relapsed SCLC since its Food and Drug Administration approval in May 2024. Patients with treated and stable brain metastases were included in the phase 1 DeLLphi-300 trial and phase 2 DeLLphi-301 trials of tarlatamab. Nevertheless, it remains unknown if tarlatamab is safe and efficacious in the setting of untreated, active or symptomatic brain metastases. Our case series provides, to our knowledge, the first reported evidence of the safety and efficacy of tarlatamab in patients with untreated brain metastases. In our cohort of 10 patients with relapsed SCLC and untreated brain metastases, including those with symptomatic intracranial disease and one with suspected leptomeningeal disease, clinical response or stability was seen in 90% of patients. We present several cases in which rapid, dramatic radiographic responses and clinical improvement were observed in patients with innumerable growing brain metastases (>20 lesions) who would otherwise require whole brain radiation, suggesting that tarlatamab can control intracranial metastases as monotherapy, potentially sparing or deferring the need for brain radiation.</p>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cemiplimab Monotherapy for First-Line Treatment of Patients with Advanced NSCLC with PD-L1 Expression ≥50%: 5-Year Outcomes of EMPOWER-Lung 1.","authors":"Saadettin Kilickap, Ana Baramidze, Ahmet Sezer, Mustafa Özgüroğlu, Mahmut Gumus, Igor Bondarenko, Miranda Gogishvili, Marina Nechaeva, Michael Schenker, Irfan Cicin, Ho Gwo Fuang, Yaroslav Kulyaba, Kasimova Zyuhal, Roxana-Ioana Scheusan, Marina Chiara Garassino, Yuntong Li, Cong Zhu, Manika Kaul, Javier Perez, Frank Seebach, Israel Lowy, Jean-Francois Pouliot, Eric Kim, Heather Magnan","doi":"10.1016/j.jtho.2025.03.033","DOIUrl":"https://doi.org/10.1016/j.jtho.2025.03.033","url":null,"abstract":"<p><strong>Introduction: </strong>Earlier results from the phase 3 EMPOWER-Lung 1 trial demonstrated significant survival benefits and a generally acceptable safety profile of first-line cemiplimab monotherapy versus chemotherapy for patients with advanced non-small cell lung cancer (NSCLC) with programmed cell death-ligand 1 (PD-L1) expression in ≥50% of tumor cells and no EGFR, ALK, or ROS1 aberrations. Here, we report the 5-year outcomes.</p><p><strong>Methods: </strong>Patients were randomized 1:1 to cemiplimab 350 mg intravenous every 3 weeks for 2 years or investigator's choice of chemotherapy. The primary endpoints were overall survival (OS) and progression-free survival (PFS).</p><p><strong>Results: </strong>A total of 712 patients were randomized to cemiplimab (n = 357) or chemotherapy (n = 355). Median duration of follow-up was 59.6 months (interquartile range: 55.1-66.7 months) at the data cutoff (January 16, 2024). In patients with verified PD-L1 ≥50% (n = 565), median OS was 26.1 months for cemiplimab vs. 13.3 months for chemotherapy (hazard ratio [HR] 0.59, 95% confidence interval [CI]: 0.48-0.72); median PFS was 8.1 months versus 5.3 months (HR 0.50, 95% CI: 0.41-0.61); the objective response rate was 46.5% versus 20.6%. The 5-year OS probability was 29.0% for cemiplimab and 15.0% for chemotherapy. Improved survival outcomes were observed with both squamous and non-squamous histology, and increasing activity of cemiplimab was correlated with higher PD-L1 expression, with the highest PD-L1 expression having the best outcome. The safety profile remains consistent with previous results. Grade ≥3 treatment-related adverse events occurred in 18.3% of patients for cemiplimab and 39.9% for chemotherapy.</p><p><strong>Conclusions: </strong>At 5-year follow-up, first-line cemiplimab monotherapy continued to show durable clinical benefits versus chemotherapy in patients with advanced NSCLC with PD-L1 ≥50%. Patients with PD-L1 ≥90% derived the largest clinical benefits.</p>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut Microbiota in Advanced Non-small-cell Lung Cancer Receiving Chemo-immunotherapy: An Ancillary Biomarker Study from the Phase III trial JCOG2007 (NIPPON).","authors":"Taiki Hakozaki, Kentaro Tanaka, Yoshimasa Shiraishi, Yuta Sekino, Noriko Mitome, Yusuke Okuma, Tomoiki Aiba, Takahiro Utsumi, Junko Tanizaki, Koichi Azuma, Satoshi Hara, Ryo Morita, Seiji Niho, Toshihide Yokoyama, Ryo Toyozawa, Hidehito Horinouchi, Isamu Okamoto, Yukio Hosomi, Yuichiro Ohe","doi":"10.1016/j.jtho.2025.02.026","DOIUrl":"https://doi.org/10.1016/j.jtho.2025.02.026","url":null,"abstract":"<p><strong>Background: </strong>Immunotherapy has transformed treatment for non-small cell lung cancer (NSCLC). However, reliable biomarkers for treatment selection remain scarce. Gut microbiota has emerged as a potential biomarker, but its role in chemo-immunotherapy for NSCLC is unclear.</p><p><strong>Methods: </strong>The phase III trial (JCOG2007, NIPPON) compared pembrolizumab plus platinum doublet chemotherapy (PC) and nivolumab-ipilimumab plus platinum doublet chemotherapy (NIC) in treatment-naïve advanced NSCLC patients without driver gene alterations. As an ancillary biomarker study, 270 patients with baseline fecal samples were analyzed for gut microbiota composition out of 295 patients enrolled. 16S rDNA sequencing was performed for the diversity and differential abundance analysis.</p><p><strong>Results: </strong>The beta diversity analysis of the overall cohort (n=270) revealed distinct microbial structures between the subpopulations defined by whether overall survival (OS) exceeds 12 or 18 months. Subsequent LEfSe analysis identified specific bacterial genera that differed between the subpopulations, with Fusicatenibacter, Butyricicoccus, and Blautia being enriched in patients with longer OS. Regarding adverse events (AEs), lower microbial alpha diversity and the presence of certain taxa were linked to a higher risk of serious (≥ Grade 4) AEs. Additionally, favorable genera, including Fusicatenibacter and Butyricicoccus, were associated with a lower risk of serious AEs. Lastly, regimen-specific analysis showed that higher abundance of Fusicatenibacter and Butyricicoccus were linked to better OS in the NIC arm compared to that in the CP arm (Hazard Ratio (HR) for OS = 0.56 and 0.52, respectively). Conversely, the higher abundance of Prevotellaceae NK3B31 was associated with higher mortality risk in the NIC arm (HR for OS = 2.33).</p><p><strong>Conclusions: </strong>Gut microbiota may serve as a biomarker for chemo-immunotherapy in advanced NSCLC. Differences in microbial diversity and specific bacterial genera were associated with prognosis and serious AEs, with potential regimen-specific effects. These findings support integrating gut microbiota profiling into clinical practice to optimize first-line treatment strategies.</p>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective depletion of CCR8+Treg cells enhances anti-tumor immunity of cytotoxic T cells in lung cancer via dendritic cells.","authors":"Peixin Chen, Haowei Wang, Zhuoran Tang, Jinpeng Shi, Lei Cheng, Chao Zhao, Xuefei Li, Caicun Zhou","doi":"10.1016/j.jtho.2025.02.029","DOIUrl":"https://doi.org/10.1016/j.jtho.2025.02.029","url":null,"abstract":"<p><p>Accumulation of regulatory T (Treg) cells, an immunosuppressive population, limits the efficacy of immunotherapy in non-small cell lung cancer (NSCLC). C-C Motif Chemokine Receptor 8 (CCR8) is selectively expressed in tumor-infiltrating Treg cells and, thus considered an ideal target. Across four NSCLC-bearing mice models, the combination of CCR8 antibody and programmed cell death protein-1 (PD1) inhibitor significantly reduced tumor growth without obvious mouse body weight drops and systemic cytokine storm. The single-cell RNA and T-cell receptor sequencing analysis demonstrated that anti-CCR8 therapy synergizes with PD1 blockade by remodeling the tumor microenvironment and disrupting CCR8+Treg - CCL5+ dendritic cells (DC) interaction. Mechanistically, therapeutic depletion of CCR8+Treg cells combined with PD1 inhibitor extremely increased interleukin-12 secretion by the JAK-STAT pathway activation on CCL5+ DCs, thereby promoting cytotoxic activity of CD8+ T cells. The therapeutic potential of the CCR8 antibody LM-108 in combination with immunotherapy was observed in clinical patients with advanced NSCLC. Overall, CCR8 expression on tumor-infiltrating Treg cells is correlated with immunosuppressive function on DCs and CD8+ T cells, thus impeding anti-tumor immunity.</p>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"10.1016/S1556-0864(25)00039-5","DOIUrl":"10.1016/S1556-0864(25)00039-5","url":null,"abstract":"","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages A11-A12"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143534643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phase II Randomized Study of Maintenance Atezolizumab Versus Atezolizumab Plus Talazoparib in Patients With SLFN11 Positive Extensive-Stage SCLC: S1929","authors":"Nagla Abdel Karim MD, PhD ,&nbsp;Jieling Miao MS ,&nbsp;Karen L. Reckamp MD ,&nbsp;Carl M. Gay MD, PhD ,&nbsp;Lauren A. Byers MD, MS ,&nbsp;Ying-Qi Zhao PhD ,&nbsp;Mary W. Redman PhD ,&nbsp;Daniel R. Carrizosa MD, MS ,&nbsp;Wei-Lien Wang MD ,&nbsp;William J. Petty MD ,&nbsp;Kathan Mehta MD, MPH ,&nbsp;Bryan A. Faller MD ,&nbsp;Edem S. Agamah MD ,&nbsp;Samer S. Kasbari MD, MS ,&nbsp;Rajini K. Malisetti MD ,&nbsp;Atul Kumar MD, PhD ,&nbsp;John Schallenkamp MD, MBA ,&nbsp;Krishna C. Alluri MD ,&nbsp;Jhanelle E. Gray MD ,&nbsp;Karen Kelly MD","doi":"10.1016/j.jtho.2024.10.021","DOIUrl":"10.1016/j.jtho.2024.10.021","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate whether the addition of a poly (adenosine diphosphate–ribose) polymerase inhibitor talazoparib to maintenance immune checkpoint inhibitor atezolizumab after frontline chemoimmunotherapy improved outcomes in patients with Schlafen 11 (SLFN11)-positive extensive-stage SCLC (ES-SCLC).</div></div><div><h3>Methods</h3><div>Patients with newly diagnosed SLFN11 expressing (H-score ≥ 1, evaluated centrally) ES-SCLC were randomized to maintenance atezolizumab (A) versus atezolizumab plus talazoparib (AT) after frontline chemotherapy plus atezolizumab. The primary objective was to compare progression-free survival (PFS) using a one-sided 10% level stratified log-rank test. Secondary endpoints included objective response rate, overall survival, and toxicity. The target sample size was 84 eligible patients.</div></div><div><h3>Results</h3><div>From June 15, 2020, to December 15, 2022, 106 eligible patients were randomized (54 to AT and 52 to A). Progression-free survival was improved with AT versus A (hazard ratio = 0.66, 80% confidence interval: 0.50–0.86, one-sided <em>p</em> = 0.019) with a median PFS of 2.9 and 2.4 months; overall survival was not different between groups (hazard ratio = 0.98, 80% confidence interval: 0.71–1.36, one-sided <em>p</em> = 0.47). Grade 3 and higher non-hematologic treatment-related adverse events occurred in 17% of patients with AT and 14% of patients with A. Grade 3 and higher hematological treatment-related adverse events were more common in AT (50%) than in A (4%) (<em>p</em> &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>Maintenance AT improved PFS in patients with SLFN11-positive ES-SCLC that did not progress after initial chemo-immunotherapy. Hematologic toxicity, primarily grade 3 anemia, was increased with AT, as expected. Prospective biomarker selection was demonstrated, paving the way for future evaluation of novel therapies in molecularly defined SCLC populations.</div></div>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages 383-394"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Durvalumab Versus Chemotherapy as First-line Treatment for Metastatic NSCLC With Tumor PD-L1 Expression of 25% or Higher: Results From the Randomized Phase 3 PEARL Study","authors":"Shun Lu MD, PhD ,&nbsp;Lin Wu MD, PhD ,&nbsp;Qiming Wang MD ,&nbsp;Ziping Wang MD ,&nbsp;Dongqing Lv MD ,&nbsp;Rui Ma MD ,&nbsp;Bo Zhu MD, PhD ,&nbsp;Ngoc van Tran MD, PhD ,&nbsp;Liyan Jiang MD, PhD ,&nbsp;Kejun Nan PhD ,&nbsp;Konstantin Laktionov MD ,&nbsp;Stephen Clarke MD, PhD ,&nbsp;Minghao Song MD ,&nbsp;Helen Mann MSc ,&nbsp;Yinglei Liu MD ,&nbsp;Xiaojin Shi MD ,&nbsp;Yi-Long Wu MD","doi":"10.1016/j.jtho.2024.10.024","DOIUrl":"10.1016/j.jtho.2024.10.024","url":null,"abstract":"<div><h3>Introduction</h3><div>PEARL (NCT03003962) is an open-label, phase 3 study comparing first-line durvalumab monotherapy with chemotherapy in patients with metastatic NSCLC (mNSCLC [<em>EGFR/ALK</em> wild type]) with programmed cell death ligand 1 (PD-L1) tumor cell (TC) membrane expression status of 25% or higher. We report the final analysis of PEARL.</div></div><div><h3>Methods</h3><div>Adults (N = 669) with previously untreated stage IV mNSCLC were randomized (1:1) to durvalumab 20 mg/kg every four weeks or chemotherapy every three weeks for four to six cycles. The dual primary endpoints were overall survival (OS) in the population with PD-L1 TC of 25% or higher and OS in the population at low risk of early mortality (LREM) with PD-L1 TC of 25% or higher.</div></div><div><h3>Results</h3><div>Durvalumab was associated with a numerical reduction in the risk of death versus chemotherapy in the 25% and higher PD-L1 TC population (OS hazard ratio [HR] = 0.84, 95% confidence interval [CI]: 0.71–0.99, <em>p</em> = 0.037; median OS 14.6 months, 95% CI: 12.2–16.9 versus 12.8 months, 95% CI: 10.1–14.7, respectively). In the 25% and higher PD-L1 TC low risk of early mortality population the OS hazard ratio for durvalumab versus chemotherapy was 0.96 (95% CI: 0.79–1.15, <em>p</em> = 0.628); median OS 14.6 months (95% CI: 12.6–17.2) versus 15.0 months (95% CI: 13.1–16.8), respectively. In the safety population, the incidence of grade 3 or 4 treatment-related adverse events was 15.5% (durvalumab) and 45.9% (chemotherapy).</div></div><div><h3>Conclusions</h3><div>Durvalumab did not statistically significantly improve OS versus chemotherapy as first-line treatment in patients with mNSCLC and 25% and higher PD-L1 TC. The numerical improvement in OS was consistent with previous studies of first-line immune checkpoint inhibitor monotherapy in patients with mNSCLC.</div></div>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages 366-382"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FGTI-2734 Inhibits ERK Reactivation to Overcome Sotorasib Resistance in KRAS G12C Lung Cancer","authors":"Aslamuzzaman Kazi PhD ,&nbsp;Hitesh Vasiyani PhD ,&nbsp;Deblina Ghosh PhD ,&nbsp;Dipankar Bandyopadhyay PhD ,&nbsp;Rachit D. Shah MD ,&nbsp;Vignesh Vudatha MD ,&nbsp;Jose Trevino MD ,&nbsp;Said M. Sebti PhD","doi":"10.1016/j.jtho.2024.11.022","DOIUrl":"10.1016/j.jtho.2024.11.022","url":null,"abstract":"<div><h3>Introduction</h3><div>KRAS G12C targeted therapies, such as sotorasib, represent a major breakthrough, but overall response rates and progression-free survival for patients with KRAS G12C lung cancer are modest due to the emergence of resistance mechanisms involving adaptive reactivation of ERK, which requires wild-type HRAS and NRAS membrane localization.</div></div><div><h3>Methods and Results</h3><div>Here, we demonstrate that the dual farnesyltransferase and geranylgeranyltransferase-1 inhibitor FGTI-2734 inhibits wild-type RAS membrane localization and sotorasib-induced ERK feedback reactivation, and overcomes sotorasib adaptive resistance. The combination of FGTI-2734 and sotorasib is synergistic at inhibiting the viability and inducing apoptosis of KRAS G12C lung cancer cells, including those highly resistant to sotorasib. FGTI-2734 enhances sotorasib’s anti-tumor activity <em>in vivo</em> leading to significant tumor regression of a patient-derived xenograft (PDX) from a patient with KRAS G12C lung cancer and several xenografts from highly sotorasib-resistant KRAS G12C human lung cancer cells. Importantly, treatment of mice with FGTI-2734 inhibited sotorasib-induced ERK reactivation in KRAS G12C PDX, and treatment of mice with the combination of FGTI-2734 and sotorasib was also significantly more effective at suppressing <em>in vivo</em> the levels of P-ERK in sotorasib-resistant human KRAS G12C lung cancer xenografts and the NSCLC PDX.</div></div><div><h3>Conclusion</h3><div>Our findings provide a foundation for overcoming sotorasib resistance and potentially improving the treatment outcomes of KRAS G12C lung cancer.</div></div>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages 331-344"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reducing pERKs to Break “RAS”istance to Sotorasib","authors":"Steven G. Gray PhD ,&nbsp;Diarmuid O’Connor MB BCH BAO ,&nbsp;Luciano Mutti MD, PhD ,&nbsp;Tomer Meirson MD, PhD","doi":"10.1016/j.jtho.2025.01.002","DOIUrl":"10.1016/j.jtho.2025.01.002","url":null,"abstract":"","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages 259-261"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143535272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicted Effect of Incidental Pulmonary Nodule Findings on NSCLC Mortality","authors":"S. Tuminello PhD ,&nbsp;R. Flores MD ,&nbsp;M. Untalan MPH ,&nbsp;T. Ivic-Pavlicic MPH ,&nbsp;C.I. Henschke MD ,&nbsp;R. Yip PhD ,&nbsp;D.F. Yankelevitz MD ,&nbsp;Emanuela Taioli MD, PhD","doi":"10.1016/j.jtho.2024.11.009","DOIUrl":"10.1016/j.jtho.2024.11.009","url":null,"abstract":"<div><h3>Introduction</h3><div>Despite the reduction in mortality by low-dose computed tomography lung cancer screening, the uptake is still low. Patients undergo chest imaging for several other medical reasons, and this is a unique opportunity to detect lung nodules.</div></div><div><h3>Methods</h3><div>In a cohort of patients with NSCLC from the Surveillance, Epidemiology, and End Results-Medicare–linked data, tumor size at previous imaging was calculated as follows: volume doubling time = [(T₂-T₁)·ln2]/ln(V₂/V₁), solving for the diameter of V₁. V₁ and V₂ are tumor volume at times T₁ (previous imaging) and T₂ (diagnostic procedure) according to three different growth models. The 10-year lung cancer-specific mortality was calculated as follows: lung cancer survival rate = (−0.0098 × maximum tumor diameter) + 1.</div></div><div><h3>Results</h3><div>A total of 1007 patients who had a chest imaging performed up to 1 year before lung cancer diagnosis were included in this study. The median size of the tumor at diagnosis was 25 mm, and the predicted median tumor size at previous imaging was 12.16 mm, 17.3 mm, and 20.42 mm under the fast, medium, and slow growth model, respectively. Under the fast growth model, a detection of the nodule at previous imaging would have yield a decrease in mortality of 7.79%; the corresponding value for the medium growth model is 4.5% and for the slow growth model 2.45%.</div></div><div><h3>Conclusions</h3><div>Identifying malignant lung nodules in imaging performed for other clinical reasons can help decrease the burden of NSCLC, especially for patients not eligible for low-dose computed tomography and the medically vulnerable. We reveal here that clinical benefits, especially among patients with aggressive disease, can be considerable.</div></div>","PeriodicalId":17515,"journal":{"name":"Journal of Thoracic Oncology","volume":"20 3","pages":"Pages 273-284"},"PeriodicalIF":21.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}