Introduction: Although the efficacy of molecular targeted therapies varies across actionable genomic alterations in NSCLC, comparisons within a single real-world cohort remain limited. Methods: We conducted a retrospective multi-institutional study of 810 consecutive Japanese patients with advanced or recurrent NSCLC harboring actionable genomic alterations who received molecular targeted therapy from 2017 to 2023. Patients were classified into the following three genomic groups: EGFR mutations (group A), ALK/ROS1/RET fusion oncogenes (group B), and others, including MET exon 14 skipping, BRAF V600E, and KRAS G12C mutations (group C). Treatment efficacy and safety were compared across the groups. Results: Treatment outcomes differed between the subgroups. Group B demonstrated the highest objective response rate (85.8%) and the longest median real-world progression-free survival (rwPFS; 42.5 mo); median overall survival (OS) was not reached. Group A had intermediate outcomes. Group C exhibited the shortest rwPFS (9.2 mo), poorer OS, and higher rates of treatment discontinuation due to adverse events. Such hierarchical differences were observed in patients with baseline central nervous system metastases and in those receiving first-line treatment. In multivariate analysis, genomic subgroup remained associated with rwPFS and OS, with fusion-driven tumors maintaining superior outcomes irrespective of other factors. Conclusions: This large real-world analysis yielded a hierarchy of therapeutic benefits across actionable genomic alterations in NSCLC. Patients with fusion-driven tumors benefited from targeted therapy, whereas those with EGFR-mutated tumors had intermediate outcomes. Treatment of patients with MET exon 14 skipping, BRAF V600E, and KRAS G12C mutations had limited efficacy and higher toxicity, underscoring the need for improved therapeutic strategies.

8528 Background: EGFR blockade enhances tumor antigen presentation and may potentiate PD-1 inhibition. This phase I/II study evaluated the safety and efficacy of adding necitumumab to pembrolizumab plus platinum-based chemotherapy in patients with previously untreated advanced squamous non–small cell lung cancer (NSCLC), a population with limited biomarker-driven treatment options. Methods: Patients received necitumumab (400–800 mg on days 1 and 8), pembrolizumab (200 mg on day 1), nab-paclitaxel (100 mg/m² on days 1, 8, and 15), and carboplatin (AUC 5 on day 1) every 3 weeks for four cycles, followed by necitumumab plus pembrolizumab maintenance. Phase I used a standard 3+3 dose-escalation design. Per protocol amendment, patients treated at the recommended dose (RD) in phase I (n = 6) and all phase II patients (n = 6) were pooled for efficacy analyses (n = 12). Tumor assessments were performed every 6 weeks per RECIST v1.1. Primary endpoints were safety and objective response rate (ORR). Data cutoff was September 14, 2025. Results: Twenty-one patients were enrolled, including 15 in phase I (400 mg, n = 6; 600 mg, n = 3; 800 mg, n = 6). One dose-limiting toxicity (DLT) occurred in the 800 mg cohort, which was determined as the RD and maximum tolerated dose (MTD). Among the 12 patients treated at the RD, the ORR was 75.0% (9/12; 95% CI, 42.8–94.5), with partial response in 9 patients, stable disease in 1 patient, and progressive disease in 2 patients. The disease control rate was 83.3%. The 24-week survival rate was 95.2%. Median progression-free survival and overall survival were not reached at the time of analysis. The most frequent adverse events (AEs) in 21 patients were hypomagnesemia (66.7%), acneiform dermatitis (66.7%), neutropenia (61.9%), decreased appetite (52.4%), anemia (52.4%), constipation (47.6%), stomatitis (42.9%), and leukopenia (42.9%). Grade 3 and 4 AEs occurred in 66.7% and 28.6% of patients, respectively, with no grade 5 events. Conclusions: The addition of necitumumab to pembrolizumab and platinum-based chemotherapy demonstrated manageable toxicity and resulted in a high ORR in patients with untreated squamous NSCLC. These findings support the potential activity of EGFR blockade–based immunochemotherapy and warrant further clinical investigation. Clinical trial information: 2031210387.

Background Antifibrotic therapies slow functional decline and improve survival in patients with idiopathic pulmonary fibrosis (IPF). Although early initiation is generally recommended, the optimal timing of treatment in real-world clinical practice remains uncertain. In particular, the relationship between the interval from diagnosis to treatment initiation and overall survival (OS), as well as the clinical implications of physician-judged deferred initiation, have not been fully clarified. Methods This multicenter retrospective cohort study included 150 patients diagnosed with IPF between April 2021 and March 2023 who received antifibrotic therapy. Treatment timing was evaluated using two definitions: 1) objectively defined intervals from diagnosis of IPF to treatment initiation (0–180, 181–364, and ≥ 365 days); and 2) physician-judged deferred initiation documented in medical records, defined as a clinician‑guided postponement based on clinical, patient‑related, or contextual considerations. The primary endpoint was OS. Landmark analyses were performed at 180 and 365 days to reduce immortal time bias. Survival outcomes were analyzed using the Kaplan–Meier method and Cox proportional hazards regression models. Multivariable analyses were used to adjust for relevant clinical covariates. In addition, reasons for delayed treatment initiation were examined. Results Among the 150 patients, longer diagnosis-to-treatment intervals were associated with longer OS in the landmark analyses. In contrast, patients with physician-judged deferred initiation showed no significant difference in OS (log-rank p = 0.164), although physician-judged deferred initiation was independently associated with OS in the multivariable analysis. In the multivariable analysis, older age, lower percent predicted forced vital capacity (%forced vital capacity), and a longer interval from referral to IPF diagnosis were also independently associated with OS. The most common reasons for delayed initiation included minimal or stable symptoms, concerns regarding adverse effects, and diagnostic uncertainty. Conclusions Physician‑judged deferred initiation was independently associated with OS, likely reflecting underlying disease activity and clinical risk stratification rather than a direct causal effect of postponing therapy. These findings underscore the limitations of evaluating treatment timing solely by elapsed time and emphasize the importance of early diagnosis, timely referral to specialized centers, and individualized clinical decision-making in the management of IPF. Clinical trial registration Not applicable.

e20712 Background: Molecular targeted therapies have transformed the management of non–small cell lung cancer (NSCLC) with actionable genomic alterations. However, direct comparisons of treatment outcomes across different genomic subtypes within a single real-world cohort remain limited. We evaluated the relative efficacy and safety of targeted therapies across major actionable genomic alterations in a large Japanese real-world population. Methods: This multicenter retrospective study included 810 consecutive Japanese patients with advanced or recurrent NSCLC harboring actionable genomic alterations who received molecular targeted therapy between 2017 and 2023. Patients were classified into three genomic groups: EGFR mutations (Group A, n = 659), fusion oncogenes involving ALK/ROS1/RET (Group B, n = 106), and other actionable alterations including MET exon 14 skipping, BRAF V600E, and KRAS G12C (Group C, n = 45). Treatment outcomes, including objective response rate (ORR), progression-free survival (PFS), overall survival (OS), and safety, were analyzed using Kaplan–Meier methods and multivariable Cox regression. Results: The median follow-up was 24.9 months overall (Group A 25.6, Group B 27.3, Group C 16.1). A total of 580 progression events and 398 deaths were observed. ORR differed significantly among groups (74.1% in Group A, 85.8% in Group B, and 68.9% in Group C; P = 0.014). Median PFS was 17.5 months in Group A, 42.5 months in Group B, and 9.2 months in Group C (P < 0.001). Median OS was not reached in Group B, compared with 39.3 months in Group A and 22.7 months in Group C (P < 0.001). In multivariable analyses adjusting for clinical covariates, genomic subgroup remained independently associated with both PFS and OS, with fusion-driven tumors demonstrating consistently superior outcomes. EGFR-mutated tumors showed intermediate outcomes, whereas Group C exhibited limited efficacy and higher treatment discontinuation due to adverse events. Conclusions: In this large Japanese real-world cohort, a clear hierarchy of therapeutic benefit across actionable genomic alterations was observed. Fusion oncogene–driven NSCLC derived exceptional and durable benefit from targeted therapy, EGFR-mutated tumors demonstrated intermediate outcomes, and MET exon 14 skipping, BRAF V600E, and KRAS G12C mutations remained associated with limited efficacy and higher toxicity. These findings underscore the clinical importance of genomic subtype–based treatment strategies and highlight unmet needs in selected molecular subsets.

Background:The effect of type 2 diabetes mellitus (T2DM) on treatments for advanced non-small cell lung cancer (NSCLC) remains unelucidated. We aimed to assess the effect of T2DM on the treatment for advanced NSCLC. Methods:We retrospectively investigated clinicopathological character, treatment effect, and adverse events (AEs) in advanced NSCLC patients started on systemic treatment at Nippon Medical School Chiba-Hokusoh Hospital from 2018 to 2024. Results:The numbers of T2DM and non-T2DM patients among those undergoing immune checkpoint inhibitor (ICI) therapy, molecular targeted therapy (MTT), and cytotoxic chemotherapy (CTT) were 37 and 78, 30 and 86, 9 and 17, respectively. The overall survival (OS) of patients complicated T2DM was significantly worse in total (19.3 vs. 34.5 months, P=0.001), the ICI (11.5 vs. 34.2 months, P=0.005) and the MTT cohort (27.4 vs. 43.4 months, P=0.03). Median progression-free survival (PFS) was significantly poor for T2DM patients in the ICI cohort (5.7 vs. 12.5 months, P=0.04). However, a significant difference was not found for the MTT cohort (13.3 vs. 12.7 months, P=0.91). There were no significant differences in AEs in either cohort. Hemoglobin A1c (HbA1c) was significantly higher in patients with derived neutrophil lymphocyte ratio (dNLR) ≥3. The PFS in T2DM patients in the ICI cohort was investigated with regard to clinicopathological factors and T2DM treatments. Specialist consultation was identified as a factor that improved PFS of ICI. Conclusions:Our research suggests that T2DM is an independent poor prognostic factor in advanced NSCLC and affects ICI treatment.

Objectives: Plasma-based testing with circulating cell-free DNA (cfDNA) is an active area of biomarker exploratory studies in patients with non-small cell lung cancer (NSCLC) harboring EGFR mutations. The Exosome-focused Translational Research for Afatinib study prospectively explored novel plasma biomarkers for afatinib monotherapy in patients with NSCLC harboring EGFR mutations using genomics, proteomics, epigenomics, and metabolomics. Herein, we present the results of the genomics part. Materials and Methods: Clinical data of afatinib were matched with next generation sequencing (NGS)-based genomics data of cfDNA (n = 101) and extracellular vesicle DNA (evDNA) (n = 99) from pretreatment plasma samples. Results: The detection sensitivity of cfDNA and evDNA mutations was 86 % (87/101) and 37 % (37/99), respectively. When cfDNA mutations were classified into tissue-matched (any EGFR mutations consistent with those identified in tissue) (n = 28), tissue-unmatched (n = 59), and mutation-undetected (n = 14) groups, cfDNA mutation status was a predictor of progression-free survival (PFS) (p < 0.01) and overall survival (OS) (p < 0.01). EvDNA mutation status was a predictor of OS (p < 0.01) rather than PFS (p = 0.48). When the tissue-unmatched cfDNA group was subclassified into EGFR-related (n = 49) and EGFR-unrelated (n = 10) groups, the EGFR-unrelated group had a median PFS and 3-year OS rate of 31.2 months and 80.0 %, respectively. EGFR-unrelated and mutation-undetected cfDNA groups (n = 24) exhibited a median PFS and 3-year OS rate of >30 months and >80 %, respectively, with afatinib monotherapy. Conclusion: This is the first large-scale prospective study of NGS-based concurrent testing for plasma cfDNA and evDNA mutations. The findings suggest that cfDNA mutation status is a promising plasma biomarker for afatinib monotherapy.

BACKGROUND:Long-term maintenance steroid therapy (MST) is often necessary for repeated relapses of chronic eosinophilic pneumonia (CEP). Because relapse does not indicate a worse prognosis, determining the optimal steroid dose to avoid overtreatment presents a clinical challenge. Our primary objective was to evaluate the optimal MST dose to prevent repeated relapses, and the secondary objectives included identifying serum eosinophil count at relapse and background factors of relapse. METHODS:A multicentre retrospective study was conducted on patients with steroid-treated CEP. Background characteristics were compared between the non-relapse and relapse groups. The optimal MST dose was determined based on dose at relapse and the final relapse prevention dose. Additionally, serum eosinophil count at relapse was assessed. RESULTS:A total of 79 patients were included, with 44 in the non-relapse group and 35 in the relapse group. The prednisolone doses required to achieve relapse-free rates of 50% (ED50) were 7.2 mg (95% CI, 4.6 to 23.6). The median serum eosinophil count at relapse was 1125 /µL (IQR, 735-2108). No clinically significant background factors were identified between the non-relapse and relapse groups. CONCLUSION:Our study demonstrated that a prednisolone dose of 7.2 mg achieved a 50% relapse-free rate in the relapse group. Based on these findings, we encourage clinicians to evaluate individual minimum effective steroid doses.

8631 Background: The VISION study demonstrated that tepotinib, a MET inhibitor, is effective against MET exon 14 (METex14) skipping NSCLC, but the clinical data on the efficacy and safety of this drug are scarce, and the utility of immune checkpoint inhibitors (ICIs) in patients with METex14 requires further investigation. The present, multicentric, retrospective study evaluated the clinical efficacy and safety of tepotinib and ICIs in patients with METex14 skipping NSCLC. Methods: Data on the patient characteristics, treatment details, efficacy, and safety of tepotinib and ICIs in patients with METex14 skipping NSCLC diagnosed at any of six Japanese hospitals between August 2020 and December 2024 were extracted from electronic medical records and retrospectively analyzed. Results: Of the 98 patients enrolled, 57 (58.2%) and 41 (41.8%) were male and female, respectively. 60 patients (61.2%) had a smoking history. Histological data indicated adenocarcinoma in most of the patients (68.4%). There were 50 patients (51.0%) with PD-L1 > 50%. Tepotinib was administered to 79 patients with a median age of 75 years (range: 55–90 years). Most of these patients had advanced-stage cancer. Tepotinib was administered as the first-line therapy in 62 patients (78.5%), with 19.0, 55.7, 17.7, 6.3, and 1.3% of this subgroup having ECOG PS 0, 1, 2, 3, and 4, respectively. The median observation period was 29.1 months (range: 1.5–51.5 months). First-line tepotinib therapy achieved a 61.4% overall response rate (ORR; 95% confidence interval [CI]: 48.8–74.0), median progression-free survival (PFS) of 8.2 months (95% CI: 6.3–10.1), and median overall survival (OS) of 24.4 months (95% CI: 9.5–39.2). The most common adverse event (AE) was edema (71.0%), with Grade 3 or higher edema occurring in 12.9% of the patients. Notably, these patients had significantly longer PFS than those without edema (10.8 months [95% CI: 8.0–13.6] vs. 4.2 months [95% CI: 2.8–5.5]; hazard ratio: 0.31; 95% CI: 0.16 to 0.60; P < 0.001). Treatment-related AEs led to tepotinib discontinuation in 15.0% of the cohort, and dose interruption and dose reduction were required in 59.5% and 62.0% of the cohort, respectively. ICI therapy, which was administered to 34 patients at various times, achieved a median PFS of 28.8 months (95% CI: 9.3–52.5) and a median OS of 45.2 months (95% CI: 20.9–77.0). Conclusions: The present, real-world analysis corroborated the findings of the VISION study demonstrating the efficacy and safety of tepotinib therapy against METex14 skipping NSCLC. The association between tepotinib-related edema and longer PFS warrants further investigation. Importantly, ICIs appear to be a promising treatment option for this population and deserve further study.

Objectives: Osimertinib is a standard treatment for patients with EGFR-mutant non-small cell lung cancer (NSCLC) and is highly effective for brain metastases (BMs). However, it is unclear whether local treatment (LT) for BMs prior to osimertinib administration improves survival in EGFR-mutant NSCLC. We aimed to reveal the survival benefit of upfront local treatment (LT) for BMs in patients treated with osimertinib. Materials and Methods: This multicenter retrospective study included consecutive patients with EGFR mutation (19del or L858R)-positive NSCLC who had BMs before osimertinib initiation between August 2018 and October 2021. We compared overall survival (OS) and central nervous system progression-free survival (CNS-PFS) between patients who received upfront LT for BMs (the upfront LT group), and patients who received osimertinib only (the osimertinib-alone group). Inverse-probability treatment weighting (IPTW) analysis was performed to adjust for potential confounding factors. Results: Of the 121 patients analyzed, 57 and 64 patients had 19del and L858R, respectively. Forty-five and 76 patients were included in the upfront LT group and the osimertinib-alone groups, respectively. IPTW-adjusted Kaplan-Meier curves showed that the OS of the upfront LT group was significantly longer than that of the osimertinib-alone group (median, 95 % confidence intervals [95 %CI]: Not reached [NR], NR-NR vs. 31.2, 21.7-33.2; p = 0.021). The hazard ratio (HR) for OS and CNS-PFS was 0.37 (95 %CI, 0.16-0.87) and 0.36 (95 %CI, 0.15-0.87), respectively. Conclusions: The OS and CNS-PFS of patients who received upfront LT for BMs followed by osimertinib were significantly longer than those of patients who received osimertinib alone. Upfront LT for BMs may be beneficial in patients with EGFR-mutant NSCLC treated with osimertinib.

The relationship between lung cancer surgery and venous thromboembolism (VTE) in Japan has not been elucidated. This was a post hoc analysis of the Cancer-VTE Registry. The 1057 patients who underwent surgery for lung cancer were divided into the surgery alone (SA) group (n = 598) and the surgery plus chemotherapy (SC) group (n = 459), and the 1-year incidences of VTE and cerebral ischemia were analyzed. In the SA and SC groups, composite VTE was observed in one (0.2%) and 15 (3.3%) patients, respectively, and cerebral ischemia was observed in eight (1.3%) and four (0.9%) patients, respectively. Lymph node metastasis was more common in patients with D-dimer >1.2 mu g/ml (odds ratio: 1.781, P = .004). SA had a low risk of VTE but a high risk of cerebral ischemia. Chemotherapy increases the risk of VTE. The D-dimer level was related to VTE and advanced cancer.

A 69-year-old woman was diagnosed with idiopathic interstitial pneumonia (IIP). The patient underwent a combination therapy of steroid therapy and intravenous cyclophosphamide, long-term oxygen therapy, and the initiation of Nintedanib. However, there was no improvement in IIP, and as a result, the activities of daily living also declined. As one of the various examinations conducted, the results of the right heart catheterization diagnosed the patient with mild pulmonary hypertension, and Macitentan therapy was initiated. The subsequent clinical course appeared to show an improvement in Idiopathic Interstitial Pneumonia (IIP) by adding Macitentan therapy to Nintedanib therapy.

Background The data on bosentan were lacking for the treatment of exercise-induced elevation of pulmonary artery pressure (eePAP) or less severe PH in COPD. This study was conducted to investigate long-term efficacy and safety of bosentan for the treatment of eePAP or less severe PH in COPD. Methods COPD patients diagnosed at this hospital as having COPD (WHO functional class II, III or IV) with eePAP or less severe PH whose respiratory symptoms were stable but remained and gradually progressed even after COPD therapy were randomly assigned in a 1:1 ratio to receive either bosentan or no PH treatment for two years and assessed at baseline and every 6 months for respiratory failure, activities of daily living (ADL), lung and heart functions by right heart catheterization (RHC), and other parameters. Results A total of 29 patients who underwent RHC for detail examination were enrolled in the current study between August 2010 and October 2018.No death occurred in drug-treated group ( n = 14) for 2 years; 5 patients died in untreated group ( n = 15). Significant differences were noted between the 2 group in hospital-free survival (686.00 ± 55.87 days vs. 499.94 ± 53.27 days; hazard ratio [HR], 0.18; P = 0.026) and overall survival (727 days vs. 516.36 ± 55.38 days; HR, 0.095; P = 0.030) in all causes of death analysis, but not in overall survival in analysis of respiratory-related death. Bosentan was not associated with increased adverse events including requiring O 2 inhalation. Conclusions This study suggested that the prognosis for COPD patients with eePAP or less severe PH presenting with respiratory symptoms was very poor and that bosentan tended to improve their prognosis and suppress ADL deterioration without worsening respiratory failure. Trial registration This study was registered with UMIN-CTR Clinical Trial as UMIN000004749 . First trial registration at 18/12/2010.

Supplementary Fig. S1 from Antitumor activity of histone deacetylase inhibitors in non-small cell lung cancer cells: development of a molecular predictive model

We present a case of a drug-induced sarcoidosis-like reaction (DISR) in a 34-year-old female patient who had been receiving dupilumab for eosinophilic rhinosinusitis, for seven months. Computerized tomography scans revealed multiple lymphadenopathies, and biopsies performed on the lung and skin lesions showed the presence of non-caseating granulomas. The patient's serum levels of soluble interleukin-2 receptor and angiotensin-converting enzyme were elevated. There were no findings of Mycobacterium spp, or any other bacterial infections. Based on these findings, it was suspected that the sarcoidosis-like reaction observed in this patient was caused by dupilumab. Switching the patient's treatment from dupilumab to mepolizumab improved the DISR.

Supplementary Fig. S2 from Antitumor activity of histone deacetylase inhibitors in non-small cell lung cancer cells: development of a molecular predictive model

Background: Rechallenge with platinum-combination chemotherapy in patients with advanced non-small cell lung cancer (NSCLC) after disease progression on platinum-combination chemotherapy occasionally leads to a favorable response. The efficacy and safety of platinum-combination chemotherapy with or without immune-check-point inhibitor (ICI) for patients with recurrent NSCLC after surgery followed by adjuvant platinum-doublet chemotherapy remains uncertain.Methods: Patients who relapsed after surgery plus adjuvant platinum-doublet chemo-therapy and received platinum-combination chemotherapy with or without ICI between April 2011 and March 2021 at four Nippon Medical School hospitals were retrospectively analyzed.Results: Among 177 patients who received adjuvant platinum-doublet chemotherapy after surgery, a total of 30 patients who received platinum-combination rechemotherapy with or without ICI after relapse were included in this study. Seven patients received ICI-combined chemotherapy. The median disease-free survival (DFS) after surgery was 13.6 months. The objective response rate and disease-control rate were 46.7% and 80.0%, respectively. The median progression-free survival and overall survival were 10.2 and 37.5 months, respectively. Patients with longer DFS (=12 months) had a better prognosis than others. The most common grade =3 toxicity associated with this treatment was neutropenia (33%). Grade =3 immune-related adverse events were pneumonitis (14%) and colitis (14%). Treatment-related deaths did not occur in this study.Conclusion: Platinum-combination chemotherapy with or without ICI for patients with postoperative recurrent NSCLC who previously received adjuvant platinum-doublet chemotherapy was effective and safe. In particular, this therapy may be prom-ising for patients with longer DFS.

BACKGROUND:Platinum-based combination therapy plus a programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) inhibitor is a standard treatment for patients with stage IV non-small cell lung cancer. However, necitumumab is used with gemcitabine and cisplatin as a first-line treatment option for squamous cell lung cancer (SqCLC). Furthermore, the combination of necitumumab with immune checkpoint inhibitors has the potential to enhance tumor immunity and improve the therapeutic effect. Thus, we planned and initiated this phase I/II study to evaluate the safety and efficacy of necitumumab plus pembrolizumab, nanoparticle albumin-bound (nab)-paclitaxel), and carboplatin therapy for patients with previously untreated SqCLC. PATIENTS AND METHODS:In phase I, the primary endpoint is the tolerability and recommended dose of necitumumab combined with pembrolizumab plus nab-paclitaxel and carboplatin. In phase II, the primary endpoint is the overall response rate. Secondary endpoints are disease control rate, progression-free survival, overall survival, and safety. Forty-two patients will be enrolled in phase II. CONCLUSION:This is the first study to investigate the efficacy and safety of necitumumab plus pembrolizumab combined with platinum-based chemotherapy in patients with previously untreated SqCLC.

Supplementary Figure 1 from Proteomic Signature Corresponding to the Response to Gefitinib (Iressa, ZD1839), an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor in Lung Adenocarcinoma

The Cancer-VTE Registry (UMIN000024942) is a multicenter, prospective, observational study carried out to investigate the incidence of venous thromboembolism (VTE) in Japanese patients with six types of solid cancer. We present the results of a pre-specified subgroup analysis of data from patients with lung cancer. Of 10,202 patients enrolled in the Cancer-VTE registry, 2386 patients with lung cancer were included in this subgroup analysis. VTE screening results (including D-dimer concentration) and data on cancer type and stage before the start of cancer treatment were obtained, and the 1-year incidence of VTE and other events was determined. The baseline characteristics of lung cancer patients were as follows: mean age, 69.3 years; male, 71.1%; cancer stage IB, 19.3%, II, 21.8%, III, 25.2%, and IV, 33.7%; small-cell lung cancer, 11.7%; non-small-cell lung cancer, 84.3%; mean D-dimer concentration, 1.89 μg/mL; VTE prevalence, 5.0%. In the 1-year follow-up period, the cumulative incidence of symptomatic VTE was 0.6%; incidental VTE requiring treatment, 1.3%; composite VTE, 1.8%; bleeding (major or clinically relevant non-major) events, 1.2%; cerebral infarction, transient ischemic attack or systemic embolism, 1.3%; and all-cause death, 19.1%. These events occurred more frequently in patients with VTE at baseline than in those without it. Data for subgroups divided by cancer stage, type of cancer, and cancer treatment (including anti-cancer agents used) will be presented at the conference. Among lung cancer patients enrolled in the Cancer-VTE Registry, those with VTE before cancer treatment were at higher risk of VTE and other events during cancer treatment. This finding underlines importance of VTE screening at the time of cancer diagnosis.