Open AccessArticle LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population 1 Thoracic Surgery Unit, Catholic University of the Sacred Heart, 00168 Rome, Italy 2 Thoracic Surgery Unit, A. Gemelli University Hospital Foundation IRCCS, 00168 Rome, Italy 3 OncoRay—National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Helmholtz-Zentrum Dresden-Rossendorf, 01062 Dresden, Germany 4 Department of Radiotherapy and Radiation Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, 01062 Dresden, Germany 5 Departmental Unit of Molecular and Genomic Diagnostics, Genomics Core Facility, Gemelli Science and Technology Park (G-STeP), Fondazione Policlinico Universitario A. Gemelli IRCCS, 00168 Rome, Italy 6 Clinical Chemistry, Biochemistry and Molecular Biology Operations (UOC), Fondazione Policlinico Universitario A. Gemelli IRCCS, 00168 Rome, Italy 7 Pathology Unit, Department of Woman and Child’s Health and Public Health Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy 8 Advanced Radiotherapy Center, A. Gemelli University Hospital Foundation IRCCS, 00168 Rome, Italy 9 Institute of Radiooncology—OncoRay, Helmholtz-Zentrum Dresden-Rossendorf, 01062 Dresden, Germany 10 ELKH-DE Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary add Show full affiliation list remove Hide full affiliation list * Authors to whom correspondence should be addressed. Genes 2026, 17(6), 677; https://doi.org/10.3390/genes17060677 (registering DOI) Submission received: 17 April 2026 / Revised: 21 May 2026 / Accepted: 6 June 2026 / Published: 9 June 2026 Introduction: Lung cancer, the leading cause of cancer-related mortality worldwide, is a heterogeneous malignancy comprising distinct histological and molecular subtypes, with non-small cell lung cancer (NSCLC) accounting for approximately 85% of cases and adenocarcinoma (ADC) representing the most prevalent histotype. An emerging pathological feature of NSCLC, spread through air spaces (STAS)—defined as the extension of tumor cells into the lung parenchyma beyond the main tumor margin—has been associated with worse disease-free and overall survival and has been proposed as a possible predictor of recurrence to guide surgical extent. Concurrently, recent comprehensive genomic profiling of early-stage NSCLC has highlighted the need to interpret multi-omics data and their relationship with pathological variables, including IASLC histological subtypes, to better personalize treatment strategies. In this context, we investigated the overall distribution of STAS and its association with tumor mutational profiles and IASLC histological subtypes in a large real-world cohort of lung adenocarcinoma patients from the LANTERN project. Materials and Methods: In a prospective, multicenter observational study (March 2023–December 2024), 271 NSCLC patients were enrolled, and clinicopathological, immunohistochemical, and genomic data were collected; comprehensive genomic profiling was performed using the TruSight Oncology 500 assay to analyze 523 cancer-related genes, tumor mutational burden (TMB), and microsatellite instability; and STAS was assessed according to IASLC criteria. Adenocarcinoma accounted for roughly 90% of the cases, with a median age of 69 years and a predominance of stage IV disease (49.5%). STAS was evaluable in 162 cases and was detected in 17.9% of tumors. Results: STAS-positive tumors showed a higher trend towards locally advanced and advanced disease; no differences were observed in sex, age, smoking status, tumor mutational burden, or PD-L1 expression. Additionally, STAS-positive tumors showed a higher association with micropapillary, mucinous, and papillary patterns, whereas the acinar pattern was more frequent in STAS-negative tumors. The most frequently mutated genes were TP53, KRAS, EGFR, and STK11, with no significant differences between groups; ROS1 alterations were absent in STAS-negative tumors but detected more frequently in STAS-positive cases. Conclusions: Overall, these findings indicate that STAS positivity is associated with high-risk histological subtypes and advanced disease, suggesting its importance as a marker of tumor aggressiveness and emphasizing the need for its systematic evaluation in lung adenocarcinoma to better guide surgical planning and patient risk assessment. STAS; NSCLC; genomic alterations 1. Introduction Lung cancer remains the leading cause of cancer death in the world, still presenting an overall dismal prognosis [ 1]. It remains a highly heterogeneous neoplasm in which various histological subgroups have been clearly identified, each with specific features and molecular characteristics [ 2]. Among non-small cell lung cancers (NSCLCs) (the most representative histology accounting for approximately 85% of all lung tumors), adenocarcinoma (ADC) represents the most frequent histotype (more than 60% of all NSCLCs) with specific histological patterns defined by IASLC/ATS/ERS and potentially associated with different prognostic outcomes [ 1]. Another pathological feature of NSCLC emerging in the last decade is the “Spread through air spaces” (STAS) that has been defined by Travis and coworkers in the current World Health Organization (WHO) Classification of Lung Tumors as the spread of micropapillary clusters, solid nests, and/or single cancer cells into air spaces in the lung parenchyma beyond the edge of the main tumor [ 3]. Although the definition of STAS varies across different studies, STAS has been shown to be associated with decreased disease-free survival and overall survival in multivariate analyses [ 4]. Regarding treatment, approximately 30% of patients with NSCLC are candidates for radical surgery (stages I–IIIA) and, in general, show a better prognosis than the advanced ones [ 5]. Sublobar resection (pulmonary parenchyma sparing surgery) for smaller peripheral nodules, instead of more extensive lobar resection, has become more common recently [ 6]. However, since the indications for performing sublobar resection are still a matter of large debate, there is an urgent need for identifying multiple predictive factors for recurrence that should be considered when choosing the best surgical resection option, especially pathological and molecular factors. In this framework, some researchers have suggested that STAS could be considered to tailor treatment to more extensive lung resection (i.e., lobar resection), as it appears to act as an independent predictor of disease recurrence in patients undergoing sublobar resections for early-stage lung adenocarcinoma, despite the data available still being scarce and controversial [ 7]. On the other hand, a new grading system for pulmonary adenocarcinoma was recently proposed by IASLC/ATS/ERS [ 8], as reported above. The grading system is based on a combination of histological patterns, with an emphasis on high-grade patterns, which offers better prognostic correlation than the adenocarcinoma classification system, which is based solely on the predominant pattern. Finally, there is an increasing interest in exploring the molecular landscape of genomic profiles even in early-stage NSCLC because it appears clear that every treatment (including surgery) should be personalized according to several tumor characteristics (i.e., biological aggressiveness). Indeed, in the last decade, the wide implementation of high-throughput technologies and comprehensive genomic profiling (CGP) in lung cancer allowed for the identification of a broad spectrum of molecular aberrations and altered signaling pathways, leading to the definition of distinct molecular profiles. Thus, the interpretation of these complex data (mostly genomic and pathological variables) and their inter-relationship in NSCLC patients is pivotal for tailoring more precise therapeutic approaches. Within this context, the LANTERN (Lung cancer multi-omics digital human avatars for integrating precision medicine) project [ 9] arises, with the aim of delivering a novel approach for comprehensive lung cancer decision-making solutions, based on predictive digital platforms powered by the integration of complex data. In the present analysis, we analyze the LANTERN population, consisting of a large prospective cohort of Caucasian lung adenocarcinoma patients, with the following aims: (1) To explore the overall expression of STAS and its distribution according to staging and other clinical factors; (2) To analyze the inter-relationship between STAS positivity, tumor mutational profile, and IASLC morphological classification. 2. Materials and Methods 2.1. Ethics The protocol of the study was designed in accordance with the Standards of Good Clinical Practice of the European Union and the current review of the Helsinki Declaration and was approved by the respective Ethics Committee. All methods were carried out in accordance with relevant guidelines and regulations. Informed consent was obtained from all subjects and/or their legal guardian(s). Approval of Fondazione Policlinico Universitario Agostino Gemelli IRCCS—Università Cattolica del Sacro Cuore Ethics Committee Number: 5420-0002485/23; Trial registration—clinicaltrial.gov: NCT05802771. 2.2. Patients This study was conducted on a prospective, multicenter observational cohort of 271 patients with non-small cell lung cancer (NSCLC), enrolled between March 2023 and December 2024 in the LANTERN consortium (see Consort Diagram— Supplementary Figure S1) [ 9]. No restrictions regarding sex or disease stage were applied at enrollment in order to ensure a representative NSCLC cohort and minimize potential selection bias. The inclusion criteria were as follows: (1) age ≥ 18 years; (2) provision of written informed consent; and (3) histopathological confirmation of NSCLC. Patients were excluded in the presence of: (1) a diagnosis of neuroendocrine carcinoma, small cell lung carcinoma, or other non-NSCLC lung malignancies (see details below); and (2) a diagnosis based solely on cytological specimens. Tumor staging was performed according to the eighth edition of the TNM classification established by the American Joint Committee on Cancer (AJCC) for lung cancer [ 10]. Clinicopathological variables were retrieved from electronic medical records, including age, sex, smoking status, tumor site, histopathological characteristics, presence of STAS, PD-L1 expression, treatment details, and pathological TNM stage. Clinical and molecular data were collected and managed with REDCap (Research Electronic Data Capture) and hosted at Fondazione Policlinico Universitario A. Gemelli IRCCS. All patient information was pseudonymized, and a unique alphanumeric identifier was assigned to each case to ensure secure data linkage. 2.3. STAS and IASLC Pattern Evaluation on Surgical Specimens STAS is defined as the presence of tumor cells within the air spaces beyond the edge of the primary tumor, as previously documented in the literature [ 11] ( Figure 1A,B). Tumor cells were considered STAS if they were present continuously in the air spaces from the tumor edge, and individual isolated tumor cells or rare tumor clusters were found far away from the tumor without spreading [ 12]. STAS detection was finally performed on 162 NSCLC patients according to the criteria described below (see Consort Diagram— Supplementary Figure S1). STAS expression was properly evaluated in all anatomical lung resections (137 cases) and non-anatomical ones (i.e., wedge resections) (25 cases), while this factor was not evaluated in biopsies performed in other organs or small lung biopsies, as recommended by the IASLC definition of STAS detection [ 11]. As reported by Yu and coworkers [ 13], a false-positive STAS evaluation included: (I) random distribution of tumor cells with irregular edges at the tissue section margins or outside the plane; (II) lack of continuous spread process from the main tumor; (III) serrated edges of tumor cell clusters; (IV) linear bands of cells detached from the alveolar walls; (V) artifacts caused by sectioning blades. We did not perform a further sub-classification according to the “grade” of STAS (single cells, cell nests, micropapillary components) because this has not been largely validated to date. Similarly, IASLC pattern evaluation was conducted according to the criteria reported in [ 14]. In cases presenting with more different patterns, the predominant one was reported. Adenocarcinoma grade was not derived in our series, and only the predominant pattern was accounted for. Expert lung pathologists led the evaluations for STAS and IASLC patterns according to the above-mentioned criteria. Usually, these evaluations were performed by two distinct pathologists who were unaware of the clinical stage and molecular analysis and a consensus was reached in cases of disagreement. 2.4. Molecular Analysis All patients enrolled in the present study were tested via NGS analysis regardless of histology and stage. Hematoxylin and eosin-stained sections were independently reviewed by experienced pathologists to select tumor areas containing a minimum of 20% neoplastic cells. Genomic DNA was isolated from formalin-fixed, paraffin-embedded (FFPE) specimens using the AllPrep ପ୍ପ DNA/RNA FFPE Kit (QIAGEN ପ୍ପ) (Germantown, MD, USA), following the manufacturer’s instructions. Comprehensive genomic profiling (CGP) was carried out using the TruSight Oncology 500 High Throughput (TSO500HT) panel (Illumina, Inc., San Diego, CA, USA), which allows for the identification of single-nucleotide variants (SNVs), insertions and deletions (indels), and copy number variations (CNVs) across 523 cancer-associated genes. The test is validated for the detection of CNAs, specifically gene amplifications (gain), in 59 genes included in the panel, with a detection limit of 2.2× fold. The TSO500HT is able to identify known and novel fusions in 55 genes of the panel, as well as splicing variants in 3 genes. The assay also provides evaluation of tumor mutational burden (TMB) and microsatellite instability (MSI) status. For MSI status, the TSO500HT analyzes 130 homopolymeric sites to calculate an accurate quantitative score. A cutoff of 20% is used to define MSI status (stable 20%). A TMB 10 high. DNA and RNA secondary data analysis are performed using the default parameters on the local TSO500 v2.2 application of Illumina software and within the Clinical Genomics Workspace software platform by PierianDx, TSO500, DRAGEN solid v2.5. The minimum coverage accepted for variant calling is 100× over 90% of the sequenced regions and at least 250× over hotspot regions. Variants with VAF 100×) and are reported if present in genes relevant to the clinical question. Copy-number fold change was reported according to the tumor fraction estimation. Only fusion-calling supported by a minimum of 20 fusion-supporting unique reads was reported (DNA quality requirements: >3.5 ng/µL, RNA quality requirements: >10 ng/µL; DV200 > 40%). Library preparation and next-generation sequencing (NGS) procedures were performed in accordance with the manufacturer’s recommendations and previously published protocols. Concerning PDL1 analysis, it was performed on formalin-fixed, paraffin-embedded tissue using immunohistochemical detection with the PD-L1 IHC 22C3 pharmDx kit (Agilent Technologies, Inc., Santa Clara, CA, USA) (Dako, REF: SK006), employing the mouse anti-PD-L1 monoclonal antibody (clone 22C3) and the EnVision FLEX visualization system on the Autostainer Link 48 platform (Dako). PD-L1 expression was determined using the Tumor Proportion Score (TPS), defined as the percentage of viable tumor cells showing partial or complete membrane staining. TPS categories are: TPS 50% 85/229 37.12% Histotype Adenocarcinoma 234/271 86.3% Adenosquamous 2/271 0.74% NEC/NSCLC 6/271 2.2% Squamous cell carcinoma 19/271 7.1% NOS 10/271 3.66% STAS expression 133/162 82.1% Yes 29/162 17.9% TMB Median (min–max) 6.28 (0–94.3) TMB grade Low 92/219 42.01% Medium 69/219 31.51% High 58/219 26.48% MSI grade Stable 220/222 99.1% Unstable 2/222 0.9% ADC subtype growth pattern Acinar pattern 48/140 34.29% Adenocarcinoma in situ 1/140 0.71% Colloid/fetal/enteric pattern 1/140 0.71% Complex/cribriform glandular pattern 1/140 0.71% Lepidic pattern 5/140 3.57% Micropapillary pattern 10/140 7.14% Mucinous pattern 17/140 12.14% Papillary pattern 22/140 15.71% Solid pattern 35/140 25% Clinicopathological features in the STAS-analyzed cohort. Clinicopathological features in the STAS-analyzed cohort. Clinical Features STAS-Negative STAS-Positive p-Value Sex 0.8385 Female 64/133 (48.12%) 13/29 (44.83%) Male 69/133 (51.88%) 16/29 (55.17%) Age at diagnosis 0.815 Median (min–max) 69 (28–85) 69 (50–86) Stage 0.0617 Early 85/133 (63.91%) 12/29 (41.38%) Locally Advanced 28/133 (21.05%) 11/29 (37.93%) Advanced 20/133 (15.04%) 6/29 (20.69%) Histotype 0.0799 Adenocarcinoma 108/133 (81–2%) 29/29 (100%) Atypical carcinoid 2/133 (1.51%) 0/29 (0%) NEC 4/133 (3.01%) 0/29 (0%) Squamous cell carcinoma 19/133(14.28%) 0/29 (0%) TMB grade 0.5165 Low 43/107 (40.19%) 9/19 (47.37%) Medium 37/107 (34.58%) 4/19 (21.05%) High 27/107 (25.23%) 6/19 (31.58%) Smoker 0.1876 Yes 40/132 (30.3%) 5/29 (17.24%) Ex-smoker 68/132 (51.52%) 15/29 (51.72%) 24/132 (18.18%) 9/29 (31.03%) PDL1 expression 0.5341 50% 27/106 (25.47%) 9/24 (37.5%) 1–49% 26/106 (24.53%) 5/24 (20.83%) ADC subtype growth pattern ୨.୫୦ ୍ଠ ୧୦ −6Acinar pattern 45/88 (51.14%) 3/28 (10.71%) Lepidic pattern 5/88 (5.68%) 0/28 (0%) Micropapillary pattern 1/88 (1.14%) 7/28 (25%) Mucinous pattern 6/88 (6.82%) 6/28 (21.43%) Papillary pattern 13/88 (14.77%) 7/28 (25%) Solid pattern 18/88 (20.45%) 5/28 (17.86%) Distribution of RNA-level somatic alterations across the STAS-analyzed cohort. The table details the frequency of gene fusions and RNA-level events stratified by STAS status (Negative vs. Positive). To rigorously account for multiple hypothesis testing across the six evaluated genes, False Discovery Rate (FDR)-adjusted q-values were used. Distribution of RNA-level somatic alterations across the STAS-analyzed cohort. The table details the frequency of gene fusions and RNA-level events stratified by STAS status (Negative vs. Positive). To rigorously account for multiple hypothesis testing across the six evaluated genes, False Discovery Rate (FDR)-adjusted q-values were used. Gene STAS-Negative STAS-Positive p-Value q-Value ALK 4/133 (3.01%) 1/29 (3.45%) 1 1 RET 3/133 (2.26%) 0/29 (0%) 1 1 EML4 0/133 (0%) 1/29 (3.45%) 0.1790 0.5370 ROS1 0/133 (0%) 2/29 (6.9%) 0.0311 0.1866 BRAF 1/133 (0.75%) 0/29 (0%) 1 1 NRG1 1/133 (0.75%) 0/29 (0%) 1 1 Clinicopathological features in the early and locally advanced stage cohort. Clinicopathological features in the early and locally advanced stage cohort. Clinical Features STAS-Negative STAS-Positive p-Value Sex 0.8199 Female 54/113 (47.79%) 10/23 (43.48%) Male 59/113 (52.21%) 13/23 (56.52%) Age at diagnosis 0.5809 Median (min–max) 70 (28–85) 69 (50–86) Stage 0.0409 Early 85/113 (75.22%) 12/23 (52.17%) Locally Advanced 28/113 (24.78%) 11/23 (47.83%) Histotype 0.0966 Adenocarcinoma 84/108 (77.78%) 23/23 (100%) Atypical carcinoid 2/108 (1.85%) 0/23 (0%) NEC 4/108 (3.7%) 0/23 (0%) Squamous cell carcinoma 18/108 (16.67%) 0/23 (0%) TMB grade 0.4279 Low 37/91 (40.66%) 8/16 (50%) Medium 32/91 (35.16%) 3/16 (18.75%) High 22/91 (24.18%) 5/16 (31.25%) Smoker 0.2044 Yes 34/113 (30.09%) 3/23 (13.04%) Ex-smoker 59/113 (52.21%) 14/23 (60.87%) 20/113 (17.7%) 6/23 (26.09%) PDL1 expression 0.2733 50% 21/88 (23.86%) 8/18 (44.44%) 1–49% 19/88 (21.59%) 3/18 (16.67%) ADC subtype growth pattern ୬.୩୦ ୍ଠ ୧୦ −5Acinar pattern 43/78 (55.13%) 3/22 (13.64%) Lepidic pattern 4/78 (5.13%) 0/22 (0%) Micropapillary pattern 1/78 (1.28%) 6/22 (27.27%) Mucinous pattern 6/78 (7.69%) 3/22 (13.64%) Papillary pattern 13/78 (16.67%) 7/22 (31.82%) Solid pattern 11/78 (14.1%) 3/22 (13.64%) Distribution of RNA-level somatic alterations in the early and locally advanced stage cohort. The table details the frequency of gene fusions and RNA-level events stratified by STAS status (Negative vs. Positive). To rigorously account for multiple hypothesis testing across the six evaluated genes, False Discovery Rate (FDR)-adjusted q-values were used. Distribution of RNA-level somatic alterations in the early and locally advanced stage cohort. The table details the frequency of gene fusions and RNA-level events stratified by STAS status (Negative vs. Positive). To rigorously account for multiple hypothesis testing across the six evaluated genes, False Discovery Rate (FDR)-adjusted q-values were used. Gene STAS-Negative STAS-Positive p-Value q-Value ALK 2/113 (1.77%) 1/23 (4.35%) 0.429 1 RET 2/113 (1.77%) 0/23 (0%) 1 1 ROS1 0/113 (0%) 2/23 (8.7%) 0.0276 0.1380 BRAF 1/113 (0.88%) 0/23 (0%) 1 1 NRG1 1/113 (0.88%) 0/23 (0%) 1 1 Clinicopathological features in the advanced stage cohort. Clinicopathological features in the advanced stage cohort. Clinical Features STAS-Negative STAS-Positive Sex Female 10/20 (50%) 3/6 (50%) Male 10/20 (50%) 3/6 (50%) Age at Diagnosis Median (min–max) 68.5 (48–79) 68 (56–74) Stage Advanced 20/20 (100%) 6/6 (100%) Histotype Adenocarcinoma 19/20 (95%) 6/6 (100%) Squamous cell carcinoma 1/20 (5%) 0/6 (0%) TMB grade Low 6/16 (37.5%) 1/3 (33.33%) Medium 5/16 (31.25%) 1/3 (33.33%) High 5/16 (31.25%) 1/3 (33.33%) Smoker Yes 6/19 (31.58%) 2/6 (33.33%) Ex-smoker 9/19 (47.37%) 1/6 (16.67%) 4/19 (21.05%) 3/6 (50%) PDL1 expression 50% 6/18 (33.33%) 1/6 (16.67%) 1–49% 7/18 (38.89%) 2/6 (33.33%) ADC subtype growth pattern Acinar pattern 2/10 (20%) 0/6 (0%) Lepidic pattern 1/10 (10%) 0/6 (0%) Micropapillary pattern 0/10 (0%) 1/6 (16.67%) Mucinous pattern 0/10 (0%) 3/6 (50%) Solid pattern 7/10 (70%) 2/6 (33.33%) Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. Sassorossi, C.; Dalfovo, D.; De Paolis, E.; Evangelista, J.; Cancellieri, A.; Campanella, A.; Boldrini, L.; Troost, E.G.C.; Ádány, R.; Farré, N.; et al. LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population. Genes 2026, 17, 677. https://doi.org/10.3390/genes17060677 Sassorossi C, Dalfovo D, De Paolis E, Evangelista J, Cancellieri A, Campanella A, Boldrini L, Troost EGC, Ádány R, Farré N, et al. LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population. Genes. 2026; 17(6):677. https://doi.org/10.3390/genes17060677 Sassorossi, Carolina, Davide Dalfovo, Elisa De Paolis, Jessica Evangelista, Alessandra Cancellieri, Annalisa Campanella, Luca Boldrini, Esther G. C. Troost, Róza Ádány, Núria Farré, and et al. 2026. "LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population" Genes 17, no. 6: 677. https://doi.org/10.3390/genes17060677 Sassorossi, C., Dalfovo, D., De Paolis, E., Evangelista, J., Cancellieri, A., Campanella, A., Boldrini, L., Troost, E. G. C., Ádány, R., Farré, N., Öztürk, E., Minucci, A., Trisolini, R., Bria, E., Margaritora, S., Löck, S., & Lococo, F. (2026). LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population. Genes, 17(6), 677. https://doi.org/10.3390/genes17060677 Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details .
LANTERN 2: Association Between Gene Molecular Profile and STAS in Lung Adenocarcinoma: A Comparative Analysis in a Prospective Real-World Population
