Head and neck squamous cell carcinoma (HNSCC) is a major health concern with considerable morbidity and mortality worldwide. Previous studies have applied single-cell sequencing to characterize the tumor microenvironment in HNSCC, providing insights into immune cell composition, stromal interactions, and malignant cell states. However, there remains a gap in analyzing lymph node metastasis (LM) and normal lymph node tissues (LN) by using single-cell RNA sequencing (scRNA-seq) analysis. We performed comparative scRNA-seq analysis on seven lymph node metastatic tissues of HNSCC patients and five non-metastatic tissues. We identified several cell types with significantly altered expression levels, such as CD8+ Tex cells, Macrophages, and Cancer-associated fibroblasts (CAFs). Tumor cells were classified into seven clusters, with cluster2 strongly linked to tumorigenesis and metastasis. Specific subsets such as CD4_Tfh_CXCL13, CD4_Treg_RPL26, CD8_teff_CREM, NK_GZMB, Macrophages_OLFML3 and macrophages_SPP1 cells were also associated with HNSCC progression and metastasis. Based on these findings, we constructed and validated a prognostic model for HNSCC using the expression of INHBA, SFRP2, SPP1, and IFI27. This model provides a tool for risk stratification and informs potential therapeutic strategies for HNSCC.

BackgroundHead and neck squamous cell carcinoma (HNSC) is a highly heterogeneous malignancy with poor prognosis and frequent recurrence. Beyond tumor-intrinsic alterations, the immune microenvironment plays a decisive role in tumor initiation and progression. However, the causal contribution of systemic plasma proteins to immune regulation and HNSC susceptibility remains poorly defined.MethodsWe conducted a multi-sample Mendelian randomization (MR) study integrating large-scale plasma proteomics, immune cell phenotypes, and HNSC. Mediation analyses were performed to identify immune cell phenotypes that potentially mediate protein-HNSC associations. The findings were further supported by immune infiltration analyses, molecular docking and molecular dynamics simulations and validation using clinical HNSC specimens, including single-cell RNA sequencing of collected samples, scTenifoldKnk virtual knockout modeling and immunofluorescence staining/histological assessment of HNSC tissues.ResultsAmong 4907 plasma proteins, MR identified prefoldin subunit 2 (PFDN2) as a protective factor against hypopharyngeal carcinoma, with no evidence of reverse causality. Immune phenotype MR analyses revealed CD64 on monocyte (FCGR1A+ monocytes) as the only immune trait causally linked to both PFDN2 and cancer risk. Analysis using multiple deconvolution algorithms demonstrated a consistent negative correlation between PFDN2 expression and monocyte infiltration. Single-cell RNA sequencing revealed predominant PFDN2 expression in epithelial tumor cells, whereas FCGR1A expression was restricted to monocytes. Virtual knockout of PFDN2 selectively activated monocyte-associated inflammatory programs. Molecular docking and dynamics simulations supported a stable protein-protein interaction between PFDN2 and CD64. Tissue analyses further confirmed PFDN2 downregulation and CD64 upregulation in HNSC, correlating with advanced tumor grade and stage.ConclusionsOur findings establish PFDN2 as a protective plasma protein that restrains HNSC progression by suppressing CD64 on monocyte-mediated inflammatory immune microenvironments, highlighting the PFDN2-CD64 axis as a potential prognostic biomarker and therapeutic target.

Hypopharyngeal squamous cell carcinoma (HSCC) is an aggressive subtype of head and neck squamous cell carcinoma with insidious onset, early metastasis, and dismal prognosis. Conventional multimodal therapy achieves limited survival benefit, highlighting an urgent need for refined precision strategies. This review systematically summarizes the latest progress in HSCC, covering epidemiological characteristics, imaging diagnosis, prognostic prediction, surgical and non-surgical treatment advances, as well as coding and non-coding therapeutic targets, biomarkers, and candidate drugs. It further introduces the application of multi-omics and machine learning in HSCC research, analyzes current challenges and future directions, and provides a theoretical reference for precise diagnosis, individualized treatment, and prognostic evaluation of HSCC.

Background:Immune checkpoint inhibitors (ICIs) have transformed lung cancer treatment, but clinical trials often miss rare, life-threatening toxicities and safety patterns in complex combinations. Real-world pharmacovigilance is essential to identify toxicity profiles in unselected populations. This study aimed to characterize adverse event reporting patterns associated with ICI monotherapy and ICI-based combination regimens in lung cancer using real-world data. Methods:We analyzed 34,223 adverse event reports from the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database (Q1 2016-Q3 2025) for pembrolizumab, atezolizumab, and nivolumab and their combinations. Disproportionality analysis, time-to-onset, and stratified analysis were conducted. Results:Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) inhibitors primarily caused endocrine and respiratory toxicities; ipilimumab caused dermatologic and hepatobiliary effects. Stress cardiomyopathy occurred across all agents, with pembrolizumab showed highest disproportionality signal. Males on atezolizumab had 73% lower odds of reported stress cardiomyopathy [odds ratio (OR) =0.27, P<0.01]. Combination-regimen analyses showed heterogeneous reporting profiles. For example, pembrolizumab-chemotherapy was associated with an earlier onset of duodenitis, atezolizumab-bevacizumab-platinum was uniquely associated with duodenal ulcer hemorrhage, and ventricular fibrillation was highlighted in by nivolumab-ipilimumab combination. Conclusions:ICI toxicity is highly regimen-specific and combination therapy was associated with a shorter reported time-to-onset and increased odds of reporting cardiac and gastrointestinal events, informing tailored surveillance strategies.

Immunotherapy has emerged as a transformative approach in cancer treatment. However, its efficacy remains limited in many cases. A key factor contributing to this limitation is metabolic reprogramming within the tumor microenvironment (TME), which suppresses immune cell function and promotes tumor progression. Recently, nanotechnology-based approaches have opened new ways to modulate tumor metabolism and enhance immunotherapy. This review outlines nanoscale strategies aimed at reprogramming tumor metabolism to potentiate antitumor immunity. We begin by discussing the rational design of immune-metabolic nanoregulators, along with key immunometabolic pathways and their regulatory mechanisms. Next, nanotechnology strategies for targeted metabolic intervention at the cellular and microbial levels, as well as the metabolic characteristics of TME are systematically summarized. Furthermore, we highlight recent advances in nanomedicine-based metabolic regulators and evaluate their potential for clinical translation, addressing both opportunities and challenges.

Microsatellite instability-high (MSI-H) metastatic colorectal cancer (CRC) patients are the dominant population in immune checkpoint blockade treatments, while more than half of them could not benefit from single-agent immunotherapy. We tried to identify the biomarker of MSI-H CRC and explore its role and mechanism in anti-PD-1 treatments. Tumor-specific MHC-II was linked to a better response to anti-PD-1 in MSI-H CRC and CD74 promoted assembly and transport of HLA-DR dimers. The characteristic gene was screened by data analysis of single-cell and bulk transcriptome sequencing from public datasets. MSI-H CRC cells co-cultured with peripheral blood mononuclear cells and syngeneic model in C57BL/6 mice were performed to detect the sensitivity to anti-PD-1 treatments respectively. ANXA10 was identified as a characteristic gene of MSI-H CRC and its expression was obviously greater in MSI-H than MSS CRC. ANXA10 significantly sensitized MSI-H CRC to anti-PD-1 treatments in vitro and in vivo. Specifically, ANXA10 promoted HLA-DR dimers in and on the surface of MSI-H CRC by increasing CD74 expression. Besides, this work demonstrated that ANXA10 contributed to better clinical benefits with anti-PD-1 therapy in MSI-H CRC patients. Our results provided a novel molecular marker ANXA10 to identify benefit population of MSI-H CRC for improving efficacy of anti-PD-1 and contributed to selection of treatment strategies.

More than 90% of advanced gastric cancers (GC) are microsatellite-stable (MSS). Compared to the high response rate of immune checkpoint inhibitors (ICI) in microsatellite-instability-high (MSI-H) GCs, only 10% of unstratified MSS GCs respond to ICIs. In this study, we apply semi-supervised learning to stratify potential ICI responders in MSS GCs, achieving high accuracy, quantified by an area under the curve of 0.924. Spatial analysis of the tumor microenvironment of ICI-sensitive GCs reveals a high level of T-bet+ CD8 + T cell infiltration in their tumor compartments. T-bet+ CD8 + T cells exhibit superior anti-tumor activity due to their increased ability to infiltrate tumors and secrete cytotoxic molecules. Adoptive transfer of T-bet+ CD8 + T cells boosts anti-tumor immunity and confers susceptibility to ICIs in immune-ignorant MSS GCs in a humanized mouse model. Spatial RNA sequencing suggests a positive-feedback loop between T-bet+ T cells and PD-L1+ tumor cells, which eventually drives T cell exhaustion and can therefore be leveraged for ICI therapy. In summary, our research provides insights into the underlying mechanism of anti-tumor immunity and deepens our understanding of varied ICI responses in MSS GCs.

Head and neck squamous cell carcinoma (HNSCC) constitutes a major clinical challenge that severely affects patient survival. Mitochondrial ribosomal protein (MRP) family plays an important role in energy metabolism by participating in mitochondrial oxidative phosphorylation. However, their roles in HNSCC and the underlying mechanisms are still unclear. Single-cell analysis highlighted MRPL21 as a notable biomarker of HNSCC. Human HNSCC tissues, cell lines, and xenograft models in nude mice were used to explore the expression and function of MRPL21. The mass spectrometry was performed to analyze the potential binding targets of MRPL21. In vitro and in vivo experiments were performed to evaluate the effect of MRPL21 on autophagy and cisplatin resistance. The inhibitory actions of siMRPL21 nanodelivery systems on HNSCC progression were also evaluated in vivo. Clinically, relatively high expression level of MRPL21 was associated with poor prognosis in HNSCC patients, and overexpression of MRPL21 significantly promoted HNSCC tumorigenesis, metastasis, and cisplatin resistance. Mechanistically, MRPL21 upregulated mitochondrial oxidative phosphorylation (OXPHOS) and increased PARylation level, inhibited autophagy through activating the downstream PI3K/AKT/mTOR signaling pathway, and ultimately led to tumor progression and cisplatin resistance in HNSCC. We conclude that MRPL21 is a novel biomarker and therapeutic target of HNSCC progression and cisplatin resistant, which may provide a new approach for overcoming cisplatin resistance in HNSCC patients.

BACKGROUND:The cellular origin of hypopharyngeal diseases is crucial for further diagnosis and treatment, and the microenvironment in tissues may also be associated with specific cell types at the same time. Normal adjacent tissues (NATs) of hypopharyngeal carcinoma differ from non-tumor-bearing tissues, and can influenced by the tumor. However, the heterogeneity in kinds of disease samples remains little known, and the transcriptomic profile about biological information associated with disease occurrence and clinical outcome contained in it has yet to be fully evaluated. For these reasons, we should quickly investigate the taxonomic and transcriptomic information of NATs in human hypopharynx.RESULTS:Single-cell suspensions of normal adjacent tissues (NATs) of hypopharyngeal carcinoma were obtained and single-cell RNA sequencing (scRNA-seq) was performed. We present scRNA-seq data from 39,315 high-quality cells in the hypopharyngeal from five human donors, nine clusters of normal adjacent human hypopharyngeal cells were presented, including epithelial cells, endothelial cells (ECs), mononuclear phagocyte system cells (MPs), fibroblasts, T cells, plasma cells, B cells, mural cells and mast cells. Nonimmune components in the microenvironment, including epithelial cells, endothelial cells, fibroblasts and the subpopulations of them were performed.CONCLUSIONS:Our data provide a solid basis for the study of single-cell landscape in human normal adjacent hypopharyngeal tissues biology and related diseases.

Background Hypopharyngeal squamous cell carcinoma (HSCC) is a type of head and neck tumor with malignant behavior and poor prognosis. Spatial transcriptomics is a method that spatially analyzes gene expression patterns in tissues and has been used to discover tumor microenvironment and molecular markers in various tumors. However, there are no published reports on spatial transcriptomic analysis of HSCC. Methods In this study, spatial transcriptomic analysis was performed on tumor tissues in situ, peritumoral tissues, and lymphatic metastatic tissues of four patients with HSCC. Morphological markers, including panCK, SMA, and CD45, were used to identify epithelial, fibroblast, and immune cells, respectively. By analyzing the expression of more than 18, 000 genes within the transcriptome of all ROIs, differentially expressed genes of three cell types in different tissues were identified, and differentially expressed signaling pathways and immune infiltration were analyzed. Results The spatial distribution of cells suggests that fibroblast cells in tumor tissues may be involved in the genesis and development of tumors, and the immune infiltration of lymphatic tumor metastasis is lower than that of tumors in situ. For epithelial cells, SLCO2A1, which is a favorable prognosis marker in head and neck squamous cell carcinoma (HNSCC), was significantly down-regulated in tumor tissues and lymphatic metastatic tissues compared with adjacent normal tissues. For immune cells, KANK3, which is a favorable prognosis markers in HNSCC, was significantly down-regulated in lymphatic metastatic tissues compared with adjacent normal tissues. For fibroblast cells, AQP1, CLEC3B and SLCO2A1, which are favorable prognosis markers in HNSCC, were significantly down-regulated in tumor tissues compared with adjacent normal tissues. ITGA8, which is a favorable prognosis markers in HNSCC, was significantly down-regulated in lymphatic metastatic tissues compared with normal lymphatic tissues. CSRP1, DES, and SLCO2A1 positively correlate with immune infiltration in HNSCC. Moreover, SLCO2A1 overexpression suppressed Fadu cells proliferation and metastasis and significantly correlated with favorable survival overcome in HSCC. Conclusions We investigated tumor and fibroblast heterogeneity, as well as the immune microenvironment in HSCC by using spatial transcriptomics. SLCO2A1 may be a tumor suppressor gene and correlates with immune infiltration for HSCC and could serve as a potential target for its diagnosis and treatment.

Abstract Background To explore the pulmonary-vascular-stump filling-defect on CT and investigate its association with cancer progression. Methods Records in our institutional database from 2018 to 2022 were retrospectively analyzed to identify filling-defects in the pulmonary-vascular-stump after lung cancer resection and collect imaging and clinical data of patients. Results Among the 1714 patients analyzed, 95 cases of filling-defects in the vascular stump after lung cancer resection were identified. After excluding lost-to-follow-up cases, a total of 77 cases were included in the final study. Morphologically, the filling-defects were dichotomized as 46 convex-shape and 31 concave-shape cases. Concave defects exhibited a higher incidence of increase compared to convex defects (51.7% v. 9.4%, P = 0.001). Among 61 filling defects in the pulmonary arterial stump, four (6.5%) increasing concave defects showed the nuclide concentration on PET and extravascular extension. The progression-free survival (PFS) time differed significantly among the concave, convex, and non-filling-defect groups (log-rank P < 0.0001), with concave defects having the shortest survival time. Multivariate Cox proportional hazards analysis indicated that the shape of filling-defects independently predicted PFS in early onset on CT (HR: 0.46; 95% CI: 0.39–1.99; P = 0.04). In follow-ups, the growth of filling-effects was an independent predictor of PFS (HR: 0.26; 95% CI: 0.11–0.65; P = 0.004). Conclusions Certain filling-defects in the pulmonary-arterial-stump post lung tumor resection exhibit malignant growth. In the early onset of filling-defects on CT, the concave-shape independently predicted cancer-progression, while during the subsequent follow-up, the growth of filling-defects could be used independently to forecast cancer-progression.

BACKGROUND:Coronary artery wall contrast enhancement (CE) has been applied to non-invasive visualization of changes to the coronary artery wall in systemic lupus erythematosus (SLE). This study investigated the feasibility of quantifying CE to detect coronary involvement in IgG4-related disease (IgG4-RD), as well as the influence on disease activity assessment. METHODS:A total of 93 subjects (31 IgG4-RD; 29 SLE; 33 controls) were recruited in the study. Coronary artery wall imaging was performed in a 3.0 T MRI scanner. Serological markers and IgG4-RD Responder Index (IgG4-RD-RI) scores were collected for correlation analysis. RESULTS:Coronary wall CE was observed in 29 (94 %) IgG4-RD patients and 22 (76 %) SLE patients. Contrast-to-noise ratio (CNR) and total CE area were significantly higher in patient groups compared to controls (CNR: 6.1 ± 2.7 [IgG4-RD] v. 4.2 ± 2.3 [SLE] v. 1.9 ± 1.5 [control], P < 0.001; Total CE area: 3.0 [3.0-6.6] v. 1.7 [1.5-2.6] v. 0.3 [0.3-0.9], P < 0.001). In the IgG4-RD group, CNR and total CE area were correlated with the RI (CNR: r = 0.55, P = 0.002; total CE area: r = 0.39, P = 0.031). RI´ scored considering coronary involvement by CE, differed significantly from RI scored without consideration of CE (RI v. RI´: 15 ± 6 v. 16 ± 6, P < 0.001). CONCLUSIONS:Visualization and quantification of CMR coronary CE by CNR and total CE area could be utilized to detect subclinical and clinical coronary wall involvement, which is prevalent in IgG4-RD. The potential inclusion of small and medium-sized vessel involvements in the assessment of disease activity in IgG4-RD is worthy of further investigation.

The relationship between left ventricular (LV) torsion and myocardial fibrosis (MF) in hypertrophic cardiomyopathy (HCM) patients with preserved ejection fraction was still not well understood. New developments in cardiac magnetic resonance (CMR) enable a much fuller assessment of cardiac characteristics. This study sought to assess the impact of HCM on myocardial function as assessed by LV torsion and its relationship with MF. HCM (n = 79) and healthy controls (n = 40) underwent CMR. According to whether there was late gadolinium enhancement (LGE), patients were divided into LGE+ group and LGE− group. LV torsion and torsion rate were measured by CMR feature-tracking (CMR-FT). MF was quantitatively evaluated through LGE imaging. LGE was present in 44 patients (56

Background The combinations of PD-1 inhibitors with paclitaxel/cisplatinum (PD-1 + TP) and fluoropyrimidine/cisplatinum (PD-1 + FP) both have been shown to improve overall survival (OS) and progression-free survival (PFS) in patients with previously untreated, advanced esophageal squamous cell carcinoma (ESCC). However, there is no consensus on which chemotherapy regimen combined with PD-1 has better efficacy. To deal with this important issue in the first-line treatment of patients with ESCC, a network meta-analysis (NMA) was performed. Methods Data were collected from eligible studies searched in Medline, Web of Science, PubMed, the Cochrane Library and Embase. The pooled hazard ratio (HR) for the OS, and PFS, odds ratio (OR) for the objective response rate (ORR) and ≥ 3 grade treatment-related adverse events (≥ 3TRAEs) were estimated to evaluate the efficacy of PD-1 inhibitors combined with TP or FP. Results Five RCTs and one retrospective study involving 3685 patients and evaluating four treatments were included in this NMA. Compared to other treatments, PD-1 + TP was better. For the PFS, the HRs for PD-1 + TP compared to PD-1 + FP, TP and FP were 0.59 (0.44, 0.80), 0.56 (0.51, 0.61) and 0.45 (0.37, 0.56) respectively. For the OS, PD-1 + TP was also a better treatment compared to other treatments. The HRs were 0.74 (0.56, 0.96), 0.64 (0.57, 0.71), 0.53 (0.43, 0.67) respectively. For the ORR, there was no significant difference between PD-1 + TP and PD-1 + FP, and the ORs were 1.2 (0.69, 2.11). Compare with TP and FP, PD-1 + TP had an obvious advantage, ORs were 2.5 (2.04, 3.04) and 2.95 (1.91, 4.63). For ≥ 3TRAEs, PD-1 + TP compared to other treatments, ORs were 1.34 (0.74, 2.46) and 1.13 (0.92, 1.38) and 2.23 (1.35, 3.69). Conclusion PD-1 + TP significantly improved both PFS and OS compared to PD-1 + FP. Taking into account both efficacy and safety, PD-1 + TP may be a superior first-line treatment option for ESCC.

Supplementary Data for publication

Head neck squamous cell carcinoma (HNSCC) is one of the most common malignant tumors which ranks the sixth incidence in the world. Although treatments for HNSCC have improved significantly in recent years, its recurrence rate and mortality rate remain high. Myosin genes have been studied in a variety of tumors, however its role in HNSCC has not been elucidated. GSE58911 and GSE30784 gene expression profile analysis were performed to detect significantly dys-regulated myosin genes in HNSCC. The Cancer Genome Atlas (TCGA) HNSCC database was used to verify the dys-regulated myosin genes and study the relationship between these genes and prognosis in HNSCC. The results showed that MYL1, MYL2, MYL3, MYH2, and MYH7 were down-regulated, while MYH10 was up-regulated in patients with HNSCC. Interestingly, MYL1, MYL2, MYH1, MYH2, and MYH7 were shown to be unfavorable prognostic markers in HNSCC. It is also worth noting that MYL1 was a specific unfavorable prognostic biomarker in HNSCC. MYL1, MYL2, MYL3, MYH2, MYH7, and MYH10 promoted CD4 + T cells activation in HNSCC. MYL1 was proved to be down-regulated in HNSCC tissues compared to normal tissues at protein levels. MYL1 overexpression had no effect on proliferation, but significantly promoted migration of Fadu cells. MYL1 increased EGF and EGFR protein expression levels. Moreover, there is a positive correlation between MYL1 expression and Tcm CD8 cells, Tcm CD4 + cells, NK cells, Mast cells, NKT cells, Tfh cells and Treg cells in HNSCC. Overall, MYL1 facilitates tumor metastasis and correlates with tumor immune infiltration in HNSCC and these effects may be associated with the EGF/EGFR pathway.

HomeCirculation: Cardiovascular ImagingAhead of PrintQuantitative Characterization of Intertumor Heterogeneity of Primary Cardiac Diffuse Large B-Cell Lymphoma Using Cardiac Magnetic Resonance No AccessCase ReportRequest AccessAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessCase ReportRequest AccessQuantitative Characterization of Intertumor Heterogeneity of Primary Cardiac Diffuse Large B-Cell Lymphoma Using Cardiac Magnetic Resonance Lei Ni, MD, Ce Li, MD, PhD, Yaqi Du, MD, Zhenggang Sun, MD, Guoguang Fan, MD, PhD and Guan Wang, MD, PhD Lei NiLei Ni Department of Radiology, the First Hospital of China Medical University, Shenyang, China (L.N., Y.D., Z.S., G.F., G.W.). , Ce LiCe Li Department of Medical Oncology, the First Hospital of China Medical University, Shenyang, China (C.L.). , Yaqi DuYaqi Du Department of Radiology, the First Hospital of China Medical University, Shenyang, China (L.N., Y.D., Z.S., G.F., G.W.). , Zhenggang SunZhenggang Sun Department of Radiology, the First Hospital of China Medical University, Shenyang, China (L.N., Y.D., Z.S., G.F., G.W.). , Guoguang FanGuoguang Fan Correspondence to: Guoguang Fan, MD, PhD, Department of Radiology, the First Hospital of China Medical University, No.155, North Nanjing St, Shenyang, Liaoning, China 110001 Email E-mail Address: [email protected] https://orcid.org/0000-0001-8114-5727 Department of Radiology, the First Hospital of China Medical University, Shenyang, China (L.N., Y.D., Z.S., G.F., G.W.). and Guan WangGuan Wang Guan Wang, MD, PhD, Department of Radiology, the First Hospital of China Medical University, No.155, North Nanjing St, Shenyang, Liaoning, China 110001Email E-mail Address: [email protected] https://orcid.org/0000-0001-8626-5824 Department of Radiology, the First Hospital of China Medical University, Shenyang, China (L.N., Y.D., Z.S., G.F., G.W.). Originally published3 Feb 2023https://doi.org/10.1161/CIRCIMAGING.122.014884Circulation: Cardiovascular Imaging. 2023;0:e014884"Quantitative Characterization of Intertumor Heterogeneity of Primary Cardiac Diffuse Large B-Cell Lymphoma Using Cardiac Magnetic Resonance." Circulation: Cardiovascular Imaging, , pp. –Footnotes*L. Ni and C. Li contributed equallyFor Sources of Funding and Disclosures, see page xxx.Correspondence to: Guoguang Fan, MD, PhD, Department of Radiology, the First Hospital of China Medical University, No.155, North Nanjing St, Shenyang, Liaoning, China 110001 Email [email protected]comGuan Wang, MD, PhD, Department of Radiology, the First Hospital of China Medical University, No.155, North Nanjing St, Shenyang, Liaoning, China 110001Email [email protected]com Previous Back to top Next FiguresReferencesRelatedDetails Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.122.014884PMID: 36734239 Originally publishedFebruary 3, 2023 Keywordsmagnetic resonance imagingneoplasmprognosispositron emission tomographypericardial effusionPDF download Advertisement SubjectsMagnetic Resonance Imaging (MRI)

S1. Separation of patients with the same TNM substaging into different risk subgroups by the immunoscore system.