Characteristics of Genomic Mutations and Signaling Pathway Alterations in Thymic Epithelial Tumors

Abstract Purpose: To elucidate mechanisms of thymic epithelial tumor (TET) canceration through characterization of genomic mutations and signal pathway alterations.Methods: Primary tumor and blood samples were collected from 21 patients diagnosed with TETs (thymoma and thymic cancer), 15 of whom were screened by nucleic acid extraction and total exon sequencing. Bioinformatics was used to comprehensively analyze sequencing data for these samples, including differences in tumor mutation burden (TMB) and signaling pathways.Results: We found that the gene with the highest mutation frequency in thymic carcinoma was ZNF429 (36%). In addition, mutations in BAP1 (14%), ABI1 (7%), BCL9L (7%), CHEK2 (7%) were only detected in thymic carcinoma, whereas ZNF721 mutations (7%) were found only in thymoma. Mean TMB values for thymic carcinoma and thymoma groups were 0.722 and 0.663 mutations per megabase (Mb), respectively, differences that were not statistically significant. There were significant differences in enriched pathways for cellular components between tumor metastasis and non-metastatic samples. The ErbB signaling pathway was enriched in both the thymoma group and the intersection group, whereas “pathways in cancer” was found in both the thymoma group and thymic cancer group. In contrast, enrichment of longevity-regulating and MAPK signaling pathways was found only in the thymoma group.Conclusions: We identified multiple differences in somatic genes and pathways, providing insights into differences between thymoma and thymic carcinoma that could aid in designing personalized clinical therapy.

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Targeting ERK-Hippo Interplay in Cancer Therapy

International Journal of Molecular Sciences ◽

10.3390/ijms21093236 ◽

2020 ◽

Vol 21 (9) ◽

pp. 3236 ◽

Cited By ~ 2

Author(s):

Karel Vališ ◽

Petr Novák

Keyword(s):

Cancer Therapy ◽

Signaling Pathways ◽

Signaling Pathway ◽

Cross Talk ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Mitogen Activated Protein Kinase ◽

Cancer Therapies ◽

Anti Cancer ◽

Targeted Inhibition

Extracellular signal-regulated kinase (ERK) is a part of the mitogen-activated protein kinase (MAPK) signaling pathway which allows the transduction of various cellular signals to final effectors and regulation of elementary cellular processes. Deregulation of the MAPK signaling occurs under many pathological conditions including neurodegenerative disorders, metabolic syndromes and cancers. Targeted inhibition of individual kinases of the MAPK signaling pathway using synthetic compounds represents a promising way to effective anti-cancer therapy. Cross-talk of the MAPK signaling pathway with other proteins and signaling pathways have a crucial impact on clinical outcomes of targeted therapies and plays important role during development of drug resistance in cancers. We discuss cross-talk of the MAPK/ERK signaling pathway with other signaling pathways, in particular interplay with the Hippo/MST pathway. We demonstrate the mechanism of cell death induction shared between MAPK/ERK and Hippo/MST signaling pathways and discuss the potential of combination targeting of these pathways in the development of more effective anti-cancer therapies.

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Proteins in cord blood as a new target for prevention and treatment of bronchopulmonary dysplasia: a proteomic analysis

10.21203/rs.3.rs-514982/v1 ◽

2021 ◽

Author(s):

Juan Wang ◽

Jianping Mao ◽

Gang Chen ◽

Yuanmei Huang ◽

Jinjin Zhou ◽

...

Keyword(s):

Cord Blood ◽

Signaling Pathways ◽

Signaling Pathway ◽

Bronchopulmonary Dysplasia ◽

Proteomic Analysis ◽

Mapk Signaling ◽

Term Infants ◽

Reproductive Process ◽

Prevention And Treatment ◽

Differential Proteins

Abstract This study aimed to explore the proteins in cord blood that could regulate the development of neonatal bronchi and lungs, and to find a new target for the prevention and treatment of bronchopulmonary dysplasia (BPD). In this study, proteomic analysis was used to analyze the proteins in cord blood of preterm and term infants. A total of 100 differentially expressed (57 up-regulated and 43 down-regulated) proteins were identified from preterm with BPD and term infants cord blood (fold change ≥ 1.5, P value < 0.05). GO analysis revealed that the major enrichment functions of these differential proteins were multi-organism process, stimulus, immune system process growth, reproductive process, development process and antioxidant activity. The signaling pathways involved included insulin resistance, insulin signaling pathway, IL−17 signaling pathway, PI3K−Akt signaling pathway, NF−kappa B signaling pathway, glucagon signaling pathway, apoptosis, MAPK signaling pathway, as well as glycolysis/gluconeogenesis. Further protein and protein interact (PPI) analysis revealed that the interacting proteins involved were PGAM1, CNN2, HSP90AA and DAG1, which were all crucial in the development of BPD. We found that these differential proteins in cord blood might regulate bronchopulmonary development through the abovementioned signaling pathways or their interaction proteins, which may provide a new research direction for the intervention of BPD.

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Five Circular RNAs in Metabolism Pathways Related to Prostate Cancer

Frontiers in Genetics ◽

10.3389/fgene.2021.636419 ◽

2021 ◽

Vol 12 ◽

Author(s):

Lili Zhang ◽

Wei Zhang ◽

Hexin Li ◽

Xiaokun Tang ◽

Siyuan Xu ◽

...

Keyword(s):

Prostate Cancer ◽

Signaling Pathway ◽

High Throughput Sequencing ◽

Specific Antigen ◽

Mapk Signaling ◽

Circular Rnas ◽

Sequencing Data ◽

Clinical Indicators ◽

High Throughput Sequencing Data ◽

Differentially Expressed Mrna

Prostate cancer (PCa) is the most common malignant tumor in men, and its incidence increases with age. Serum prostate-specific antigen and tissue biopsy remain the standard for diagnosis of suspected PCa. However, these clinical indicators may lead to aggressive overtreatment in patients who have been treated sufficiently with active surveillance. Circular RNAs (circRNAs) have been recently recognized as a new type of regulatory RNA that is not easily degraded by RNases and other exonucleases because of their covalent closed cyclic structure. Thus, we utilized high-throughput sequencing data and bioinformatics analysis to identify specifically expressed circRNAs in PCa and filtered out five specific circRNAs for further analysis—hsa_circ_0006410, hsa_circ_0003970, hsa_circ_0006754, hsa_circ_0005848, and a novel circRNA, hsa_circ_AKAP7. We constructed a circRNA-miRNA regulatory network and used miRNA and differentially expressed mRNA interactions to predict the function of the selected circRNAs. Furthermore, survival analysis of their cognate genes and PCR verification of these five circRNAs revealed that they are closely related to well-known PCa pathways such as the MAPK signaling pathway, P53 pathway, androgen receptor signaling pathway, cell cycle, hormone-mediated signaling pathway, and cellular lipid metabolic process. By understanding the related metabolism of circRNAs, these circRNAs could act as metabolic biomarkers, and monitoring their levels could help diagnose PCa. Meanwhile, the exact regulatory mechanism for AR-related regulation in PCa is still unclear. The circRNAs we found can provide new solutions for research in this field.

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Identification of the Crucial Gene in Overflow Arteriovenous Fistula by Bioinformatics Analysis

Frontiers in Physiology ◽

10.3389/fphys.2021.621830 ◽

2021 ◽

Vol 12 ◽

Author(s):

Zhengde Zhao ◽

Qining Fu ◽

Liangzhu Hu ◽

Yangdong Liu

Keyword(s):

Signaling Pathways ◽

Signaling Pathway ◽

Intimal Hyperplasia ◽

Enrichment Analysis ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Biological Processes ◽

Hub Genes ◽

Av Fistula ◽

Core Genes

Objective: The aim was to study the preliminary screening of the crucial genes in intimal hyperplasia in the venous segment of arteriovenous (AV) fistula and the underlying potential molecular mechanisms of intimal hyperplasia with bioinformatics analysis.Methods: The gene expression profile data (GSE39488) was analyzed to identify differentially expressed genes (DEGs). We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of DEGs. Gene set enrichment analysis (GSEA) was used to understand the potential activated signaling pathway. The protein–protein interaction (PPI) network was constructed with the STRING database and Cytoscape software. The Venn diagram between 10 hub genes and gene sets of 4 crucial signaling pathways was used to obtain core genes and relevant potential pathways. Furthermore, GSEAs were performed to understand their biological functions.Results: A total of 185 DEGs were screened in this study. The main biological function of the 111 upregulated genes in AV fistula primarily concentrated on cell proliferation and vascular remodeling, and the 74 downregulated genes in AV fistula were enriched in the biological function mainly relevant to inflammation. GSEA found four signaling pathways crucial for intimal hyperplasia, namely, MAPK, NOD-like, Cell Cycle, and TGF-beta signaling pathway. A total of 10 hub genes were identified, namely, EGR1, EGR2, EGR3, NR4A1, NR4A2, DUSP1, CXCR4, ATF3, CCL4, and CYR61. Particularly, DUSP1 and NR4A1 were identified as core genes that potentially participate in the MAPK signaling pathway. In AV fistula, the biological processes and pathways were primarily involved with MAPK signaling pathway and MAPK-mediated pathway with the high expression of DUSP1 and were highly relevant to cell proliferation and inflammation with the low expression of DUSP1. Besides, the biological processes and pathways in AV fistula with the high expression of NR4A1 similarly included the MAPK signaling pathway and the pathway mediated by MAPK signaling, and it was mainly involved with inflammation in AV fistula with the low expression of NR4A1.Conclusion: We screened four potential signaling pathways relevant to intimal hyperplasia and identified 10 hub genes, including two core genes (i.e., DUSP1 and NR4A1). Two core genes potentially participate in the MAPK signaling pathway and might serve as the therapeutic targets of intimal hyperplasia to prevent stenosis after AV fistula creation.

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Cross-talk of Signaling Pathways in the Pathogenesis of Allergic Asthma and Cataract

Protein and Peptide Letters ◽

10.2174/0929866527666200207113439 ◽

2020 ◽

Vol 27 (9) ◽

pp. 810-822

Author(s):

Yang Zhao ◽

Sumei Liu ◽

Xiangsheng Li ◽

Zhenzhen Xu ◽

Lifang Hao ◽

...

Keyword(s):

Signaling Pathways ◽

Allergic Asthma ◽

Signaling Pathway ◽

Academic Research ◽

Notch Signaling Pathway ◽

Mapk Signaling ◽

Chronic Inflammatory Disease ◽

Smad Signaling Pathway ◽

Immune Imbalance ◽

Cellular Components

: Allergic asthma is a chronic inflammatory disease, which involves many cellular and cellular components. Cataract is a condition that affects the transparency of the lens, which the opacity of the lens caused by any innate or acquired factor degrades its transparency or changes in color. Both of them belong to diseases induced by immune disorders or inflammation. We want to confirm the signaling pathways involved in the regulation of asthma and cataract simultaneously, and provide reference for the later related experiments. So we conducted a scoping review of many databases and searched for studies (Academic research published in Wiley, Springer and Bentham from 2000 to 2019) about the possible relationship between asthma and cataract. It was found that during the onset of asthma and cataract, Rho/Rock signaling pathway, Notch signaling pathway, Wnt/β-catenin signaling pathway, PI3K/AKT signaling pathway, JAK/STAT signaling pathway, MAPK signaling pathway, TGF-β1/Smad signaling pathway and NF-κB signaling pathway are all active, so they may have a certain correlation in pathogenesis. Asthma may be associated with cataract through the eight signaling pathways, causing inflammation or immune imbalance based on allergy that can lead to cataract. According to these studies, we speculated that the three most likely signaling pathways are PI3K/AKT, MAPK and NF-κB signaling pathway.

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Selenoproteins and their emerging roles in signaling pathways

Regulatory Mechanisms in Biosystems ◽

10.15421/022028 ◽

2020 ◽

Vol 11 (2) ◽

pp. 186-199

Author(s):

N. V. Stanishevska

Keyword(s):

Endoplasmic Reticulum ◽

Signaling Pathways ◽

Signaling Pathway ◽

Thioredoxin Reductase ◽

Methionine Sulfoxide ◽

Mapk Signaling ◽

Methionine Sulfoxide Reductase ◽

Selenoprotein S ◽

Selenoprotein K ◽

Er Membrane

The functional activity of selenoproteins has a wide range of effects on complex pathogenetic processes, including teratogenesis, immuno-inflammatory, neurodegenerative. Being active participants and promoters of many signaling pathways, selenoproteins support the lively interest of a wide scientific community. This review is devoted to the analysis of recent data describing the participation of selenoproteins in various molecular interactions mediating important signaling pathways. Data processing was carried out by the method of complex analysis. For convenience, all selenoproteins were divided into groups depending on their location and function. Among the group of selenoproteins of the ER membrane, selenoprotein N affects the absorption of Ca2+ by the endoplasmic reticulum mediated by oxidoreductin (ERO1), a key player in the CHOP/ERO1 branch, a pathogenic mechanism that causes myopathy. Another selenoprotein of the ER membrane selenoprotein K binding to the DHHC6 protein affects the IP3R receptor that regulates Ca2+ flux. Selenoprotein K is able to affect another protein of the endoplasmic reticulum CHERP, also appearing in Ca2+ transport. Selenoprotein S, associated with the lumen of ER, is able to influence the VCP protein, which ensures the incorporation of selenoprotein K into the ER membrane. Selenoprotein M, as an ER lumen protein, affects the phosphorylation of STAT3 by leptin, which confirms that Sel M is a positive regulator of leptin signaling. Selenoprotein S also related to luminal selenoproteins ER is a modulator of the IRE1α-sXBP1 signaling pathway. Nuclear selenoprotein H will directly affect the suppressor of malignant tumours, p53 protein, the activation of which increases with Sel H deficiency. The same selenoprotein is involved in redox regulation. Among the cytoplasmic selenoproteins, abundant investigations are devoted to SelP, which affects the PI3K/Akt/Erk signaling pathway during ischemia/reperfusion, is transported into the myoblasts through the plasmalemma after binding to the apoER2 receptor, and into the neurons to the megaline receptor and in general, selenoprotein P plays the role of a pool that stores the necessary trace element and releases it, if necessary, for vital selenoproteins. The thioredoxin reductase family plays a key role in the invasion and metastasis of salivary adenoid cystic carcinoma through the influence on the TGF-β-Akt/GSK-3β pathway during epithelial-mesenchymal transition. The deletion of thioredoxin reductase 1 affects the levels of messengers of the Wnt/β-catenin signaling pathway. No less studied is the glutathione peroxidase group, of which GPX3 is able to inhibit signaling in the Wnt/β-catenin pathway and thereby inhibit thyroid metastasis, as well as suppress protein levels in the PI3K/Akt/c-fos pathway. A key observation is that in cases of carcinogenesis, a decrease in GPX3 and its hypermethylation are almost always found. Among deiodinases, deiodinase 3 acts as a promoter of the oncogenes BRAF, MEK or p38, while stimulating a decrease in the expression of cyclin D1. The dependence of the level of deiodinase 3 on the Hedgehog (SHH) signaling pathway is also noted. Methionine sulfoxide reductase A can compete for the uptake of ubiquitin, reduce p38, JNK and ERK promoters of the MAPK signaling pathway; methionine sulfoxide reductase B1 suppresses MAPK signaling messengers, and also increases PARP and caspase 3.

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Therapeutic mechanism of Toujie Quwen granules in COVID-19 based on network pharmacology

BioData Mining ◽

10.1186/s13040-020-00225-8 ◽

2020 ◽

Vol 13 (1) ◽

Author(s):

Ying Huang ◽

Wen-jiang Zheng ◽

Yong-shi Ni ◽

Mian-sha Li ◽

Jian-kun Chen ◽

...

Keyword(s):

Chinese Medicine ◽

Signaling Pathways ◽

Signaling Pathway ◽

Mapk Signaling ◽

Venn Diagram ◽

Network Pharmacology ◽

Active Ingredients ◽

Integrated Network ◽

Therapeutic Mechanism ◽

The World

Abstract Background Chinese medicine Toujie Quwen granule (TJQW) has proven to be effective in the treatment of mild coronavirus disease 2019 (COVID-19) cases by relieving symptoms, slowing the progression of the disease, and boosting the recovery of patients. But the bioactive compounds and potential mechanisms of TJQW for COVID-19 prevention and treatment are unclear. This study aimed to explore the potential therapeutic mechanism of TJQW in coronavirus disease 2019 (COVID-19) based on an integrated network pharmacology approach. Methods TCMSP were used to search and screen the active ingredients in TJQW. The Swiss TargetPrediction was used to predict the potential targets of active ingredients. Genes co-expressed with ACE2 were considered potential therapeutic targets on COVID-19. Venn diagram was created to show correlative targets of TJQW against COVID-19. Cytoscape was used to construct a “drug-active ingredient-potential target” network, STRING were used to construct protein-protein interaction network, and cytoHubba performed network topology analysis. Enrichment of biological functions and signaling pathways of core targets was performed by using the clusterProfiler package in R software and ClueGO with CluePedia plugins in Cytoscape. Results A total of 156 active ingredients were obtained through oral bioavailability and drug-likeness screenings. Two hundred twenty-seven potential targets of TJQW were related to COVID-19. The top ten core targets are EGFR, CASP3, STAT3, ESR1, FPR2, F2, BCL2L1, BDKRB2, MPO, and ACE. Based on that, we obtained 19 key active ingredients: umbelliprenin, quercetin, kaempferol, luteolin, praeruptorin E, stigmasterol, and oroxylin A. And the enrichment analysis obtained multiple related gene ontology functions and signaling pathways. Lastly, we constructed a key network of “drug-component-target-biological process-signaling pathway”. Our findings suggested that TJQW treatment for COVID-19 was associated with elevation of immunity and suppression of inflammatory stress, including regulation of inflammatory response, viral process, neutrophil mediated immunity, PI3K-Akt signaling pathway, MAPK signaling pathway, Jak-STAT signaling pathway, Complement and coagulation cascades, and HIF-1 signaling pathway. Conclusions Our study uncovered the pharmacological mechanism underlying TJQW treatment for COVID-19. These results should benefit efforts for people around the world to gain more knowledge about Chinese medicine TJQW in the treatment of this vicious epidemic COVID-19, and help to address this pressing problem currently facing the world.

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Identification and Characterization of MAPK Signaling Pathway Genes and Associated lncRNAs in the Ileum of Piglets Infected by Clostridium perfringens Type C

BioMed Research International ◽

10.1155/2020/8496872 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12

Author(s):

Ruirui Luo ◽

Xiaoyu Huang ◽

Zunqiang Yan ◽

Xiaoli Gao ◽

Pengfei Wang ◽

...

Keyword(s):

Signaling Pathway ◽

Clostridium Perfringens ◽

Expression Patterns ◽

Strong Support ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Differentially Expressed ◽

Economic Losses ◽

Sequencing Data ◽

Type C

Clostridium perfringens type C (C. perfringens type C) is one of the main microbial pathogens responsible for piglet diarrhea worldwide, causing substantial economic losses for pig-rearing industries. The mitogen-activated protein kinase (MAPK) signaling pathway is a key regulator of inflammatory bowel disease, especially necrotic enteritis. However, whether and how the MAPK signaling pathway is involved in regulating the process of piglet diarrhea when challenged by C. perfringens type C are still unknown. Here, we screened 38 differentially expressed genes (DEGs) in piglets’ ileum tissues experimentally infected with C. perfringens type C that were enriched in the Sus scrofa MAPK signaling pathway, based on our previous transcriptome data. Of these DEGs, 12 genes (TRAF2, MAPK8, and GADD45G, among others) were upregulated whereas 26 genes (MAPK1, TP53, and CHUK, among others) were downregulated in the infected group. Our results showed that MAPK1, TP53, MAPK8, MYC, and CHUK were in the core nodes of the PPI network. Additionally, we obtained 35 lncRNAs from the sequencing data, which could be trans-targeted to MAPK signaling pathway genes and were differentially expressed in the ileum tissues infected with C. perfringens. We used qRT-PCR to verify the expression levels of genes and lncRNAs related to the MAPK signaling pathway; their expression patterns were consistent with RNA sequencing data. Our results provide strong support for deeply exploring the role of the MAPK signaling pathway in diarrhea caused by C. perfringens type C.

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107 FVIIa Prevents the Progressive Hemorrhaging of a Brain Contusion by Protecting Microvessels Via Formation of the TF-FVIIa-FXa Complex

Neurosurgery ◽

10.1093/neuros/nyx417.107 ◽

2017 ◽

Vol 64 (CN_suppl_1) ◽

pp. 221-222

Author(s):

Qiang Yuan

Keyword(s):

Endothelial Cells ◽

Signaling Pathways ◽

Signaling Pathway ◽

Vascular Endothelial Cells ◽

Mapk Signaling ◽

Coagulation Cascade ◽

Cell Protein ◽

Vascular Endothelial ◽

Brain Contusion ◽

Microvessel Endothelial Cells

Abstract INTRODUCTION Factor VII (FVII) plays a key role in the initiation of the coagulation cascade and, in clinical situations, recombinant human activated FVII (rFVIIa) effectively prevents progressive hemorrhaging after a brain contusion. However, it remains unclear whether decreases in FVII activity directly lead to progressive hemorrhaging and, moreover, the precise mechanisms underlying this process are not yet known. METHODS Controlled cortical impact model of mouse brain contusion was used to examine whether decreased FVII activity would directly lead to the occurrence of progressive hemorrhaging in mice and whether administration of FVIIa would prevent the delayed catastrophic structural failure of microvessels and the progressive hemorrhaging of brain contusions by protecting vascular endothelial cells via formation of the ternary TF FVIIa FXa complex. Activations of p44/42 MAPK, p38 MAPK, and p65 NF-kB signaling pathways by ternary TF FVIIa FXa complex were tested by WB in HUVECs. RESULTS >The present study demonstrated that decreased FVII activity directly led to progressive hemorrhaging of the cerebral contusions. Administration of FVII prevented the progression of hemorrhaging from cerebral contusions by protecting microvessel endothelial cells in the penumbra of the contusion. The present study also showed that the ternary TF FVIIa FXa complex cleaved endogenous protease-activated receptor 2 (PAR2) on endothelial cells, activated the p44/42 mitogen-activated protein kinase (MAPK) signaling cascade, and inhibited p65 nuclear factor-kB (NF-kB) signaling. Furthermore, exposure to ternary TF FVIIa FXa protected endothelial cells from thrombin- or inflammatory cytokine-induced apoptosis. Although activation of the p44/42 MAPK signaling pathway is endothelial cell protein C receptor (EPCR)-dependent, inhibition of the p65 NF-kB signaling pathway is EPCR independent; thus, the regulation mechanism underlying the effects of TF FVIIa FXa in vascular endothelial cells appears to be multiple signaling pathways. CONCLUSION In summary, the present findings demonstrated that FVIIa prevented the progressive hemorrhaging of brain contusions by protecting microvessel endothelial cells via the formation of the ternary TF FVIIa FXa complex. These findings are novel and of great clinical significance because FVIIa is used to prevent the progressive hemorrhaging of brain contusions in humans.

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Extracellular volume fraction measurement correlates with lymphocyte abundance in thymic epithelial tumors

Cancer Imaging ◽

10.1186/s40644-020-00349-4 ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

Chao-Chun Chang ◽

Chia-Ying Lin ◽

Chang-Yao Chu ◽

Yi-Cheng Hsiung ◽

Ming-Tsung Chuang ◽

...

Keyword(s):

T1 Mapping ◽

Thymic Carcinoma ◽

Volume Fraction ◽

Extracellular Volume ◽

Quantitative Mri ◽

Low Grade ◽

Epithelial Tumor ◽

Thymic Epithelial Tumors ◽

Epithelial Tumors ◽

Thymic Epithelial Tumor

Abstract Background Recent advance in tissue characterization with parametric mapping imaging has the potential to be a novel biomarker for histopathologic correlation with thymic epithelial tumors (TETs). The purpose of our study is to evaluate MRI T1 mapping with the calculation of extracellular volume (ECV) fraction for histologic correlation with thymic epithelial tumor based on lymphocyte abundance. Methods A retrospective study including 31 consecutive patients (14 men and 17 women, median age, 56 years; interquartile range, 12 years) with TETs was performed. The T1 values and ECV were assessed by using quantitative MRI mapping techniques. Mann-Whitney U test, Kruskal-Wallis H test, and receiver operating characteristic curve analyses were used to assess discrimination between different types of TETs based on lymphocyte abundance. Results Extracellular volume was significantly higher in TETs with sparse lymphocyte, including type A, type B3, and thymic carcinoma, compared with those with abundant lymphocyte, including type B1, B2, and AB thymomas (42.5% vs 26.9%, respectively; p < 0.001). Extracellular volume was significantly higher in thymic carcinoma compared with low grade and high grade thymomas (48.6% vs 31.1% vs 27.6%, respectively; p = 0.002). Conclusions T1 mapping with the calculation of extracellular volume (ECV) fraction correlate with the WHO histologic classification of thymic epithelial tumor based on lymphocyte abundance.

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