International Journal of Experimental Pathology最新文献_第4页

Optimization of decellularization methods using human small intestinal submucosa for scaffold generation in regenerative medicine 人小肠粘膜下层脱细胞制备再生医学支架方法的优化。

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-08-25 DOI: 10.1111/iep.12492

Shumei Mineta, Shunji Endo, Tomio Ueno

{"title":"Optimization of decellularization methods using human small intestinal submucosa for scaffold generation in regenerative medicine","authors":"Shumei Mineta, Shunji Endo, Tomio Ueno","doi":"10.1111/iep.12492","DOIUrl":"10.1111/iep.12492","url":null,"abstract":"Porcine small intestinal submucosa, despite its successful use as a scaffold in regenerative medicine, has innate biomechanical heterogeneity. In this study, we hypothesized that human small intestinal submucosa could be a viable alternative bio-scaffold. For the first time, we characterize submucosal extraction from human small intestine and examine appropriate decellularization methods. In total, 16 human small intestinal submucosal samples were obtained and decellularized using three reported methods of porcine decellularization: Abraham, Badylak, and Luo. For each method, four specimens were decellularized. The remaining four specimens were designated as non-decellularized. We measured the amount of residual DNA and growth factors in decellularized human intestinal samples. Additionally, decellularized human small intestinal submucosa was co-cultured with mouse bone marrow-derived mesenchymal stem cells to examine mesenchymal stem cell survival and proliferation. The reference value for the amount of residual DNA deemed appropriate in decellularized tissue was established as 50 ng/mg of extracellular matrix dry weight or less. Abraham's method most successfully met this criterion. Measurement of residual growth factors revealed low levels observed in samples decellularized using the Abraham and Badylak methods. Co-culture of each small intestinal submucosal sample with mouse bone marrow-derived mesenchymal stem cells confirmed viable cell survival and proliferation in samples derived using protocols by Abraham and Badylak. Abraham's method most successfully met the criteria for efficient tissue decellularization and cell viability and proliferation. Thus, we consider this method most suitable for decellularization of human small intestinal submucosa.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 6","pages":"313-320"},"PeriodicalIF":3.0,"publicationDate":"2023-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10071861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Panx1 knockout promotes preneoplastic aberrant crypt foci development in a chemically induced model of mouse colon carcinogenesis 在化学诱导的小鼠结肠癌模型中，Panx1基因敲除促进肿瘤前异常隐窝灶的发展。

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-08-18 DOI: 10.1111/iep.12491

Sara Gomes Espírito Santo, Tereza Cristina Da Silva, Bruno Cogliati, Luís Fernando Barbisan, Guilherme Ribeiro Romualdo

{"title":"Panx1 knockout promotes preneoplastic aberrant crypt foci development in a chemically induced model of mouse colon carcinogenesis","authors":"Sara Gomes Espírito Santo, Tereza Cristina Da Silva, Bruno Cogliati, Luís Fernando Barbisan, Guilherme Ribeiro Romualdo","doi":"10.1111/iep.12491","DOIUrl":"10.1111/iep.12491","url":null,"abstract":"Colorectal cancer, which is the third leading cause of cancer-related deaths worldwide, is a multistep disease, featuring preneoplastic aberrant crypt foci (ACF) as the early morphological manifestation. The roles of hemichannel-forming transmembrane Pannexin 1 (Panx1) protein have not been investigated in the context of colon carcinogenesis yet, although it has contrasting roles in other cancer types. Thus, this study was conducted to examine the effects of Panx1 knockout (Panx1−/−) on the early events of chemically induced colon carcinogenesis in mouse. Wild type (WT) and Panx1−/− female C57BL6J mice were submitted to a chemically induced model of colon carcinogenesis by receiving six intraperitoneal administrations of 1,2-dimethylhydrazine (DMH) carcinogen. Animals were euthanized 8 h (week 7) or 30 weeks (week 37) after the last DMH administration in order to evaluate sub-acute colon toxicity outcomes or the burden of ACF, respectively. At week 7, Panx1 genetic ablation increased DMH-induced genotoxicity in peripheral blood cells, malondialdehyde levels in the colon, and apoptosis (cleaved caspase-3) in colonic crypts. Of note, at week 37, Panx1−/− animals showed an increase in aberrant crypts (AC), ACF mean number, and ACF multiplicity (AC per ACF) by 56%, 57% and 20%, respectively. In essence, our findings indicate that Panx1 genetic ablation promotes preneoplastic ACF development during chemically induced mouse colon carcinogenesis, and a protective role of Panx1 is postulated.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 6","pages":"304-312"},"PeriodicalIF":3.0,"publicationDate":"2023-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10396749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nek6 knockdown polarized macrophages into a pro-inflammatory phenotype via inhibiting STAT3 expression 通过抑制STAT3的表达，Nek6敲低极化巨噬细胞进入促炎表型

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-07-10 DOI: 10.1111/iep.12489

Xiaoyan Wu, Ke-Qiong Deng, Huan-Huan Cai, Ziyue Zeng, Jian-Lei Cao, Lin Zhang, Zhibing Lu, Wen-Lin Cheng

{"title":"Nek6 knockdown polarized macrophages into a pro-inflammatory phenotype via inhibiting STAT3 expression","authors":"Xiaoyan Wu, Ke-Qiong Deng, Huan-Huan Cai, Ziyue Zeng, Jian-Lei Cao, Lin Zhang, Zhibing Lu, Wen-Lin Cheng","doi":"10.1111/iep.12489","DOIUrl":"10.1111/iep.12489","url":null,"abstract":"Recently macrophage polarization has emerged as playing an essential role in the oathogenesis of atherosclerosis, which is the most important underlying process in many types of cardiovascular diseases. Although Nek6 has been reported to be involved in various cellular processes, the effect of Nek6 on macrophage polarization remains unknown. Macrophages exposed to lipopolysaccharide (LPS) or IL-4 were used to establish an in vitro model for the study of regulation of classically (M1) or alternatively (M2) activated macrophage. Bone marrow-derived macrophages (BMDMs) transfected with short hairpin RNA-targeting Nek6 were then in functional studies. We observed that Nek6 expression was decreased in both peritoneal macrophages (PMs) and BMDMs stimulated by LPS. This effect was seen at both mRNA and protein level. The opposite results were obtained after administration of IL-4. Macrophage-specific Nek6 knockdown significantly exacerbated pro-inflammatory M1 polarized macrophage gene expression in response to LPS challenge, but the anti-inflammatory response gene expression that is related to M2 macrophages was attenuated by Nek6 silencing followed by treatment with IL-4. Mechanistic studies exhibited that Nek6 knockdown inhibited the phosphorylated STAT3 expression that mediated the effect on macrophage polarization regulated by AdshNek6. Moreover, decreased Nek6 expression was also observed in atherosclerotic plaques. Collectively, these evidences suggested that Nek6 acts as a crucial site in macrophage polarization, and that this operates in a STAT3-dependent manner.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 5","pages":"237-246"},"PeriodicalIF":3.0,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12489","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10256930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model mRNA表达谱揭示了实验性自身免疫性脑脊髓炎模型脾细胞中差异表达的基因

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-07-10 DOI: 10.1111/iep.12488

Arshad Mehmood, Shuang Song, Xiaochen Du, Hongjing Yan, Xuan Wang, Li Guo, Bin Li

{"title":"mRNA expression profile reveals differentially expressed genes in splenocytes of experimental autoimmune encephalomyelitis model","authors":"Arshad Mehmood, Shuang Song, Xiaochen Du, Hongjing Yan, Xuan Wang, Li Guo, Bin Li","doi":"10.1111/iep.12488","DOIUrl":"10.1111/iep.12488","url":null,"abstract":"Experimental autoimmune encephalomyelitis (EAE) is a mouse model that can be used to investigate aetiology, pathogenesis, and treatment approaches for multiple sclerosis (MS). A novel integrated bioinformatics approach was used to understand the involvement of differentially expressed genes (DEGs) in the spleen of EAE mice through data mining of existing microarray and RNA-seq datasets. We screened differentially expressed mRNAs using mRNA expression profile data of EAE spleens taken from Gene Expression Omnibus (GEO). Functional and pathway enrichment analyses of DEGs were performed by Database for Annotation, Visualization, and Integrated Discovery (DAVID). Subsequently, the DEGs-encoded protein–protein interaction (PPI) network was constructed. The 784 DEGs in GSE99300 A.SW PP-EAE mice spleen mRNA profiles, 859 DEGs in GSE151701 EAE mice spleen mRNA profiles, and 646 DEGs in GSE99300 SJL/J PP-EAE mice spleen mRNA profiles were explored. Functional enrichment of 55 common DEGs among 3 sub-datasets revealed several immune-related terms, such as neutrophil extravasation, leucocyte migration, antimicrobial humoral immune response mediated by an antimicrobial peptide, toll-like receptor 4 bindings, IL-17 signalling pathway, and TGF-beta signalling pathway. In the screening of 10 hub genes, including MPO, ELANE, CTSG, LTF, LCN2, SELP, CAMP, S100A9, ITGA2B, and PRTN3, and in choosing and validating the 5 DEGs, including ANK1, MBOAT2, SLC25A21, SLC43A1, and SOX6, the results showed that SLC43A1 and SOX6 were significantly decreased in EAE mice spleen. Thus this study offers a list of genes expressed in the spleen that might play a key role in the pathogenesis of EAE.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 5","pages":"247-257"},"PeriodicalIF":3.0,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12488","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10256925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Mechanism of the HIF-1α/VEGF/VEGFR-2 pathway in the proliferation and apoptosis of human haemangioma endothelial cells HIF-1α/VEGF/VEGFR-2通路在人血管瘤内皮细胞增殖和凋亡中的作用机制

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-06-28 DOI: 10.1111/iep.12485

Wenpei Zhang, Lei Sun, Hongxia Gao, Shengquan Wang

{"title":"Mechanism of the HIF-1α/VEGF/VEGFR-2 pathway in the proliferation and apoptosis of human haemangioma endothelial cells","authors":"Wenpei Zhang, Lei Sun, Hongxia Gao, Shengquan Wang","doi":"10.1111/iep.12485","DOIUrl":"10.1111/iep.12485","url":null,"abstract":"Haemangiomas (HAs) are prevalent vascular endothelial cell tumours. With respect to the possible involvement of HIF-1α in HAs, we have explored its role in haemangioma endothelial cell (HemEC) proliferation and apoptosis. shRNA HIF-1α and pcDNA3.1 HIF-α were manipulated into HemECs. HIF-α, VEGF, and VEGFR-2 mRNA and protein levels were assessed by qRT-PCR and Western blotting. Cell proliferation and viability, cell cycle and apoptosis, migration and invasion, and ability to form tubular structures were assessed by colony formation assay, CCK-8, flow cytometry, Transwell assay, and tube formation assay. Cell cycle-related protein levels, and VEGF and VEGFR-2 protein interaction were detected by Western blot and immunoprecipitation assays. An Haemangioma nude mouse model was established by subcutaneous injection of HemECs. Ki67 expression was determined by immunohistochemical staining. HIF-1α silencing suppressed HemEC neoplastic behaviour and promoted apoptosis. HIF-1α facilitated VEGF/VEGFR-2 expression and the VEGF had interacted with VEGFR-2 at protein - protein level. HIF-1α silencing arrested HemECs at G0/G1 phase, diminished Cyclin D1 protein level, and elevated p53 protein level. VEGF overexpression partially abrogated the effects of HIF-1α knockdown on inhibiting HemEC malignant behaviours. Inhibiting HIF-1α in nude mice with HAs repressed tumour growth and Ki67-positive cells. Briefly, HIF-1α regulated HemEC cell cycle through VEGF/VEGFR-2, thus promoting cell proliferation and inhibiting apoptosis.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 5","pages":"258-268"},"PeriodicalIF":3.0,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12485","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10261853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A prognostic model based on regulatory T-cell-related genes in gastric cancer: Systematic construction and validation 基于调节性t细胞相关基因的胃癌预后模型:系统构建与验证

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-06-23 DOI: 10.1111/iep.12487

Qin Tong, Yingjie Ling

{"title":"A prognostic model based on regulatory T-cell-related genes in gastric cancer: Systematic construction and validation","authors":"Qin Tong, Yingjie Ling","doi":"10.1111/iep.12487","DOIUrl":"10.1111/iep.12487","url":null,"abstract":"Human gastrointestinal tumours have been shown to contain massive numbers of tumour infiltrating regulatory T cells (Tregs), the presence of which are closely related to tumour immunity. This study was designed to develop new Treg-related prognostic biomarkers to monitor the prognosis of patients with gastric cancer (GC). Treg-related prognostic genes were screened from Treg-related differentially expressed genes in GC patients by using Cox regression analysis, based on which a prognostic model was constructed. Then, combined with RiskScore, survival curve, survival status assessment and ROC analysis, these genes were used to verify the accuracy of the model, whose independent prognostic ability was also evaluated. Six Treg-related prognostic genes (CHRDL1, APOC3, NPTX1, TREML4, MCEMP1, GH2) in GC were identified, and a 6-gene Treg-related prognostic model was constructed. Survival analysis revealed that patients had a higher survival rate in the low-risk group. Combining clinicopathological features, we performed univariate and multivariate regression analyses, with results establishing that the RiskScore was an independent prognostic factor. Predicted 1-, 3- and 5-year survival rates of GC patients had a good fit with the actual survival rates according to nomogram results. In addition patients in the low-risk group had higher tumour mutational burden (TMB) values. Gene Set Enrichment Analysis (GSEA) demonstrated that genes in the high-risk group were significantly enriched in pathways related to immune inflammation, tumour proliferation and migration. In general, we constructed a 6-gene Treg-associated GC prognostic model with good prediction accuracy, where RiskScore could act as an independent prognostic factor. This model is expected to provide a reference for clinicians to estimate the prognosis of GC patients.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 5","pages":"226-236"},"PeriodicalIF":3.0,"publicationDate":"2023-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12487","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10256903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical applications of gene therapy for rare diseases: A review 基因治疗罕见病的临床应用综述

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-05-13 DOI: 10.1111/iep.12478

Ioannis Papaioannou, James S. Owen, Rafael J. Yáñez-Muñoz

{"title":"Clinical applications of gene therapy for rare diseases: A review","authors":"Ioannis Papaioannou, James S. Owen, Rafael J. Yáñez-Muñoz","doi":"10.1111/iep.12478","DOIUrl":"10.1111/iep.12478","url":null,"abstract":"Rare diseases collectively exact a high toll on society due to their sheer number and overall prevalence. Their heterogeneity, diversity, and nature pose daunting clinical challenges for both management and treatment. In this review, we discuss recent advances in clinical applications of gene therapy for rare diseases, focusing on a variety of viral and non-viral strategies. The use of adeno-associated virus (AAV) vectors is discussed in the context of Luxturna, licenced for the treatment of RPE65 deficiency in the retinal epithelium. Imlygic, a herpes virus vector licenced for the treatment of refractory metastatic melanoma, will be an example of oncolytic vectors developed against rare cancers. Yescarta and Kymriah will showcase the use of retrovirus and lentivirus vectors in the autologous ex vivo production of chimeric antigen receptor T cells (CAR-T), licenced for the treatment of refractory leukaemias and lymphomas. Similar retroviral and lentiviral technology can be applied to autologous haematopoietic stem cells, exemplified by Strimvelis and Zynteglo, licenced treatments for adenosine deaminase-severe combined immunodeficiency (ADA-SCID) and β-thalassaemia respectively. Antisense oligonucleotide technologies will be highlighted through Onpattro and Tegsedi, RNA interference drugs licenced for familial transthyretin (TTR) amyloidosis, and Spinraza, a splice-switching treatment for spinal muscular atrophy (SMA). An initial comparison of the effectiveness of AAV and oligonucleotide therapies in SMA is possible with Zolgensma, an AAV serotype 9 vector, and Spinraza. Through these examples of marketed gene therapies and gene cell therapies, we will discuss the expanding applications of such novel technologies to previously intractable rare diseases.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 4","pages":"154-176"},"PeriodicalIF":3.0,"publicationDate":"2023-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12478","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10151230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

RUNX1 promotes liver fibrosis progression through regulating TGF-β signalling RUNX1通过调节TGF-β信号传导促进肝纤维化进展

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-04-17 DOI: 10.1111/iep.12474

Zhaoyang Guo, Xinxin Liu, Shulei Zhao, Fengkai Sun, Wanhua Ren, Mingze Ma

{"title":"RUNX1 promotes liver fibrosis progression through regulating TGF-β signalling","authors":"Zhaoyang Guo, Xinxin Liu, Shulei Zhao, Fengkai Sun, Wanhua Ren, Mingze Ma","doi":"10.1111/iep.12474","DOIUrl":"10.1111/iep.12474","url":null,"abstract":"Liver fibrosis is caused by chronic liver injury. There are limited treatments for it, and the pathogenesis is unclear. Therefore, there is an urgent need to explore the pathogenesis of liver fibrosis, and to try to identify new potential therapeutic targets. For this study we used the carbon tetrachloride abdominal injection induced liver fibrosis animal model in mice. Primary hepatic stellate cell isolation was performed by a density-gradient separation method, and this was followed by immunofluorescence stain analyses. Signal pathway analysis was performed by dual-luciferase reporter assay and western blotting. Our results showed that RUNX1 was upregulated in cirrhotic liver tissues compared with normal liver tissues. Besides, overexpression of RUNX1 caused more severe liver fibrosis lesions than control group under CCl4-induced conditions. Moreover, α-SMA expression in the RUNX1 overexpression group was significantly higher than in the control group. Interestingly, we found that RUNX1 could promote the activation of TGF-β/Smads in a dual-luciferase reporter assay. Thus we demonstrated that RUNX1 could be considered as a new regulator of hepatic fibrosis by activating TGF-β/Smads signalling. Based on this, we concluded that RUNX1 may be developed as a new therapeutic target in the treatment of liver fibrosis in the future. In addition, this study also provides a new insight about the aetiology of liver fibrosis.","PeriodicalId":14157,"journal":{"name":"International Journal of Experimental Pathology","volume":"104 4","pages":"188-198"},"PeriodicalIF":3.0,"publicationDate":"2023-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/iep.12474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Abnormal expression and role of MicroRNA-214-3p/SLC8A1 in neonatal Hypoxic-Ischaemic encephalopathy MicroRNA-214-3p/SLC8A1在新生儿缺氧缺血性脑病中的异常表达及其作用

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-04-09 DOI: 10.1111/iep.12475

Liu Yang, Li Zhang, Jing Zhu, Yuqian Wang, Ning Zou, Zhengjuan Liu, Yingjie Wang

引用次数: 1

High density of FOXP3 predicts better prognosis in germinal and non-germinal centre diffuse large B-cell lymphoma FOXP3的高密度预示着生发和非生发中心弥漫性大b细胞淋巴瘤更好的预后

IF 3 4区医学

International Journal of Experimental Pathology Pub Date : 2023-03-28 DOI: 10.1111/iep.12477

Asmaa M. Ahmed, Sally S. Abdel-Hakeem, Maged A. F. Amine, Etemad H. Yassin, Fatma A. M. Badary

引用次数: 0