Current molecular medicine最新文献

{"title":"CCN3/NOV Serum Levels in Non-Alcoholic Fatty Liver Disease (NAFLD) Patients in Comparison with the Healthy Group and their Correlation with TNF-α and IL-6.","authors":"Reza Afrisham, Ghazal Alasvand, Yasaman Jadidi, Vida Farrokhi, Reza Fadaei, Shaban Alizadeh, Nariman Moradi","doi":"10.2174/0115665240285539240214111947","DOIUrl":"https://doi.org/10.2174/0115665240285539240214111947","url":null,"abstract":"<p><strong>Introduction: </strong>Adipokine irregularity leads to inflammation, endothelial dysfunction, insulin resistance (IR), and Non-Alcoholic Fatty Liver Disease (NAFLD). Previous studies linked NOV/CCN3 to obesity, IR, and inflammation, but no research has explored the connection between CCN3 serum levels and NAFLD.</p><p><strong>Methods: </strong>This case-control study assessed CCN3, IL-6, adiponectin, and TNF-α serum levels in 80 NAFLD patients and 80 controls using ELISA kits. Biochemical parameters were measured with commercial kits and an auto analyzer.</p><p><strong>Results: </strong>NAFLD patients exhibited significantly higher CCN3 (2399.85 ± 744.53 vs. 1712.84 ± 478.19 ng/ml), TNF-α, and IL-6 levels, and lower adiponectin levels compared to controls (P<0.0001). In the NAFLD group, CCN3 showed positive correlations with FBG, insulin, HOMA-IR, and TNF-α. Binary logistic regression analysis revealed increased NAFLD risk in the adjusted model (OR [95% CI] = 1.220 [1.315 -1.131]). A CCN3 cut-off value of 1898.0050 pg/mL differentiated NAFLD patients from controls with 78.8% sensitivity and 73.2% specificity.</p><p><strong>Conclusion: </strong>It was found that elevated CCN3 serum levels directly correlate with NAFLD incidence and inflammation markers (IL-6 and TNF-α). CCN3 could serve as a potential biomarker for NAFLD, but further research is needed to validate this finding and assess its clinical utility.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982600","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}

{"title":"Metabolic Derangement in Non-Alcoholic Fatty Liver Disease: Opportunities for Early Diagnostic and Prognostic Markers.","authors":"Verma Abhinav, Rishabh Mittal, Mathiyazhagan Navaneethakannan, Ahirwar Sonu Singh, Mukherjee Sukhes, Kotnis Ashwin","doi":"10.2174/0115665240269082240213115711","DOIUrl":"https://doi.org/10.2174/0115665240269082240213115711","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease is a globally prevalent disorder that can rapidly progress if not detected early. Currently, no accepted markers exist for early diagnosis and prognosis of NAFLD. This review describes derangement in major metabolic pathways of lipid, carbohydrate, and amino acids in NAFLD. It suggests that measuring levels of thrombospondin, TyG index, asymmetric dimethylarginine, LAL-A, GLP-1, FGF-21, and GSG index are potential markers for early diagnosis of NAFLD. A single marker may not indicate early NAFLD, and further large-scale studies on correlating levels of Thrombospondin-2, triglyceride-glucose index, and FGF-21 with NAFLD are warranted.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971302","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}

{"title":"A Systematic Review of the Impact of Resveratrol on Viral Hepatitis and Chronic Viral Hepatitis-related Hepatocellular Carcinoma.","authors":"Mohammad Darvishi, Majid Nouri, Rasoul Rahimi, Saeid Heidari-Soureshjani, Seyed Mahmood Reza Hashemi Rafsanjani","doi":"10.2174/0115665240284347240125072555","DOIUrl":"https://doi.org/10.2174/0115665240284347240125072555","url":null,"abstract":"<p><strong>Background: </strong>Resveratrol (RSV) is used for the treatment of various diseases due to their anti-inflammatory and antioxidant activities. However, its beneficial aspects on viral hepatitis have been less investigated.</p><p><strong>Objective: </strong>This report reviews the impact of resveratrol on viral hepatitis and chronic viral hepatitis-related hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>The systematic review was performed and reported according to the PRISMA 2020 statement. Several core databases, such as Cochrane Library, PubMed, Web of Science, EMBASE, and Scopus, were used for search on September 6, 2023. After extraction of the data, the desired information of the full text of the studies was recorded in Excel, and the outcomes and mechanisms were reviewed.</p><p><strong>Results: </strong>RSV inhibits viral replication through anti-HCV NS3 helicase activity, maintains redox homeostasis via glutathione (GSH) synthesis, improves T and B cell activity, and suppresses miR-155 expression. It also enhances viral replication by enhancing hepatitis C virus (HCV) RNA transcription, activating sirtuin-1 (SIRT1), which can increase peroxisome proliferator-activated receptor (PPAR), and SIRT1 activates the HBV X protein (HBx). Moreover, RSV is responsible for hepatitis-related HCC proliferation via suppression of mammalian target of rapamycin (mTOR), SIRT1 up-regulation, inhibiting expression of HBx, and reducing expression of cyclin D1.</p><p><strong>Conclusion: </strong>Despite the promising properties of RSV in inhibiting hepatitis-related HCC cell proliferation, its antiviral effects in viral hepatitis are controversial. The antihepatitis behaviors of RSV are mainly dose-dependent, and in some studies, activating some hepatoprotective pathways increases the transcription and replication of chronic HBV and HCV. Therefore, healthcare providers should be aware of viral hepatitis before using RSV supplements.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905282","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}

{"title":"Anti-Cancer and Anti-Oxidant Effects of Fenoferin-loaded Human Serum Albumin Nanoparticles Coated with Folic Acid-bound Chitosan.","authors":"Methaq Abid Said Klmohamed Almusawi, Vahid Pouresmaeil, Masoud Homayouni Tabrizi","doi":"10.2174/0115665240283529240202095254","DOIUrl":"https://doi.org/10.2174/0115665240283529240202095254","url":null,"abstract":"<p><strong>Background: </strong>Several diseases, including cancer, can be effectively treated by altering the nanocarrier surfaces so that they are more likely to be targeted.</p><p><strong>Objective: </strong>This study aimed to prepare human albumin (HSA) nanoparticles containing Fenoferin (FN) modified with folic acid (FA) attached to Chitosan (CS) to improve its anti-cancer properties.</p><p><strong>Methods: </strong>Nanoparticles were first synthesized and surface modified. Their physicochemical properties were assessed by different methods, such as FESEM, FTIR, and DLS. In addition, the percentage of drug encapsulated was measured by indirect method. Besides evaluating the cytotoxic effects of nanoparticles using the MTT assay, the antioxidant capacity of FN-HSA-CS-FA was assessed using the ABTS and DPPH methods. Nanoparticles were also investigated for their anti-cancer effects by evaluating the expression of apoptosis and metastasis genes.</p><p><strong>Results: </strong>Based on this study, FN-HSA-CS-FA was 165.46 nm in size, and a uniform dispersion distribution was identified. Particles were reported to have a zeta potential of +29 mV, which is within the range of stable nanoparticles. Approximately 75% of FN is encapsulated in nanoparticles. Cytotoxic assay determined that liver cancer cells were most sensitive to treatment with an IC50 of 144 μg/ml. Inhibition of free radicals by nanoparticles is estimated to have an IC50 value of 195.23 and 964 μg/ml, for ABTS and DPPH, respectively. In the treatment with nanoparticles, flow cytometry results of arresting the cells in the SubG1 phase and real-time qPCR results indicated increased expression of caspases-3, caspase-8, and caspase-9 genes.</p><p><strong>Conclusion: </strong>According to this study, synthesized nanoparticles inhibited free radicals and activated apoptosis in liver cancer cells, and the capability of these nanoparticles to inhibit cancer cells was also confirmed. This formulation can, therefore, be used in preclinical studies to test the efficacy of the drug.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905283","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}

{"title":"Neferine Targeted the NLRC5/NLRP3 Pathway to Inhibit M1-type Polarization and Pyroptosis of Macrophages to Improve Hyperuricemic Nephropathy.","authors":"Wei Yin, Jin-Hua Wang, Yu-Mei Liang, Kang-Han Liu, Ying Chen, Yusa Chen","doi":"10.2174/0115665240272051240122074511","DOIUrl":"https://doi.org/10.2174/0115665240272051240122074511","url":null,"abstract":"<p><strong>Background: </strong>Neferine (Nef) has a renal protective effect. This research intended to explore the impact of Nef on hyperuricemic nephropathy (HN).</p><p><strong>Methods: </strong>Adenine and potassium oxonate were administered to SD rats to induce the HN model. Bone marrow macrophages (BMDM) and NRK-52E were used to construct a transwell co-culture system. The polarization of BMDM and apoptosis levels were detected using immunofluorescence and flow cytometry. Renal pathological changes were detected using hematoxylin-eosin (HE) and Masson staining. Biochemical methods were adopted to detect serum in rats. CCK-8 and EDU staining were used to assess cell activity and proliferation. RT-qPCR and western blot were adopted to detect NLRC5, NLRP3, pyroptosis, proliferation, and apoptosis-related factor levels.</p><p><strong>Results: </strong>After Nef treatment, renal injury and fibrosis in HN rats were inhibited, and UA concentration, urinary protein, BUN, and CRE levels were decreased. After Nef intervention, M1 markers, pyroptosis-related factors, and NLRC5 levels in BMDM stimulated with uric acid (UA) treatment were decreased. Meanwhile, the proliferation level of NRK-52E cells co-cultured with UA-treated BMDM was increased, but the apoptosis level was decreased. After NLRC5 overexpression, Nef-induced regulation was reversed, accompanied by increased NLRP3 levels. After NLRP3 was knocked down, the levels of M1-type markers and pyroptosis-related factors were reduced in BMDM.</p><p><strong>Conclusion: </strong>Nef improved HN by inhibiting macrophages polarized to M1-type and pyroptosis by targeting the NLRC5/NLRP3 pathway. This research provides a scientific theoretical basis for the treatment of HN.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140317870","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}

{"title":"Explore on the Mechanism of miRNA-146a/TAB1 in the Regulation of Cellular Apoptosis and Inflammation in Ulcerative Colitis Based on NF-κB Pathway.","authors":"Xiaoying Xia, Qian Yang, Xue Han, Yulin Du, Shujun Guo, Mengqing Hua, Fang Fang, Zhigang Ma, Hua Ma, Hui Yuan, Wenjing Tian, Zebang Ding, Yanan Duan, Qi Huo, Yao Li","doi":"10.2174/0115665240273807231122052445","DOIUrl":"https://doi.org/10.2174/0115665240273807231122052445","url":null,"abstract":"<p><strong>Objective: </strong>Ulcerative colitis (UC) is a chronic non-specific inflammatory disease of the rectum and colon with unknown etiology. A growing number of evidence suggest that the pathogenesis of UC is related to excessive apoptosis and production of inflammatory cytokines. However, the functions and molecular mechanisms associated with UC remain unclear.</p><p><strong>Materials and methods: </strong>The in vivo and in vitro models of UC were established in this study. MiRNA or gene expression was measured by qRT-PCR assay. ELISA, CCK-8, TUNEL, and flow cytometry assays were applied for analyzing cellular functions. The interactions between miR-146a and TAB1 were verified by luciferase reporter and miRNA pull-down assays.</p><p><strong>Results: </strong>MiR-146a was obviously increased in UC patients, DSS-induced colitis mice, and TNF-ɑ-induced YAMC cells, when compared to the corresponding controls. MiR- 146a knockdown inhibited the inflammatory response and apoptosis in DSS-induced colitis mice and TNF-ɑ-induced YAMC cells. Mechanistically, we found that TAB1 was the target of miR-146a and miR-146a knockdown suppressed the activation of NF-κB pathway in UC. More importantly, TAB1 could overturn the inhibitory effect of antagomiR-146a on cell apoptosis and inflammation in UC.</p><p><strong>Conclusion: </strong>MiR-146a knockdown inhibited cell apoptosis and inflammation via targeting TAB1 and suppressing NF-κB pathway, suggesting that miR-146a may be a new therapeutic target for UC treatment.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722002","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}

{"title":"Targeting Ubiquitin-specific Protease 5 Overcomes Chemoresistance via Negatively Regulating p53 in Gastric Cancer.","authors":"Jing Song, Lei Liu, Fang Wang, Di Bao","doi":"10.2174/0115665240278762240202103722","DOIUrl":"https://doi.org/10.2174/0115665240278762240202103722","url":null,"abstract":"<p><strong>Background: </strong>Resistance to chemotherapy is a major obstacle in the clinical management of gastric cancer, and the mechanisms underlying chemoresistance remain largely unknown.</p><p><strong>Aims: </strong>This study aimed to investigate the involvement of ubiquitin-specific protease 5 (USP5), a deubiquitinating enzyme, in gastric cancer chemoresistance Methods: USP5 expression was analyzed in fifty paired gastric cancer and adjacent normal tissues, chemo-sensitive and chemo-resistant gastric cancer lines using quantitative ELISA. The role of USP5 was determined using loss-of-function and gainof- function methods. USP5-mediated downstream effectors were analyzed using biochemical methods focusing on p53.</p><p><strong>Results: </strong>USP5 expression was comparable in tumors and normal in the majority of the cohort. Following chemotherapy treatment, USP5 expression significantly increased in gastric cancer cells, while p53 levels remained unaltered. Overexpression of USP5 amplified growth and migration while decreasing apoptosis induced by serum withdrawal across multiple gastric cancer cell lines. Conversely, USP5 knockdown effectively heightened gastric cancer sensitivity to paclitaxel and 5-FU treatments, particularly targeting chemo-resistant gastric cancer cells by inhibiting proliferation and migration and inducing apoptosis. Additionally, USP5 knockdown increased levels of p53 but not MDM2, increased p53 activity and increased transcription of p53 target genes. In contrast, USP5 overexpression decreased the level and activity of p53 and inhibited transcription of p53 target genes. The anti-proliferative, anti-migratory, and pro-apoptotic effects of USP5 were significantly diminished upon p53 depletion, highlighting the interplay between p53 and USP5 in regulating gastric cancer cell activities. Additionally, USP5 inhibition suppressed chemo-resistant gastric cancer cell migration via suppressing epithelial-mesenchymal transition (EMT) and RhoA activity.</p><p><strong>Conclusion: </strong>Targeting USP5 inhibition has emerged as a promising alternative therapeutic approach to overcoming chemoresistance in gastric cancer. Additionally, our study sheds light on the novel role of USP5 as a regulator of p53 in gastric cancer.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722003","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}

{"title":"Exosomes Derived from Astragaloside IV-pretreated Endothelial Progenitor Cells (AS-IV-Exos) Alleviated Endothelial Oxidative Stress and Dysfunction Via the miR-210/ Nox2/ROS Pathway.","authors":"Wu Xiong, Xi Zhang, Xiao-Ling Zou, Sai Peng, Hua-Juan Lei, Xiang-Nan Liu, Lan Zhao, Zi-Xin Huang","doi":"10.2174/0115665240262982240109104620","DOIUrl":"https://doi.org/10.2174/0115665240262982240109104620","url":null,"abstract":"<p><strong>Background: </strong>Chronic hyperglycemia in diabetes induces oxidative stress, leading to damage to the vascular system. In this study, we aimed to evaluate the effects and mechanisms of AS-IV-Exos in alleviating endothelial oxidative stress and dysfunction caused by high glucose (HG).</p><p><strong>Methods: </strong>Histopathological changes were observed using HE staining, and CD31 expression was assessed through immunohistochemistry (IHC). Cell proliferation was evaluated through CCK8 and EDU assays. The levels of ROS, SOD, and GSH-Px in the skin tissues of each group were measured using ELISA. Cell adhesion, migration, and tube formation abilities were assessed using adhesion, Transwell, and tube formation experiments. ROS levels in HUVEC cells were measured using flow cytometry. The levels of miR-210 and Nox2 were determined through quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The expression of Nox2, SOD, GSH-Px, CD63, and CD81 was confirmed using WB.</p><p><strong>Results: </strong>The level of miR-210 was reduced in diabetes-induced skin damage, while the levels of Nox2 and ROS increased. Treatment with AS-IV increased the level of miR-210 in EPC-Exos. Compared to Exos, AS-IV-Exos significantly reduced the proliferation rate, adhesion number, migration speed, and tube-forming ability of HGdamaged HUVEC cells. AS-IV-Exos also significantly decreased the levels of SOD and GSH-Px in HG-treated HUVEC cells and reduced the levels of Nox2 and GSH-Px. However, ROS levels and Nox2 could reverse this effect.</p><p><strong>Conclusion: </strong>AS-IV-Exos effectively alleviated endothelial oxidative stress and dysfunction induced by HG through the miR-210/Nox2/ROS pathway.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650466","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}

{"title":"Advances in Monoclonal Antibody Therapies for Triple-Negative Breast Cancer: Immunotherapeutic and Targeted Strategies.","authors":"Amirreza Khalaji, Sara Hadad, Amirreza Jabbaripour Sarmadian, Fatemeh Ojaghlou, Elham Mohebi Janagard, Behzad Baradaran","doi":"10.2174/0115665240287767240115062343","DOIUrl":"10.2174/0115665240287767240115062343","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) presents considerable obstacles because of its highly aggressive characteristics and limited availability of specific therapeutic interventions. The utilization of monoclonal antibody (mAb)-based immunotherapy is a viable approach to tackle these difficulties. This review aims to examine the present state of mAb-based immunotherapy in TNBC, focusing on the underlying mechanisms of action, clinical applications, and existing challenges. The effectiveness of mAbs in reducing tumor development, regulating immune responses, and changing the tumor microenvironment has been demonstrated in many clinical investigations. The challenges encompass several aspects such as the discovery of biomarkers, understanding resistance mechanisms, managing toxicity, considering costs, and ensuring accessibility. The future is poised to bring forth significant advancements in the field of biomedicine, particularly in the areas of new mAbs, personalized medicine, and precision immunotherapy. In conclusion, mAb-based immunotherapy has promise in revolutionizing the treatment of TNBC, hence providing a possible avenue for enhanced patient outcomes and quality of life.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139575542","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}

{"title":"Large B-cell Lymphoma with IRF4 Rearrangement in the Nasolacrimal Duct: A Clinicopathological Study of One Case and Literature Review.","authors":"Wang-Xing Chen, Jun Wu, Jian-Guo He","doi":"10.2174/0115665240272361231229122203","DOIUrl":"https://doi.org/10.2174/0115665240272361231229122203","url":null,"abstract":"<p><strong>Background: </strong>Large B-cell lymphoma (LBCL) with interferon regulatory factor 4 (IRF4) rearrangement (LBCL-IRF4) is a rare subtype of LBCL, with a high prevalence in Waldeyer's ring as well as the neck, head and gastrointestinal lymph nodes.</p><p><strong>Materials and methods: </strong>A patient with 2-month clinical symptoms of nasal obstruction and facial swelling was reported in this short review. A nasal endoscopy examination revealed a neoplasm in the inferior nasal meatus. Both CT and enhanced MRI showed that a soft tissue occupied the nasolacrimal duct, with bone destruction, and extended into the left nasal cavity and left lacrimal gland area. Then, a biopsy of the neoplasm in the inferior nasal meatus was performed.</p><p><strong>Results: </strong>HE staining results showed that neoplastic cells presented diffuse growth patterns, abundant cytoplasm, vacuole shape, lightly stained nuclei, and irregular nuclear membrane. Immunohistochemistry staining results revealed MUM1(+), Bcl6(+), CD20(+), CD79α(+), and CD10(+). FISH analyses detected positive IRF4 rearrangement. LBCL-IRF4 was diagnosed in the patient. The patient received treatment with four cycles of R-CHOP and two times of rituximab, followed up for 2 years, and finally got complete remission.</p><p><strong>Conclusion: </strong>For the first time, we summarize the imaging and pathological features, drug treatment, and curative effect of LBCL-IRF4 in the nasolacrimal duct.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139566336","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}