Pathology, research and practice最新文献

{"title":"Association of ATM and ARID1A in gastric carcinoma","authors":"Inwoo Hwang ,&nbsp;Somin Lee ,&nbsp;Yuyeon Kim ,&nbsp;Deok Geun Kim ,&nbsp;So Young Kang ,&nbsp;Soomin Ahn ,&nbsp;Jeeyun Lee ,&nbsp;Kyoung-Mee Kim","doi":"10.1016/j.prp.2024.155664","DOIUrl":"10.1016/j.prp.2024.155664","url":null,"abstract":"<div><h3>Background</h3><div>The ataxia telangiectasia mutated (ATM) gene is involved in the repair of double-stranded DNA breaks and a component of the DNA damage repair pathway. Tumors with mutations or low expression of both <em>ARID1A</em> and <em>ATM</em> exhibit increased numbers of tumor-infiltrating lymphocytes and a favorable prognosis. However, the relationship between <em>ATM</em> and <em>ARID1A</em> in gastric carcinoma (GC) is unclear.</div></div><div><h3>Methods</h3><div>We used the mRNA expression data from the Asian Cancer Research Group to construct tissue microarrays (<em>N</em> = 249). Next-generation sequencing (NGS) databases of Samsung Medical Center (SMC) (<em>N</em> = 813) were used to compare genetic alterations. Tissue microarrays were used for ATM and ARID1A immunohistochemistry, and expressions were categorized as “low” and “high.” NGS data from TCGA-STAD (<em>N</em> = 431) were used as independent cohorts for genetic alterations validation.</div></div><div><h3>Results</h3><div>In GCs, 32.1 % (80/249) of the cases showed low ATM protein expression (ATM^low) and 20.9 % (52/249) showed low ARID1A expression (ARID1A^low). ATM^low was significantly associated with older age (<em>P</em> &lt;.01), gross type of tumor (<em>P</em> =.02), histology (<em>P</em> &lt;. 01), lower incidence of perineural invasion (<em>P</em> =.04), lower disease stage (<em>P</em> &lt;.01), microsatellite instability-high (<em>P</em> &lt;.01), and ARID1A^low (<em>P</em> &lt;.01). Furthermore, GCs in the SMC NGS database showed that <em>ATM</em> mutations were significantly correlated with <em>ARID1A</em> mutations (<em>P</em> &lt;.01), and this finding remained significant in TCGA-STAD validation cohort (<em>P</em> &lt;.01).</div></div><div><h3>Conclusion</h3><div>ATM^low in GCs shows a characteristic clinicopathological feature that correlates strongly with ARID1A^low. <em>ATM</em> mutation was also associated with <em>ARID1A</em> mutations, highlighting the interactions between <em>ATM</em> and <em>ARID1A</em> in GC and suggesting a potential therapeutic target.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142538697","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}

{"title":"Association of viral infection with bladder cancer: A systematic review and meta-analysis","authors":"Saeed Motlaghzadeh ,&nbsp;Farbod Tabatabaei ,&nbsp;Fatemeh Eshragh ,&nbsp;Ahmad Tavakoli ,&nbsp;Nafise Mobasheri ,&nbsp;Seyed Jalal Kiani ,&nbsp;Hassan Saadati ,&nbsp;Samira Asli ,&nbsp;Ardalan Maleki Chegeni ,&nbsp;Arash Letafati ,&nbsp;Alireza Khatami ,&nbsp;Mahdiyeh Hosseini ,&nbsp;Zahra Salavatiha ,&nbsp;Abouzar Babaei ,&nbsp;Venus Fakheri Sueini ,&nbsp;Dorna Asadi ,&nbsp;Zahra Keyvanlou ,&nbsp;Elham Jafari Maskouni ,&nbsp;Atefeh Bahavar ,&nbsp;Mahdieh Sorouri Majd ,&nbsp;Saied Ghorbani","doi":"10.1016/j.prp.2024.155633","DOIUrl":"10.1016/j.prp.2024.155633","url":null,"abstract":"<div><h3>Background</h3><div>Bladder cancer (BC) is the tenth most common cancer with the highest mortality rate. Since the etiological role of viral infection in the development of BC is less known, the aim of the present study was to examine the pooled prevalence and possible relationship between viral infection and BC.</div></div><div><h3>Methods</h3><div>A systematic search of major online databases was conducted to investigate relevant studies. We estimated the pooled odds ratio (OR), 95 % confidence interval (CI), and heterogeneity for all studies by using meta-analysis and forest plots. All data were analyzed using Stata Software v.14.1.</div></div><div><h3>Results</h3><div>We analyzed 87 articles (97 datasets), which included 59 case-control and 38 cross-sectional designs. The pooled prevalence of viral infection among BC patients was 17.59 % (95 % CI: 13.09–22.55 %; I² = 96.34 %). Our subgroup analysis indicated that the pooled prevalence of human herpesvirus (HHV), papillomavirus (HPV), polyomavirus, and adenovirus was 33.67 %, 15.18 %, 7.46 %, and 30.14 %, respectively. We detected a significant relationship between viral infection and BC [summary OR 2.34 (95 % CI 1.56–3.51; I² = 58.0 %)].</div></div><div><h3>Conclusions</h3><div>This possible association was exhibited for Epstein–Barr virus (EBV) and HPV. Our finding indicated that HPV and EBV infections with significant associations with BC can be considered as possible risk factors for BC. Although the specific molecular mechanism of the role of viruses in the development of BC has not been identified, persistent viral infection, oncogenic protein expression, apoptosis inhibition, cell cycle promotion, and disruption of signaling pathways in bladder tissue are possible pathways for the role of viruses in the development of BC.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591115","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":"Whole genome sequencing elucidates etiological differences in MCPyV-negative Merkel cell carcinoma","authors":"Carla Stephan ,&nbsp;Majd Al Assaad ,&nbsp;Max F. Levine ,&nbsp;Aditya Deshpande ,&nbsp;Michael Sigouros ,&nbsp;Jyothi Manohar ,&nbsp;Andrea Sboner ,&nbsp;Olivier Elemento ,&nbsp;Anna C. Pavlick ,&nbsp;Juan Miguel Mosquera","doi":"10.1016/j.prp.2024.155668","DOIUrl":"10.1016/j.prp.2024.155668","url":null,"abstract":"<div><div>Merkel cell carcinoma (MCC) is an aggressive neuroendocrine neoplasm of the skin. Immunosuppression, ultraviolet radiation and the integration of Merkel cell polyomavirus (MCPyV) have all been shown to be involved in the pathogenesis of this malignancy. We performed whole genome sequencing on two MCPyV-negative cases of MCC that demonstrated very different clinical presentations and outcomes, and mutational profiles. The first case exhibited a highly aggressive clinical course, absence of UV-signature mutations and a low tumor mutational burden. A rearrangement in the tumor suppressor gene <em>SUFU</em> was identified, a likely driver and potential target of the Hedgehog signaling pathway. Meanwhile, the second case exhibited a less aggressive behavior, harbored UV-signature mutations, and a high mutational burden including mutations in <em>TP53</em> and <em>RB1</em>.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472152","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":"TNF-α, and TNFRs in gastrointestinal cancers","authors":"Zahra Mozooni ,&nbsp;Rezvaneh Ghadyani ,&nbsp;Shahrzad Soleimani ,&nbsp;Ehsan Rouhollahpour Ahangar ,&nbsp;Mojgan Sheikhpour ,&nbsp;Mehrdad Haghighi ,&nbsp;Marzieh Motallebi ,&nbsp;Abolfazl Movafagh ,&nbsp;Seyed Mohsen Aghaei-Zarch","doi":"10.1016/j.prp.2024.155665","DOIUrl":"10.1016/j.prp.2024.155665","url":null,"abstract":"<div><div>Tumor necrosis factor-alpha (TNF-α) is a multifunctional cytokine that plays a role in the hemostasis of the immune system, inflammation, and cell proliferation. However, it can also have a dark side as it is involved in pro-inflammatory cytokines and pathological processes such as cell growth and death, autoimmunity, and inflammation, leading to a wide range of chronic inflammatory diseases, including digestive cancer. TNF-alpha binds to two distinct receptors, TNFRI and TNFRII. Upon binding of the ligand to these receptors, TNF receptor-associated factors (TRAFs) are recruited to the cytoplasmic receptor, triggering the activation of transcription factors such as NF-kB and Activator protein 1 (AP_1). In contrast, binding of cytokines to certain family members, such as TNF RI and Fas Ligand (Fas L), leads to the secretion and initiation of apoptosis. Gastrointestinal malignancies are among the most common types of cancer globally. Despite extensive research, the exact cause of these tumors remains a mystery. Unfortunately, they often have a poor prognosis and are often detected at a late stage. The global incidence of gastrointestinal cancers, including those of the stomach, esophagus, colon, liver, and pancreas, is on the rise, leading to a surge in both incidence and mortality. Growth factors and cytokines, which are signaling molecules found in the tumor microenvironment, are thought to be major contributors to the development and metastasis of these cancers. In this review, we explored the role of TNF-α, and its receptors in the development of digestive cancers, including its signaling pathways and functions.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505692","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":"Therapeutic Potential of lncRNAs in Regulating Disulfidptosis for Cancer Treatment","authors":"Abida ,&nbsp;Abdulmalik S.A. Altamimi ,&nbsp;Nehmat Ghaboura ,&nbsp;Ashok Kumar Balaraman ,&nbsp;Pranchal Rajput ,&nbsp;Pooja Bansal ,&nbsp;Sushama Rawat ,&nbsp;Fadiyah Jadid Alanazi ,&nbsp;Abeer Nuwayfi Alruwaili ,&nbsp;Nouf Afit Aldhafeeri ,&nbsp;Haider Ali ,&nbsp;Pran Kishore Deb","doi":"10.1016/j.prp.2024.155657","DOIUrl":"10.1016/j.prp.2024.155657","url":null,"abstract":"<div><div>Non-coding RNAs (lncRNAs) play critical roles in various cellular processes, including a novel form of regulated cell death known as disulfidptosis, characterized by accumulating protein disulfide bonds and severe endoplasmic reticulum stress. This review highlights the therapeutic potential of lncRNAs in regulating disulfidptosis for cancer treatment, emphasizing their influence on key pathway components such as GPX4, SLC7A11, and PDIA family members. Recent studies have demonstrated that targeting specific lncRNAs can sensitize cancer cells to disulfidptosis, offering a promising approach to cancer therapy. The regulation of disulfidptosis by lncRNAs involves various signaling pathways, including oxidative stress, ER stress, and calcium signaling. This review also discusses the molecular mechanisms underlying lncRNA regulation of disulfidptosis, the challenges of developing lncRNA-based therapies, and the future potential of this rapidly advancing field in cancer research.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505691","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":"trans-chalcone ameliorates CCl4-induced acute liver injury by suppressing endoplasmic reticulum stress, oxidative stress and inflammation","authors":"Suvesh Munakarmi ,&nbsp;Yamuna Gurau ,&nbsp;Juna Shrestha ,&nbsp;Lokendra Chand ,&nbsp;Ho Sung Park ,&nbsp;Geum-Hwa Lee ,&nbsp;Yeon Jun Jeong","doi":"10.1016/j.prp.2024.155663","DOIUrl":"10.1016/j.prp.2024.155663","url":null,"abstract":"<div><h3>Background</h3><div>Acute liver injury serves as a crucial marker for detecting liver damage due to toxic, viral, metabolic, and autoimmune exposures. Due to the response to adverse external stimuli and various cellular homeostasis, Endoplasmic reticulum stress (ERS), Oxidative stress, and Inflammation have great potential for treating liver injury. <em>Trans</em>-chalcones (TC) is a polyphenolic compound derived from a natural plant with anti-oxidative and anti-inflammatory abilities. Here, TC was aimed to attenuate liver injury by triggering ER stress, oxidative stress, inflammation, and apoptosis. A single dose of carbon tetrachloride (CCl₄) 1 mL/kg was administered intraperitoneally into C57BL6 mice to construct an <em>in vivo</em> NAFLD model, whereas AML12 cells were treated with lipopolysaccharides (LPS) to construct an <em>in vitro</em> NAFLD model. The mice used in the experiment were randomly assigned to two groups: a 12-hour set and a 24-hour set. Forty-nine mice were randomly divided into seven groups, the control group (Group I), TC group (Group II) 10 mg/kg TC, negative control group (Group III) CCl₄, TC + CCl₄ groups (Groups IV−VI), mice were subcutaneously treated with (5, 10, and 20) mg/kg of TC for three consecutive days before the CCl₄ injection and the positive control group (Group VII) received 10 mg/kg Silymarin. After the experiment, serum transaminase, liver histological pathology, hepatic expression levels ERS, oxidative stress, and inflammation-related markers were assessed. TC pre-treatment significantly alleviates the expression of ER stress, oxidative stress, inflammatory cytokines, and apoptosis in both <em>in vivo</em> and <em>in vitro</em> models of liver injury. TC treatment significantly reduced serum transaminase levels (ALT and AST), and improved liver histopathological scores. TC administration also led to a reduction in MDA levels and the suppression of ROS generated by CCl4 in hepatic tissue, which contributed to an increase in GSH levels. The protective effect of TC on the liver injury mouse model was achieved by inhibiting hepatocyte apoptosis. Moreover, TC pre-treatment dramatically decreased the protein levels of ER stress indicators such as CHOP, Bip, Ero-Lα, IRE1α, PERK, Calnexin, and PDI when compared to the CCl4-only treated group. TC exerts hepatoprotective effects against CCl₄-induced acute liver injuries in mice by modulating ERS, oxidative stress, and inflammation. These results suggest that TC pre-treatment at a dose of (20 mg/kg BW) was as effective as silymarin (10 mg/kg) in preventing CCl4-induced acute liver injury. Further investigations are necessary to elucidate the precise molecular mechanisms underlying the hepatoprotective effects of TC and to explore its therapeutic potential in clinical trials.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505693","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":"IDO1-mediated catabolism of tryptophan in gastric tumors: Its potential role in the axis of histopathology, differentiation and metastasis","authors":"Cem Horozoglu ,&nbsp;Mehmet Tolgahan Hakan ,&nbsp;Dilara Sonmez ,&nbsp;Asli Yildiz ,&nbsp;Seyda Demirkol ,&nbsp;Fikret Aktas ,&nbsp;Sidar Bagbudar ,&nbsp;Ozlem Kucukhuseyin ,&nbsp;Soykan Arikan ,&nbsp;Filiz Akyuz ,&nbsp;Ilhan Yaylim","doi":"10.1016/j.prp.2024.155655","DOIUrl":"10.1016/j.prp.2024.155655","url":null,"abstract":"<div><h3>Background</h3><div>Indoleamine 2,3-Dioxygenase 1 (IDO1)-mediated tryptophan degradation, which is the rate-limiting enzyme of tryptophan/kynurenine pathway, may cause immune suppression in the tumor microenvironment, while potentiating proliferative and metastatic activity in the tumor focus, Phase studies of IDO1 inhibitors are ongoing, and our study aims to evaluate the potential contribution of IDO1 gene expression to the tryptophan/kynurenine pathway in tumor and tumor microenvironment foci in gastric cancer (GC) on a clinicopathological axis,</div></div><div><h3>Method</h3><div>In the case-control study design, the determination of tryptophan and its metabolites in the serum of 51 GC and 49 healthy controls was made using High Pressure Liquid Chromatography-Fluorescence Detector (HPLC-FD). IDO1 expression in a total of 102 tissues with tumor and tumor microenvironment was detected by quantitative PCR (q-PCR).</div></div><div><h3>Results</h3><div>In gastric tumors, 3,25-fold decreased expression of IDO1 was detected according to the tumor microenvironment (p=0,05), IDO1 expression was found to be more than 2 times higher in signet ring cell carcinoma (SRCC) and poorly differentiated tumors without distant organ metastasis (p&lt;0,05), In GC, tryptophan level was found to be 1,6 times lower than in control (AUC:0889; cut off≤21,57; p&lt;0001), Low tryptophan level was found in advanced tumor stage compared to early stage and in the presence of perineural invasion compared to its absence (p&lt;0,05) The level of kynurenine was found to be approximately 1,8 times lower in SRCC (p=0,04),</div></div><div><h3>Conclusion</h3><div>Increased tryptophan accumulation in the gastric tumor and its microenvironment, when catabolized via IDO1, exhibits histological type, tumor differentiation, and metastasis-promoting effects more prominently in aggressive subtypes such as SRCC,</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505683","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":"Application of LEF-1 immunohistochemical staining in the diagnosis of solid pseudopapillary neoplasm of the pancreas","authors":"Saroja Devi Geetha ,&nbsp;Atif Khan ,&nbsp;Anam Khan ,&nbsp;Yonah Ziemba ,&nbsp;Karen Chau ,&nbsp;Sunder Sham ,&nbsp;Silvat Sheikh-Fayyaz ,&nbsp;Arvind Rishi ,&nbsp;Deepika Savant","doi":"10.1016/j.prp.2024.155662","DOIUrl":"10.1016/j.prp.2024.155662","url":null,"abstract":"<div><h3>Introduction</h3><div>Solid pseudopapillary neoplasm (SPN) is a tumor of young females with gain-of-function mutation in catenin beta 1 gene involved in Wnt signal transduction pathway. Beta-catenin immunohistochemistry (IHC) is used to diagnose SPN. Lymphoid enhancer-binding factor 1 (LEF-1) has been recognized in the transactivation of Wnt pathway. We aim to study LEF-1 IHC in SPN and other pancreatic tumors and compare it with beta-catenin IHC.</div></div><div><h3>Methods</h3><div>We retrieved cases of SPN, pancreatic neuroendocrine tumor (PanNET), serous cystadenoma (SCA), ductal adenocarcinoma (PDAC) and acinar cell carcinoma (ACC) from 2011 to 2023. Formalin-fixed, paraffin-embedded blocks with adequate tumor were cut and stained with beta-catenin (B-Catenin-1 clone) and LEF-1 (EP310 clone) IHC. Cases were reviewed by two pathologists independently. Nuclear staining with LEF-1 and beta-catenin was considered as positive.</div></div><div><h3>Results</h3><div>Our cohort consisted of 111 cases [SPN = 59 (42 resections, 11 FNA, 6 biopsies), PDAC = 24, PanNET = 22, SCA = 5, ACC = 1]. For SPN cases male to female ratio was1:8. Age ranged from 9 to 81 years (average: 32 years). Pancreatic tail was the most common location (47 %) followed by head (28 %), body (19 %) and neck (6 %). Tumor size ranged from 1.0 to 12.2 cm (average: 5 cm). Among the SPN cases 57/59 demonstrated strong nuclear LEF-1 staining. 2/49 cases were negative for LEF-1 (both pathologist in agreement). All SPN tumors demonstrated nuclear staining with beta-catenin. Among the non-SPN tumors, beta-catenin showed nuclear staining in 2/52 cases (2 PDAC). The remaining 50 cases were negative for nuclear beta-catenin and demonstrated variable staining pattern with interpretation variability between the two pathologists. The sensitivity and specificity for LEF-1 were 97 % and 100 %, respectively, while for beta-catenin, they were 100 % and 96 % respectively.</div></div><div><h3>Conclusion</h3><div>Crisp nuclear staining of LEF-1 without background staining makes diagnostic interpretation relatively easy and accurate compared to beta-catenin IHC. This is further helpful for small biopsy samples to help differentiate SPN from mimickers such as PanNET. None of the non-SPN cases displayed nuclear LEF-1 rendering it a valuable adjunct to beta-catenin in the diagnostic evaluation of SPN.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472148","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":"CircWDR37 promotes hepatocellular carcinoma tumorigenesis by mediating the miR-646/TRAF4 regulatory pathway","authors":"Jie Zhou ,&nbsp;Zhu Zhu ,&nbsp;Xi Zhang ,&nbsp;Wenli Peng ,&nbsp;Yongpeng He ,&nbsp;Qing Zhang","doi":"10.1016/j.prp.2024.155658","DOIUrl":"10.1016/j.prp.2024.155658","url":null,"abstract":"<div><h3>Background</h3><div>CircRNA has emerged as a significant player in human malignancies, including hepatocellular carcinoma (HCC). Hsa_circ_0004277 (circWDR37) is abnormally up-regulated in HCC. But, its function and underlying mechanism in HCC progression are largely unknown.</div></div><div><h3>Methods</h3><div>qRT-PCR and western blot assays were used to measure the expression of circWDR37, miR-646, and TRAF4. Cell malignant phenotypes were assessed via CCK-8, EdU, colony formation, flow cytometry, transwell, and tube formation experiments. The intermolecular interaction between miR-646 and circWDR37 or TRAF4 was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assay. The <em>in vivo</em> effect of circWDR37 on xenograft tumor growth was also investigated in mice.</div></div><div><h3>Results</h3><div>Increased CircWDR37 and TRAF4 and decreased miR-646 were found in HCC tissues and cells. Scilencing circWDR37 impeded cell proliferation, migration, invasion, and tube formation, while accelerated apoptosis. CircWDR37 directly bind to miR-646 to suppress miR-646 expression and up-regulate TRAF4 expression. MiR-646 inhibitor partially abated the cell phenotype changes caused by circWDR37 knockdown. Moreover, miR-646 exerted an inhibitory effect on cell malignant phenotypes, which were attenuated due to the increase of TRAF4. Additionally, circWDR37 knockdown blocked HCC tumor growth <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>CircWDR37 exerted an oncogenic effect in HCC by sponging miR-646 to up-regulate TRAF4 expression. Our finding elucidates a novel ‘circWDR37-miR-646-TRAF4’ regulatory axis in HCC and provides a promising target for HCC treatment.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472150","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":"High endothelial venules in the pleura: MECA-79 expression in mesothelioma, pleural metastasis and pleuritis","authors":"Ikram Kherrour ,&nbsp;Mousa Mobarki ,&nbsp;Michel Péoc’h ,&nbsp;Georgia Karpathiou","doi":"10.1016/j.prp.2024.155661","DOIUrl":"10.1016/j.prp.2024.155661","url":null,"abstract":"<div><h3>Introduction</h3><div>High endothelial venules (HEVs) are vessels specialized in the extravasation of lymphocytes from the blood to the tissue implicated in the immune microenvironment of several tumors. Their presence has been never studied in the pleural tissue.</div></div><div><h3>Material and methods</h3><div>We retrospectively studied 149 surgical pleural biopsies by immunohistochemistry for MECA-79 expression, a marker specifically recognizing HEVs. The tissues included 44 (44 %) inflammatory and 105 (56 %) neoplastic diseases. The latter corresponded to 34 (22.8 %) mesotheliomas and 71 (47.7 %) metastases from lung (n=50) or breast (n=21) primaries.</div></div><div><h3>Results</h3><div>HEVs were present in 102 (68 %) of all pleural specimens with a mean number of foci containing HEVs of 13.33 (±20.64). Neoplastic pleural pathologies harbored HEVs in 73.3 % of the cases compared to the non-neoplastic pathologies which harbored HEVs in 56.8 % of the cases (p=0.048). Their presence did not differ between pulmonary or mammary metastasis (p=0.7).</div></div><div><h3>Conclusion</h3><div>We show for the first time that HEVs are present in the pleural cavity probably participating in the immune microenvironment of inflammatory and neoplastic pleural disease.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441303","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}