Pathology, research and practice最新文献

{"title":"Correlation between immune microenvironment and clinicopathological characteristics and prognosis of primary large B-cell lymphoma of immune-privileged sites","authors":"Yawen Guo,&nbsp;Xiaoxian Zhang,&nbsp;Luyao Wu,&nbsp;Jiajia Ma,&nbsp;Ran Zhang,&nbsp;Huifang Yan,&nbsp;Xinxia Li","doi":"10.1016/j.prp.2024.155720","DOIUrl":"10.1016/j.prp.2024.155720","url":null,"abstract":"<div><h3>Objectives</h3><div>To explore the correlation between tumor-associated macrophages (TAMs), tumor-infiltrating lymphocytes (TILs), and tumor-associated angiogenesis (TAA) in the tumor microenvironment with the clinicopathological characteristics and prognosis of primary large B-cell lymphoma of immune-privileged sites (LBCL-IP).</div></div><div><h3>Methods</h3><div>A total of 46 cases of LBCL-IP from the Department of Pathology, the Third Affiliated Hospital of Xinjiang Medical University, from January 2010 to February 2024, were collected, along with clinical and follow-up data of LBCL-IP patients. Immunohistochemistry and triple immunofluorescence were used to detect related proteins of TAMs, TILs, and TAA, and to analyze the correlation between TAMs, TILs, TAA, and the polarization of TAMs with the clinical and prognostic factors of LBCL-IP patients.</div></div><div><h3>Results</h3><div>There are 30 cases (65.2 %) showed high expression of CD68 proteins, 32 cases (69.6 %) showed high expression of CD163 proteins, 19 cases (41.3 %) showed high expression of CD4 proteins, 34 cases (73.9 %) showed high expression of CD8 proteins, and 25 cases (54.3 %) showed high expression of CD34 proteins. A total of 28 cases (60.9 %) showed CD68⁺CD163⁺/CD68⁺CD86⁺≥1. The chi-square tests showed that high expression of CD163 proteins was positively correlated with elevated LDH and BMG values, and the count of CD68⁺CD163⁺/CD68⁺CD86⁺≥1 was positively correlated with ECOG scores ≥2, Ann Arbor staging III-IV, and increased BMG value. High expression of CD8 proteins was positively correlated with a Ki-67 proliferation index ≥70 %, and high MVD values were positively correlated with Ann Arbor staging III-IV. The Kaplan-Meier estimator analysis showed that LBCL-IP patients with low expression of CD68 proteins, high expression of CD163 proteins, CD68⁺CD163⁺/CD68⁺CD86⁺≥1, low expression of CD8 proteins, high MVD values, ECOG scores ≥2, Ann Arbor staging III-IV, LDH ≥250 U/L, BMG ≥2.2 mg/L, and IPI scores ≥2 had shorter survival times. Multivariate Cox regression analysis showed that low expression of CD8 proteins, CD68⁺CD163⁺/CD68⁺CD86⁺≥1, LDH ≥250 U/L, and ECOG scores ≥2 are independent risk factors affecting the survival of LBCL-IP patients.</div></div><div><h3>Conclusion</h3><div>M2-polarized TAMs and low infiltration of CD8⁺ TILs were more strongly correlated with poor clinical pathological indicators and worse prognosis, and MVD values may serve as an aiding means for the diagnosis and prognostic prediction of LBCL-IP disease.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155720"},"PeriodicalIF":2.9,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625774","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":"Germline pathogenic variants in prostate cancer","authors":"Yousif M. Shakroo ,&nbsp;Charles A. Seabury Jr. ,&nbsp;Kenneth A. Iczkowski ,&nbsp;Kinloch Nelson ,&nbsp;Junqi Qian ,&nbsp;Dharam M. Ramnani","doi":"10.1016/j.prp.2024.155718","DOIUrl":"10.1016/j.prp.2024.155718","url":null,"abstract":"<div><div>While most prostate cancer is sporadic, evidence suggests that a significant minority of cases have a hereditary component, and germline variants may play a role in this heritability. In this study, we investigated germline pathogenic variants in prostate cancer patients. All genetic variants were classified using the American College of Medical Genetics and Genomics/Association for Molecular Pathology 2015 guidelines. By retrospectively reviewing patient charts and genetic testing results, we collected clinicopathologic, demographic, and genetic data. Among the 160 prostate cancer patients who met NCCN genetic testing guidelines and underwent germline testing, 41 % had metastatic cancer, while 59 % had localized cancer, mostly high-risk. Nineteen (19) out of the 160 patients (12 %) had a pathogenic or likely pathogenic variant in the following genes: <em>MUTYH</em> (3.1 %), <em>ATM</em> (1.9 %), <em>BRCA2</em> (1.3 %), <em>CHEK2</em> (1.3 %), <em>PALB2</em> (1.3 %), <em>HOXB13</em> (1.3 %), and 5 other genes (<em>BRIP1</em>, <em>LZTR1</em>, <em>TP53</em>, <em>NTHL1</em>, and <em>NBN</em>), each at a frequency of 0.6 %. There was no significant difference in clinicopathologic data (such as age, serum prostate-specific antigen, Gleason score, and others) between those with a pathogenic or likely pathogenic variant and those without. There was also a lack of significant difference in the number of variants of uncertain significance observed between different racial and ethnic groups. Individuals with a family history of cancer were significantly more likely to have a pathogenic or likely pathogenic variant than those without one (p = 0.002). Overall, our results show the necessity for future research with a larger sample size to better explain the relationship between clinicopathologic data and genetic variants.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155718"},"PeriodicalIF":2.9,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625791","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":"BCL11A expression worsens the prognosis of DLBCL and its co-expression with C-MYC predicts poor survival","authors":"Lixin Wang ,&nbsp;Hong He ,&nbsp;Yuanxin Li ,&nbsp;Xingyu Wang ,&nbsp;Jieyang Yu ,&nbsp;Ying Huang ,&nbsp;Kuai Yu ,&nbsp;Juan He ,&nbsp;Min Zhao ,&nbsp;Tao Xie ,&nbsp;Dan Li","doi":"10.1016/j.prp.2024.155717","DOIUrl":"10.1016/j.prp.2024.155717","url":null,"abstract":"<div><div>Non-Hodgkin's lymphoma (NHL) is a significant global malignancy, with diffuse large B cell lymphoma (DLBCL) being the most prevalent subtype, accounting for 25–50 % of newly diagnosed cases in China. Despite a 60 % survival rate achieved with R-CHOP regiment for DLBCL, approximately 40 % of patients experience relapse or develop resistance to treatment. While the oncogenic transcription factor B-cell chronic lymphocytic leukaemia/lymphoma 11 A (BCL11A) has been implicated in various tumors, its specific role in DLBCL remains unclear. In this study, we conducted retrospective histomorphological and immunophenotypic analyses on paraffin sample tissues and collected fresh tissue samples for protein and mRNA analyses to investigate the relationship between BCL11A and DLBCL. Additionally, we classified DLBCL into subtypes based on cells of origin (COO) and examined the expressions of BCL11A, C-MYC, P53 and other protein expressions to better understand the factors contributing to poor clinical outcomes in DLBCL. Our findings revealed elevated BCL11A expression in DLBCL, with increased expression associated with worse prognosis and higher C-MYC expression. Patients exhibiting co-expression of C-MYC and BCL11A had significantly lower survival rates compared to those with singular expression. Furthermore, BCL11A protein expression levels demonstrated significant associations with P53 and C-MYC protein expression levels in the Germinal Center B-cell-like (GCB) subtype. These findings suggest that BCL11A may serve as a potential prognostic marker and therapeutic target for DLBCL.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155717"},"PeriodicalIF":2.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639439","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":"Dysplastic crypts with lateral buddings in tubular adenomas","authors":"Carlos A. Rubio ,&nbsp;Michael Vieth ,&nbsp;Corinna Lang-Schwarz","doi":"10.1016/j.prp.2024.155704","DOIUrl":"10.1016/j.prp.2024.155704","url":null,"abstract":"<div><div>Tubular adenomas (TA) are the most frequent of all colorectal adenomas. Current definitions of TA do not include the phenotype of the dysplastic crypts. We report a novel crypt phenotype characterized by dysplastic crypts with lateral buddings (DCLB). Out of the 309 TA, 25.9 % (n=80) exhibited DCLBs: 12.5 % (n=10) had one DCLB focus/TA, 15.0 % (n=12) had two DCLB foci/TA, 27.5 % (n=22) three had three DCLB foci/TA, 30.0 % (n=24) had four DCLB foci/TA, 12.5 % (n=10) had five DCLB foci/TA, and in the remaining 2.5 %n (n=2) most fields of view at x4 showed DCLB foci. DCLB in TA were generated independently of TA size or degree of dysplasia. The presence of DCLB was not influenced by age, gender or localization. In conclusion, a novel histologic phenotype of TA is showcased. DCLBs are integral components in some of the TA. Recently, another novel dysplastic crypt phenotype in TA characterized by dysplastic crypts in tandem was reported. The awareness that different dysplastic crypt phenotypes thrive in TA might open a new vista on research aimed to learn more about why the most prevalent of all colorectal adenomas thrive with a low capacity to invade the host.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155704"},"PeriodicalIF":2.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625776","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":"Farrerol suppresses epithelial-mesenchymal transition in hepatocellular carcinoma via suppression of TGF-β1/Smad2/3 signaling","authors":"Yaming Hao ,&nbsp;Zhixiong Long ,&nbsp;Xiufeng Gu","doi":"10.1016/j.prp.2024.155719","DOIUrl":"10.1016/j.prp.2024.155719","url":null,"abstract":"<div><h3>Background</h3><div>Epithelial-mesenchymal transition (EMT) is an essential process for the metastasis of multiple malignancies, including hepatocellular carcinoma (HCC). Farrerol is a plant-derived flavonoid and has significant pharmacological effects. However, the anticancer activities of farrerol have not been fully elucidated. Here, we investigated the effects of farrerol on HCC progression.</div></div><div><h3>Methods</h3><div>The potential of farrerol to prevent HCC cell migration and invasiveness was evaluated by wound healing and transwll matrix assays. Immunoblotting, immunofluorescence, and qPCR were used to detect the levels of EMT-related proteins. Transforming growth factor beta (TGF-β) (10 ng/ml) was used to stimulate HCC cells, followed by measurement of cell migration, invasiveness, and the EMT. TGF-β1/Smads signaling was examined by immunoblotting. A xenograft mouse model was used to assess the anticancer efficacy of farrerol <em>in vivo</em>. The expression levels of EMT- and angiogenesis-related proteins in xenograft tumors were evaluated by immunoblotting or immunohistochemistry.</div></div><div><h3>Results</h3><div>We found that farrerol blocked HCC cell migration and invasiveness. Farrerol upregulated E-cadherin levels and reduced N-cadherin and vimentin levels. Farrerol also downreuglated the expression levels of EMT-related transcription factors including slug, snail, twist, and zeb1. Furthermore, farrerol suppressed TGF-β-stimulated migration, invasiveness, and the EMT in HCC cells. The phosphorylation of Smad 2/3 induced by TGF-β was inhibited by farrerol. Importantly, farrerol suppressed HCC growth and the EMT <em>in vivo</em>. Farrerol also inhibited tumor angiogenesis by inhibiting hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>Overall, farrerol suppresss HCC by inhibiting migration, invasiveness, the EMT, and angiogenesis, implying that farrerol could be a promising antimetastasis agent for HCC.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155719"},"PeriodicalIF":2.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625788","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":"Polyribonucleotide phosphorylase is overexpressed in hepatocellular cancer, promoting epithelial phenotype maintenance and tumor progression","authors":"Francisco Revert-Ros ,&nbsp;Ignacio Ventura ,&nbsp;Jesús A. Prieto-Ruiz ,&nbsp;Eduardo Giner-Moreno ,&nbsp;Ángela Pérez-Cervera ,&nbsp;Judith Pérez-Rojas ,&nbsp;Fernando Revert ,&nbsp;José Miguel Hernández-Andreu","doi":"10.1016/j.prp.2024.155713","DOIUrl":"10.1016/j.prp.2024.155713","url":null,"abstract":"<div><div>Liver cancer, particularly hepatocellular carcinoma (HCC), is a major global health challenge, largely associated with cirrhosis caused by various factors. Prognosis is often guided by molecular and histological classifications. In this study, expression of Polyribonucleotide Phosphorylase (PNPT1) in HCC was investigated to better understand its role in tumor behavior and patient outcomes. The expression of the corresponding protein PNPase was assessed in HCC tissue samples using immunohistochemistry, while RNA-seq data from The Cancer Genome Atlas (TCGA) were analyzed via OncoDB. Additionally, PNPT1 silencing in HepG2 cells was followed by gene and protein expression analysis. The results revealed that PNPT1 is overexpressed in HCC tumors, particularly in those expressing E-cadherin. Notably, silencing PNPT1 in HepG2 cells triggered a shift towards a mesenchymal phenotype. In HCC tissues, PNPT1 expression was linked to markers of epithelial phenotype, oxidative stress, and poor prognosis, especially in non-viral HCC cases. These findings suggest that PNPase may play a crucial role in the progression of well-differentiated HCC tumors, serving as a poor prognostic biomarker.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155713"},"PeriodicalIF":2.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625810","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":"MicroRNA-146 family: Molecular insights into their role in regulation of signaling pathways in glioma progression","authors":"Sepideh Mirzaei ,&nbsp;Fatemeh Ahangari ,&nbsp;Fatemeh Faramarzi ,&nbsp;Seyedeh Mahdieh Khoshnazar ,&nbsp;Fateme Zare Khormizi ,&nbsp;Mahboobeh Aghagolzadeh ,&nbsp;Mohammadreza Rostami ,&nbsp;Vahid Asghariazar ,&nbsp;Mina Alimohammadi ,&nbsp;Payman Rahimzadeh ,&nbsp;Najma Farahani","doi":"10.1016/j.prp.2024.155707","DOIUrl":"10.1016/j.prp.2024.155707","url":null,"abstract":"<div><div>Glioma is a highly lethal brain cancer in humans. Despite advancements in treatment, the prognosis for patients remains unfavorable. Epigenetic factors, along with their interactions and non-coding RNAs (ncRNAs), are crucial in glioma cells' development and aggressive characteristics. MicroRNAs (miRNAs) are a class of small non-coding RNAs (ncRNAs) that modulate the expression of various genes by binding to target mRNA molecules. They play a critical role in regulating essential biological mechanisms such as cell proliferation and differentiation, cell cycle, and apoptosis. MiR-146a/miR-146b is a significant and prevalent miRNA whose expression alterations are linked to various pathological changes in cancer cells, as well as the modulation of several cellular signaling pathways, including NF-κB, TGF-β, PI3K/Akt, and Notch-1. Scientists may identify novel targets in clinical settings by studying the complicated link between Mir-146a/mir-146b, drug resistance, molecular pathways, and pharmacological intervention in gliomas. Additionally, its interactions with other ncRNAs, such as circular RNA and long non-coding RNA, contribute to the pathogenesis of glioma. As well as miR-146 holds potential as both a diagnostic and therapeutic biomarker for patients with this condition. In the current review, we investigate the significance of miRNAs in the context of glioma, with a particular focus on the critical role of Mir-146a/mir-146b in glioma tumors. Additionally, we examined the clinical relevance of this miRNA, highlighting its potential implications for diagnosis and treatment.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155707"},"PeriodicalIF":2.9,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625799","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":"Pathological insights into cell death pathways in diabetic wound healing","authors":"Kannan Harithpriya,&nbsp;Srinivasan Kaussikaa,&nbsp;Srikanth Kavyashree,&nbsp;AVS Geetha,&nbsp;Kunka Mohanram Ramkumar","doi":"10.1016/j.prp.2024.155715","DOIUrl":"10.1016/j.prp.2024.155715","url":null,"abstract":"<div><div>Diabetic foot ulcers (DFUs) are a microvascular complication that affects almost 21 % of the diabetic population. DFUs are characterized by lower limb abnormalities, chronic inflammation, and a heightened hypoxic environment. The challenge of healing these chronic wounds arises from impaired blood flow, neuropathy, and dysregulated cell death processes. The pathogenesis of DFUs involves intricate mechanisms of programmed cell death (PCD) in different cell types, which include keratinocytes, fibroblasts, and endothelial cells. The modes of cell death comprise apoptosis, autophagy, ferroptosis, pyroptosis, and NETosis, each defined by distinct biochemical hallmarks. These diverse mechanisms contribute to tissue injury by inducing neutrophil extracellular traps and generating cellular stressors like endoplasmic reticulum stress, oxidative stress, and inflammation. Through a comprehensive review of experimental studies identified from literature databases, this review synthesizes current knowledge on the critical signaling cascades implicated in programmed cell death within the context of diabetic foot ulcer pathology.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155715"},"PeriodicalIF":2.9,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648729","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":"LncRNA-mediated regulation of cisplatin response in breast cancer","authors":"Shirin Azizidoost ,&nbsp;Mohadeseh Sheykhi-Sabzehpoush ,&nbsp;Mahrokh Abouali Gale Dari ,&nbsp;Małgorzata Józkowiak ,&nbsp;Julia Niebora ,&nbsp;Dominika Domagała ,&nbsp;Krzysztof Data ,&nbsp;Piotr Dzięgiel ,&nbsp;Paul Mozdziak ,&nbsp;Maryam Farzaneh ,&nbsp;Bartosz Kempisty","doi":"10.1016/j.prp.2024.155716","DOIUrl":"10.1016/j.prp.2024.155716","url":null,"abstract":"<div><div>Breast cancer is a prevalent and aggressive disease characterized by high metastasis, recurrence, and mortality rates. While cisplatin is an effective chemotherapy drug, its use is limited by its toxic effects on the body. Despite advancements in therapeutic strategies, the therapeutic response is often unsatisfactory due to drug resistance, leading to poor prognosis. Recent studies have shown that cisplatin interacts with long non-coding RNAs (lncRNAs) and accelerates the development of resistance in tumor cells to therapy. This interaction highlights the complex mechanisms involved in the response of cancer cells to chemotherapy. Several lncRNAs have been identified as key players in mediating cisplatin resistance in breast cancer. These lncRNAs include SNHG15, HULC, HCP5, MT1JP, LncMat2B, DLX6-ASL, Linc00665, CARMN, and Lnc-EinRP44–3:6. These lncRNAs have been shown to target microRNAs and mRNAs and modulate the expression of genes involved in cisplatin resistance, which is important in treating breast cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155716"},"PeriodicalIF":2.9,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625795","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":"The role of programmed death-ligand 1 (PDL-1) in high-grade cervical intraepithelial neoplasia (CIN2+) development and recurrence: A systematic review of literature about HPV-CIN2+-PDL-1 axis","authors":"Mattia Dominoni ,&nbsp;Frediano Socrate Inzani ,&nbsp;Andrea Gritti ,&nbsp;Marianna Francesca Pasquali ,&nbsp;Matteo Mauri ,&nbsp;Asaf Eldar ,&nbsp;Barbara Gardella","doi":"10.1016/j.prp.2024.155712","DOIUrl":"10.1016/j.prp.2024.155712","url":null,"abstract":"<div><h3>Background and aims</h3><div>Cervical intraepithelial neoplasia(CIN)and persistent high-risk human papillomavirus (HR-HPV)infection are associated with impaired local cellular immunity; however, the molecular mechanisms underlying these processes are not well understood. The involvement of the programmed death 1/programmed death 1 ligand (PD-1/PD-L1) pathway in the downregulation of T cell function has been demonstrated recently and it is believed to have a role in the onset and persistence of HPV infection and cervical cancer. Our aim is to analyze the role of PD-L1 in the CIN to identify a possible biomarker of HSIL (CIN2+) progression and persistence.</div></div><div><h3>Methods</h3><div>We performed a systematic review, considering papers published from January 2000 to May 2024, according to PRISMA guideline, in order to obtain a Comprehensive analysis of the literature regarding the role of PD-L1 expression in CIN. The most important medical databases, such as PubMed, Cochrane Database of narrative Reviews, EMBASE, and Web of Science, were consulted. Articles documenting the characteristics and clinical implications of PDL-1 expression in cervical dysplasia were given special consideration.</div></div><div><h3>Results</h3><div>HR-HPV lesions show a positive expression of PD-L1, which level increase from LSIL (CIN1) to cervical cancer. The expression of PD-L1 in both mononuclear and cervical epithelial cells also exhibit an elevation with the progression of the lesions followed by a overexpression of pro-inflammatory cytokines IFN-γ and IL-12 and downregulation of anti-inflammatory cytokine IL-10 indicating a role of PD-1/PD-L1 pathway in cervical immunity.</div></div><div><h3>Conclusions</h3><div>PD-1 and PD-L1 may serve as diagnostic and prognostic biomarkers as well as valuable tools in immunotherapy for treating cancer and CIN.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"264 ","pages":"Article 155712"},"PeriodicalIF":2.9,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625817","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}