International journal of clinical and experimental pathology最新文献

{"title":"Prophylactic administration of PEPITEM in experimental autoimmune encephalomyelitis delays disease onset, inhibits leukocyte infiltration, and alleviates severity.","authors":"Mohammed Alassiri, Fahd Al Sufiani, Mohammed Aljohi, Asma Alanazi, Aiman S Alhazmi, Bahauddeen M Alrfaei, Hasan Alnakhli, Mohammed Alasseiri, Nora Alorf, Mashan L Abdullah","doi":"10.62347/LTAO2386","DOIUrl":"10.62347/LTAO2386","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS) is a chronic, immune-mediated neurological disorder in which the immune system mistakenly attacks the myelin sheath, affecting the communication between the brain and the rest of the body.</p><p><strong>Objective: </strong>This study investigated the prophylactic use of peptide inhibitor of trans-endothelial migration (PEPITEM), a novel peptide, in alleviating experimental autoimmune encephalomyelitis (EAE), a mouse model for Multiple Sclerosis (MS).</p><p><strong>Methods: </strong>Female C57BL/6 female mice were assigned to the control, untreated EAE, or PEPITEM group. EAE was induced in mice in the untreated EAE and PEPITEM groups through immunization by injecting an emulsion containing myelin oligodendrocyte glycoprotein 35-55 in complete Freund's adjuvant. Mice in these groups subsequently received PEPITEM or scramble peptide injections daily for 21 days. Then, all mice were euthanized to obtain samples for histologic and immunohistochemical analyses of central nervous system lymphocytic infiltrate. Levels of biomarkers, including myelin basic protein, microtubule-associated protein 2 (MAP-2), interleukin-17 (IL-17), and forkhead box P3 (Foxp3), were evaluated in both serum and spinal cord lysates using western blotting and enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>In the PEPITEM group, EAE onset was significantly delayed and disease severity was reduced compared to the untreated EAE group. Analysis of spinal cord tissues revealed a marked reduction in inflammatory cell infiltration following PEPITEM administration. Furthermore, PEPITEM treatment led to significantly reduced IL-17 and Foxp3 levels, highlighting its potential in mitigating inflammatory responses.</p><p><strong>Conclusion: </strong>PEPITEM has potent prophylactic potential against MS, providing a robust foundation for further exploration.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 12","pages":"492-505"},"PeriodicalIF":1.1,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of cGAS confers PARP inhibitor resistance in ovarian cancer via the TBK1-IRF3 axis.","authors":"Hongxia Guo, Rui Lu, Shuibin Yuan, Falin Xu, Chunyan Huang, Jingzhi Li, Wuqiong Ge, Yue Geng, Yan Zhang, Qiong Liu, Peng Wang, Wenqing Li","doi":"10.62347/XOPN6908","DOIUrl":"10.62347/XOPN6908","url":null,"abstract":"<p><strong>Objectives: </strong>Ovarian cancer is a gynecologic tumor with the highest mortality rate worldwide. Nonetheless, chemoresistance remains a significant obstacle in treating ovarian cancer. PARP inhibitors (PARPis) are effective drugs approved for maintenance therapy in ovarian cancer. However, the development of natural or acquired resistance to PARPis poses a major challenge for ovarian cancer treatment.</p><p><strong>Methods: </strong>Public database analysis of cGAS expression in relation to PARPi resistance. cCK-8 assay was used to determine cell survival. qPCR assay with Western Blot was implemented to determine gene expression and protein activation status.</p><p><strong>Results: </strong>Analysis of public databases revealed significantly higher cGAS expression in Olaparib-resistant cells and in recurrent ovarian tumors. Furthermore, high cGAS expression significantly promoted Olaparib tolerance in ovarian cancer cells. Our findings demonstrate that Olaparib treatment induces activation of the TBK1-IRF3 signaling axis downstream of cGAS, leading to the production of type I interferon. This, in turn, activates NF-κB and IL-6-STAT3 signaling, contributing to inflammation and PARPi resistance. Consequently, targeting cGAS effectively counteracts Olaparib resistance and enhances its efficacy in suppressing cancer cell growth, ultimately leading to cell death.</p><p><strong>Conclusions: </strong>Our study highlights the crucial function of cGAS signaling in mediating PARPi resistance in ovarian cancer cells. These findings provide valuable novel therapeutic strategies targeting cGAS to improve the efficacy of PARPi-based treatments for ovarian cancer.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"429-438"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Down-regulation of BRMS1 by DNA hypermethylation and its association with metastatic progression in triple-negative breast cancer.","authors":"Bin Kong, Zhi-Dong Lv, Yu Wang, Li-Ying Jin, Lei Ding, Zhao-Chuan Yang","doi":"10.62347/PBKP4984","DOIUrl":"https://doi.org/10.62347/PBKP4984","url":null,"abstract":"<p><p>[This corrects the article on p. 11076 in vol. 8, PMID: 26617826.].</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"439-441"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic anticancer activity of resveratrol with cisplatin and carboplatin in A549 lung adenocarcinoma cells.","authors":"Kareena Moar, Mettle Brahma, Anuja Pant, Mulaka Maruthi, Pawan Kumar Maurya","doi":"10.62347/RYSQ1416","DOIUrl":"10.62347/RYSQ1416","url":null,"abstract":"<p><strong>Background: </strong>This study looked at the efficacy of combining the phytochemical resveratrol with the anticancer drugs cisplatin and carboplatin on lung adenocarcinoma cell lines.</p><p><strong>Materials and methods: </strong>We used MTT assay and generation of Reactive Oxygen Species levels using molecular fluorogenic probe 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) to investigate the effects of resveratrol in combination with cisplatin and carboplatin on the proliferation and viability of cells and levels of reactive oxygen species (ROS).</p><p><strong>Results: </strong>Resveratrol has an anti-proliferative effect on A549 lung cancer cells, inhibiting cell proliferation in a dose and time-dependent manner. Resveratrol in conjunction with cisplatin and carboplatin inhibited cell proliferation synergistically. The combination therapy of cisplatin and carboplatin with Resveratrol showed enhanced growth inhibition of lung cancer cells in <i>in-vitro</i> with IC50 values of 15.09 ± 0.71 µM and IC50 values of 21.72 ± 1.9 µM, respectively. The present investigation also revealed the significant dose-dependent ROS generation in A549 cells by cisplatin, carboplatin, and their combination with resveratrol. Carboplatin treatment in combination with Resveratrol induced a higher generation of ROS (3.4-fold) when compared to carboplatin treatment (2.4-fold) at the highest concentration.</p><p><strong>Conclusions: </strong>Our findings offered a basis for further research for assessing the potential of Resveratrol as a therapeutic agent to treat lung adenocarcinoma and whether it can be used as an adjuvant with drugs like cisplatin and carboplatin for improving their efficacies. However, the underlying processes of cell inhibition and cell death should be thoroughly investigated.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"411-420"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between EPCAM upregulation and clinicopathological parameters and outcomes of breast cancer.","authors":"Nahid Nafissi, Saeed Azad Armaki, Ebrahim Babaee, Pegah Babaheidarian, Elaheh Safari, Soheila Sayad, Samine Saghafinia, Masoumeh Safaee","doi":"10.62347/EGXS1506","DOIUrl":"10.62347/EGXS1506","url":null,"abstract":"<p><strong>Introduction: </strong>EpCAM (epithelial cell adhesion molecule) protein expression was detected in 45 to 90% of breast cancers in different studies, and high expression levels were associated with poor outcomes in several retrospective analyses. This study aims to investigate the relationship between EpCAM and clinicopathological parameters and survival in breast cancer.</p><p><strong>Methodology: </strong>This study was conducted as a Quasi-Experimental Cohort Study to explore 100 breast cancer patients. After the surgical excision of breast cancer, pathology blocks were deparaffinized and subjected to IHC (immunohistochemistry) for EpCAM examination. Using a Roche VENTANA Benchmark GX automated staining instrument and a well-established IHC staining protocol, the expression of EpCAM in breast cancer tissue was assessed. Independent sample T-test and Chi squared and Logistic Regression test with STATA version 17 software were used for data analysis.</p><p><strong>Results: </strong>The difference in the distribution of the negative state of biomarkers (ER = estrogen receptor, PR = Progesterone receptor) and EPCAM positive group was significant (<i>P</i>-value = 0.002) (<i>P</i>-value = 0.006). A statistically insignificant distinction was observed in the distribution of the HER2 (human epidermal growth factor receptor) and EPCAM groups (<i>P</i>-value = 0.198). With 30.95% of those in the EPCAM-positive cohort experienced metastasis or recurrence. ER+ and PR+ decreased the chance of EPCAM positive by 0.25 and 0.29, respectively. HER2+ and Basal like breast cancer increase the chances of EPCAM being positive by 1.9 and 2.08, respectively. Basal like breast cancer increases the odds of EpCAM positive 2.19 times. Similarly, N2 and stage 3 increase the odds of EpCAM positive by 1.95 and 0.5 times, respectively.</p><p><strong>Conclusion: </strong>We found that Basal like breast cancer, HER2+, and stage 3 increase the chance of EpCAM positivity. It seems that EPCAM positive cancer has more chance for recurrence and metastasis.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"421-428"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: DLC-3 suppresses cellular proliferation, migration, and invasion in triple-negative breast cancer by the Wnt/β-catenin pathway.","authors":"Bin Kong, Zhi-Dong Lv, Jing Xia, Li-Ying Jin, Zhao-Chuan Yang","doi":"10.62347/WTHX6766","DOIUrl":"https://doi.org/10.62347/WTHX6766","url":null,"abstract":"<p><p>[This corrects the article on p. 1224 in vol. 12, PMID: 31933937.].</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"442-443"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment and analysis of a prognostic model of pancreatic ductal adenocarcinomas based on nerve-cancer crosstalk-related genes.","authors":"Lei Jiang, Xiaozhi Lu, Yuran Dai, Kuirong Jiang, Yi Miao, Jun Yu, Lingdi Yin, Jishu Wei","doi":"10.62347/GHUM8504","DOIUrl":"10.62347/GHUM8504","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant tumor with a five-year survival rate of 13%, the lowest among all malignant tumors. The work aims to use bioinformatics methods to mine Nerve-cancer crosstalk-related genes (NCCGs) in pancreatic cancer and evaluate their correlation with tumor stage and prognosis, thereby providing a new direction of development and experimental basis for pancreatic cancer treatment. This study included 185 individuals with PDAC from the TCGA database, together with clinical and RNA sequencing data. A review of prior studies revealed the mechanism of neural-cancer crosstalk and identified 42 neural-cancer crosstalk-related genes (NCCGs). Multivariate logistic regression analysis showed that NGFR (OR=39.076, 95% CI; P<0.05), CHRNB2 (OR=41.076, 95% CI; P<0.05), and CHRNA10 (OR=39.038, 95% CI; P<0.05) were identified as independent risk factors for PNI development. Pearson correlation analysis revealed that CHRNA10 was negatively connected with PDAC microsatellite instability, whereas CHRNA10, CHRNB2, and NGFR were negatively correlated with PDAC tumor mutation burden. The GEPIA database revealed that CHRNB2 expression was higher in stage I PDAC. The pancreatic cancer single-cell dataset PAAD_CRA001160 revealed that malignant tumor cells, ductal cells, endothelial cells and fibroblasts accounted for a large proportion in the tumor microenvironment of pancreatic cancer. Furthermore, the NGFR gene was shown to be more significantly expressed in various pancreatic cancer cells. Bioinformatics analysis was used to create a validated prognostic model of pancreatic cancer, which explored the critical mechanisms of neural-tumor interactions and revealed the potential of cancer-neural crosstalk-related genes as prognostic biomarkers and anti-tumor therapy targets.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"396-410"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha-fetoprotein, glypican-3, and kininogen-1 as biomarkers for the diagnosis of hepatocellular carcinoma.","authors":"Diana Gabriela Domínguez-Lazcano, Ingrid Simón-Lara, Jaime Morales-Romero, Verónica Rocío Vásquez-Garzón, Omar Elind Arroyo-Helguera, Julieta López-Vazquez, Alma D Campos-Parra, Brayan Hernández-Nopaltecatl, Ximena Andrea Rivera-Hernández, Sofía Quintana, Rebeca García-Román","doi":"10.62347/QSII4050","DOIUrl":"10.62347/QSII4050","url":null,"abstract":"<p><p>The hepatocarcinoma (HCC) is the most important liver tumor. It represents 90% of liver cancer cases. One of the main problems is the limited prompt cancer diagnosis and the advanced stages where the chances of treatment are limited. The main diagnostic methods for HCC are imaging techniques and liver biopsy. With advances in technology, proteins as significant diagnostic biomarkers have increased. The objective of this review is to describe the role of Alpha-fetoprotein (AFP), Glipican 3 (GPC-3), and Kininogen 1 (KNG-1) as biomarkers for the diagnosis of hepatocellular carcinoma. A systematic search of studies was carried out in the literature and the diagnostic values of these proteins were compared. The results showed that the combined use of biomarkers increases the diagnostic capacity for the detection of hepatocellular carcinoma.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 11","pages":"383-395"},"PeriodicalIF":1.1,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: CXCL12 chemokine expression suppresses human breast cancer growth and metastasis in vitro and in vivo.","authors":"Zhi-Dong Lv, Bin Kong, Xiang-Ping Liu, Qian Dong, Hai-Tao Niu, Yong-Hua Wang, Fu-Nian Li, Hai-Bo Wang","doi":"10.62347/GEVX3778","DOIUrl":"10.62347/GEVX3778","url":null,"abstract":"<p><p>[This corrects the article on p. 6671 in vol. 7, PMID: 25400746.].</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 10","pages":"381-382"},"PeriodicalIF":1.1,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PCSK7, a potential target for the treatment of age-related macular degeneration: inhibition of retinal epithelial cell death.","authors":"Xiaolong Zhang, Xin Zhao, Xiangyang Xin","doi":"10.62347/LEHU9944","DOIUrl":"10.62347/LEHU9944","url":null,"abstract":"<p><strong>Background: </strong>Age-related macular degeneration (AMD) is a complex disease with a pathophysiology that remains incompletely understood. PCSK7 is closely related to the normal development of ocular tissues; however, the roles and mechanisms of PCSK7 in AMD have yet to be elucidated. Therefore, the purpose of this study was to investigate the specific manifestations of PCSK7 in AMD.</p><p><strong>Methods: </strong>An AMD cell model was established by using hydrogen peroxide (H₂O₂)-treated ARPE-19 cells. The efficiency of PCSK7 overexpression was analyzed by western blotting (WB) and quantitative reverse transcription PCR (RT-qPCR). Subsequently, a Cell Counting Kit 8 (CCK-8) assay was employed to assess the proliferation of ARPE-19 cells, while flow cytometry and immunofluorescence were utilized to examine apoptosis. Iron accumulation and glutathione (GSH) levels in cells were measured using Enzyme-linked immunosorbent assay (ELISA), and WB was conducted to evaluate the expression of anti-ferroptosis protein. Finally, JC-1 staining was performed to assess mitochondrial membrane potential.</p><p><strong>Results: </strong>Overexpressing of PCSK7 enhanced the proliferation and inhibited the apoptosis of ARPE-19 cells treated with H₂O₂. Additionally, increased PCSK7 expression suppressed intracellular iron levels and GSH content, thereby inhibiting the ferroptosis process. Furthermore, overexpression of PCSK7 restored mitochondrial membrane potential, alleviating H₂O₂-induced mitochondrial damage.</p><p><strong>Conclusions: </strong>PCSK7 might be one of the targets for the treatment of AMD through the regulation of retinal epithelial cell death.</p>","PeriodicalId":13943,"journal":{"name":"International journal of clinical and experimental pathology","volume":"17 10","pages":"371-380"},"PeriodicalIF":1.1,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}