CytojournalPub Date : 2026-02-04eCollection Date: 2026-01-01DOI: 10.25259/Cytojournal_62_2025
Chenwei Jiao, Lichao Zhu, Anzhi Zhu, Xiaoqing Xu
{"title":"Actin-related protein 6 regulates the Hedgehog signaling pathway: Molecular basis for stemness maintenance of hepatoma cells.","authors":"Chenwei Jiao, Lichao Zhu, Anzhi Zhu, Xiaoqing Xu","doi":"10.25259/Cytojournal_62_2025","DOIUrl":"10.25259/Cytojournal_62_2025","url":null,"abstract":"<p><strong>Objective: </strong>The liver is a common primary cancer site in humans. Actin-related protein 6 (ACTR6) plays a key role in liver cancer. The aim of this study was to further explore the regulatory molecular mechanism of ACTR6 in liver cancer.</p><p><strong>Material and methods: </strong>In this study, hepatoma cell HuH-7 was evaluated by 5-ethynyl-2'-deoxyuridine staining, colony formation, Transwell assay, and wound healing assay. The possible mechanism of the action of ACTR6 on hepatocellular carcinoma cells was evaluated by analyzing sphere formation, the key factors of the Hedgehog (Hh) signaling pathway, and molecules related to cell stemness. Then, xenografted mouse tumor models were used to demonstrate the promotion effect of ACTR6 on liver cancer <i>in vivo</i>.</p><p><strong>Results: </strong>ACTR6 was highly expressed in HuH-7h and HepG2 cells (<i>P</i> < 0.001). Silencing ACTR6 inhibited the migration, invasion capacity, and activity of HuH-7 (<i>P</i> < 0.01). ACTR6 activated the Hh signaling pathway by upregulating the expression of Sonic Hedgehog, patched 1, smoothened, and glioma-associated transcription factor 1. In addition, ACTR6 increased the molecular level of cell stemness by increasing the level of cellular myelocytomatosis oncogene, octamer-binding transcription factor 4, Nanog homeobox, and SRY-box transcription factor 2. Vismodegib reversed the promoting effect of ACTR6 on the Hh signaling pathway and stem-related proteins in cells.</p><p><strong>Conclusion: </strong>ACTR6 regulates the molecular basis of stemness maintenance of liver cancer cells through the Hh signaling pathway and promotes the occurrence of liver cancer. This study provides possible targets for the clinical treatment of liver cancer.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"9"},"PeriodicalIF":2.2,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147311547","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}
CytojournalPub Date : 2026-02-03eCollection Date: 2026-01-01DOI: 10.25259/Cytojournal_184_2025
Nadir Paksoy
{"title":"Quo vadis? Evolving trends in fine-needle aspiration cytology practice: A personal perspective.","authors":"Nadir Paksoy","doi":"10.25259/Cytojournal_184_2025","DOIUrl":"10.25259/Cytojournal_184_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"8"},"PeriodicalIF":2.2,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291692","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":"Current situation and future prospect of biobank.","authors":"Ruizhe Wang, Xiaotong Han, Lvcheng Jin, Zitong Wang, Huimin Sun, Yunxiang Zhang","doi":"10.25259/Cytojournal_82_2025","DOIUrl":"10.25259/Cytojournal_82_2025","url":null,"abstract":"<p><p>Biobanks are essential infrastructures dedicated to the systematic collection, processing, storage, and distribution of biological samples and related data, serving as fundamental resources for biomedical research. Their application ranges from clinical research and epidemiological investigations to public health monitoring, facilitating the identification of disease-associated genetic variations and the exploration of gene-environment interactions. Biobanks provide valuable resources for systems biology and interdisciplinary research, significantly broadening the scope and depth of scientific inquiry. This review explores the development history, current landscape, and future prospects of global biobanking initiatives, highlighting notable advancements in technological innovation and methodological practices. It also scrutinizes prevailing challenges and envisions future trajectories for development. In the era of personalized medicine, biobanks are expected to play a more critical role by providing the data and samples needed for the development of individualized therapies. By surmounting existing impediments and fostering international collaboration, biobanks are poised to propel scientific breakthroughs and elevate global healthcare standards. This article aims to comprehensively elucidate the trajectory of biobanking development and its profound influence on biomedical research.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"7"},"PeriodicalIF":2.2,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291649","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-15a-5p suppresses triple-negative breast cancer cell proliferation and invasion by modulating T-cell immunoreceptor associated with immunoglobulin and ITIM domain expression.","authors":"Shaopeng Feng, Yunjie Song, Jintao Cui, Zhihao Wu, Limin Wei","doi":"10.25259/Cytojournal_40_2025","DOIUrl":"10.25259/Cytojournal_40_2025","url":null,"abstract":"<p><strong>Objective: </strong>Treating triple-negative breast cancer (TNBC) is a major challenge owing to its unique biological characteristics. This study aimed to elucidate the molecular interaction between microRNA-15a-5p and T-cell immunoreceptor associated with immunoglobulin and ITIM domains (TIGIT) in TNBC.</p><p><strong>Material and methods: </strong>The GSE22513 microarray dataset was subjected to bioinformatic analysis. MDA-MB-231 and MDA-MB-468 cells were transfected with lentiviral constructs for overexpressing TIGIT and microRNA (miRNA) mimics for overexpressing miR-15a-5p. Western blot and quantitative real-time polymerase chain reaction analyses were conducted to quantify TIGIT and miR-15a-5p levels of pre- and post-transfection. Cell proliferation, migration, invasiveness, cell cycle distribution, and apoptosis were assessed using cell counting kit-8, wound-healing, colony formation, transwell assays, and flow cytometry, respectively.</p><p><strong>Results: </strong>This study identified 139 genes (37 upregulated and 102 downregulated genes). Elevated TIGIT levels exhibited a significant link to unfavorable outcomes in individuals with breast cancer (BC). Additional analyses demonstrated that TIGIT expression in BC cell lines was substantially increased compared with that in normal breast cells. Overexpressing miR-15a-5p effectively inhibited TIGIT expression and consequently suppressed TNBC cell proliferation, invasion, and migration. This inhibition prompted G2/M phase accumulation and enhanced cellular mortality.</p><p><strong>Conclusion: </strong>miR-15a-5p exerts tumor-suppressive effects through TIGIT downregulation, thereby mitigating the malignant phenotype of TNBC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"6"},"PeriodicalIF":2.2,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291643","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}
CytojournalPub Date : 2026-01-23eCollection Date: 2026-01-01DOI: 10.25259/Cytojournal_90_2025
Le Xin, Shuoyu Han, Zixin Wang, Xinyu Yuan, Yiwei Ye, Jidong Liu, Xing Bao, Jinjun Ye
{"title":"Tripartite motif-containing protein 28 promotes drug resistance to bortezomib in gastric cancer through proteasome activity regulation.","authors":"Le Xin, Shuoyu Han, Zixin Wang, Xinyu Yuan, Yiwei Ye, Jidong Liu, Xing Bao, Jinjun Ye","doi":"10.25259/Cytojournal_90_2025","DOIUrl":"10.25259/Cytojournal_90_2025","url":null,"abstract":"<p><strong>Objective: </strong>Gastric cancer (GC) persists as a leading global cause of cancer-related mortality. Although bortezomib (BTZ), a proteasome inhibitor, has demonstrated efficacy in treating various cancers, its therapeutic potential is hindered by drug resistance in GC. This study aims to explore the regulatory role of tripartite motif-containing protein 28 (TRIM28) in BTZ resistance in GC cells and to evaluate the antitumor effect of targeting TRIM28 in combination with BTZ.</p><p><strong>Material and methods: </strong>We established control groups (including Lenti-control and short hairpin non-targeting control groups), TRIM28-overexpressing (OE), and TRIM28-knockdown models using the MGC-803 gastric cancer cell line to investigate TRIM28-mediated BTZ resistance. A series of assays was performed, including cell counting kit-8 analysis to assess cell viability, flow cytometry for apoptosis analysis, colony formation assays to evaluate cell proliferation, western blot to measure the protein expression of 20S proteasome subunits (α1/4 and β1/2/5), proteasome activity assays, and immunohistochemistry to assess TRIM28 expression in clinical samples. Bioinformatic tools were also used to analyze the clinical correlation of TRIM28 expression with cancer stage and grade.</p><p><strong>Results: </strong>Our results demonstrate that TRIM28 markedly enhanced BTZ resistance in GC cells. TRIM28 OE increased cell viability, inhibited apoptosis, enhanced colony-forming ability, upregulated the expression of proteasome subunits, and increased proteasome activity, contributing to a protective effect against BTZ-induced cytotoxicity. For the clinical GC samples, TRIM28 was highly expressed in tumor tissues, and its expression was correlated with advanced cancer stages and high tumor grades.</p><p><strong>Conclusion: </strong>TRIM28 is critical in promoting BTZ resistance in GC cells. Targeting TRIM28 could potentiate BTZ treatment outcomes and offer a promising therapeutic strategy for overcoming drug resistance in GC treatment.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"5"},"PeriodicalIF":2.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291641","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}
CytojournalPub Date : 2026-01-23eCollection Date: 2026-01-01DOI: 10.25259/Cytojournal_16_2025
Bo Su, Lianjie Cheng, Fanding Meng, Hongfei Yan, Peng Su, Longbin Bai
{"title":"Melanocortin 1 receptor alleviates collagen-induced arthritis by upregulating T helper 1/T helper 17 cells and downregulating regulatory T cells.","authors":"Bo Su, Lianjie Cheng, Fanding Meng, Hongfei Yan, Peng Su, Longbin Bai","doi":"10.25259/Cytojournal_16_2025","DOIUrl":"10.25259/Cytojournal_16_2025","url":null,"abstract":"<p><strong>Objective: </strong>Arthritis is a common chronic disease. The T cell subpopulation, as a key element in the immune system, plays a crucial role in arthritis. This work aimed to explore the involvement of melanocortin 1 receptor (MC1R) in collagen-induced arthritis (CIA) and how it affects the balance of proinflammatory and anti-inflammatory T cell subsets.</p><p><strong>Material and methods: </strong>Using flow cytometry, the ratios of T helper (Th)1, Th17, and regulatory T (Treg) cells were examined. Using the enzyme-linked immunosorbent assay, pro-interleukin (IL)-17, interferon (IFN)-g, anti-IL-10, and IL-4 were measured.</p><p><strong>Results: </strong>MC1R knockout (MC1R-KO) mice exhibited an increase in the proportion of Th1 and Th17 cells compared with wild-type mice. The proportion of Treg cells in MC1R-KO mice was reduced. The levels of IL-17 and IFN-g in MC1R-KO mice increased, whereas those of IL-10 and IL-4 decreased.</p><p><strong>Conclusion: </strong>MC1R-KO mice exacerbated CIA by upregulating the numbers of Th1 and Th17 cells and decreasing the proportion of Treg cells. The increased production of IL-17 and IFN-g, along with the reduced IL-10 and IL-4 levels, further contributed to the enhanced inflammatory response. These findings suggest that MC1R plays a crucial role in the regulation of immune responses and inflammation in CIA. Targeting MC1R may have therapeutic potential for autoimmune diseases characterized by dysregulated T cell subsets.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"4"},"PeriodicalIF":2.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291703","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":"Transcription factor EGR1 orchestrates ferroptosis to mitigate sepsis-induced myocardial injury by enhancing ferroportin expression.","authors":"Sihua Jiang, Guolin Song, Hangqi Zhu, Xiaosong Wang, Tingting Pan, Zhuoqing Dai","doi":"10.25259/Cytojournal_68_2025","DOIUrl":"10.25259/Cytojournal_68_2025","url":null,"abstract":"<p><strong>Objective: </strong>Myocardial injury is a devastating complication of sepsis and a leading cause of mortality in critically ill patients. This study aimed to investigate the role and underlying mechanisms of early growth response factor 1 (EGR1) in sepsis-induced myocardial injury (SIMI).</p><p><strong>Material and methods: </strong>A rat model of SIMI was established using cecal ligation and puncture, and <i>in vivo</i> and <i>in vitro</i> experiments were conducted. <i>In vivo</i>, the myocardial tissue levels of cytokines, myocardial injury markers, apoptosis, and reactive oxygen species (ROS) were measured, along with the expression levels of EGR1, ferroportin (FPN), cystine/glutamate transporter ( xCT), and glutathione peroxidase 4 (GPX4). <i>In vitro</i>, H9c2 cardiomyoblast cell line ( H9c2) cardiomyocytes were transfected to overexpress or silence EGR1, and cell viability, oxidative stress, ferroptosis-related indicators, and mitochondrial membrane potential (ΔYm) were assessed. Transcriptome sequencing and dual-luciferase reporter gene assays were performed to analyze the mechanism of EGR1-mediated transcriptional regulation of FPN.</p><p><strong>Results: </strong>Septic rats exhibited significant inflammation, myocardial injury, apoptosis, and oxidative stress. Transcriptome sequencing revealed that EGR1 expression was downregulated in the myocardium of septic rats and associated with the ferroptosis pathway. Dual-luciferase reporter gene assays confirmed that EGR1 is directly bound to and activates the FPN promoter. <i>In vitro</i>, EGR1 overexpression significantly promoted H9c2 cardiomyocyte viability, reduced malondialdehyde (MDA) and iron (II) ion (Fe<sup>2+</sup>) levels, increased glutathione (GSH) levels, upregulated the FPN/xCT/GPX4 axis, maintained ΔYm, and inhibited ROS production. Conversely, EGR1 knockdown exhibited opposite effects. <i>In vivo</i>, EGR1 overexpression effectively attenuated myocardial injury; improved myocardial histopathology; significantly increased EGR1, FPN, xCT, and GPX4 expression levels; significantly reduced serum Fe<sup>2+</sup> and MDA levels; increased GSH levels; and improved the survival rate of septic rats.</p><p><strong>Conclusion: </strong>This study provides a novel finding that EGR1 plays a pivotal protective role in myocardial injury through the direct transcriptional activation of FPN. Mechanistically, EGR1 alleviates SIMI by transcriptionally activating the FPN/xCT/GPX4 axis, which leads to the suppression of ferroptosis and oxidative stress and the preservation of mitochondrial function.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"3"},"PeriodicalIF":2.2,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291659","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":"Jumonji domain-containing 6 promotes the expansion of neuroblastoma stem cells by activating the wingless/ integrated pathway.","authors":"Zuoqing Li, Wenzong Gao, Pengfei Gao, Yingchun Fei, Huadong Chen, Hong Jiang, Juntao Xie, Zhe Xu","doi":"10.25259/Cytojournal_41_2025","DOIUrl":"10.25259/Cytojournal_41_2025","url":null,"abstract":"<p><strong>Objective: </strong>Cancer stem cells are involved in chemotherapy resistance. Neuroblastoma (NB) is a common solid tumor in children, which is responsible for about 15% of pediatric cancer deaths. Jumonji domain-containing 6 (JMJD6), which is an arginine demethylase and lysine hydroxylase, regulates the progression of various tumors. However, the molecular mechanism underlying JMJD6's activity in NB stem cells remains unclear. Thus, this study aims to explore the role of JMJD6 in NB stem cells.</p><p><strong>Material and methods: </strong>Side population and sphere formation assays were used to investigate the role of JMJD6 in NB stem cell expansion. Immunohistochemistry was performed to determine the expression level of JMJD6 in NB tissues. Luciferase reporter assays were used to discover the effect of JMJD6 on the wingless/integrated (WNT) pathway.</p><p><strong>Results: </strong>JMJD6 was upregulated in NB tissues and cells (<i>P</i> < 0.05). NB patients with high JMJD6 levels had poor outcomes. JMJD6 could serve as an independent prognostic factor for NB. <i>JMJD6</i> overexpression promoted NB stem cell expansion, whereas <i>JMJD6</i> knockdown had the opposite effect, as determined by cell and animal models. Mechanism Roche studies showed that JMJD6 promoted NB stem cell expansion by activating the WNT pathway.</p><p><strong>Conclusion: </strong>JMJD6 promotes NB stem cell expansion by activating the WNT pathway, thereby providing a new target for NB therapy and a prognostic factor for patients with NB.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"2"},"PeriodicalIF":2.2,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291700","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}
CytojournalPub Date : 2026-01-12eCollection Date: 2026-01-01DOI: 10.25259/Cytojournal_263_2024
Madhuri Dindalkoppa, Prajna K Shetty, U S Dinesh, Shruti Vimal, Anita P Javalgi
{"title":"Usefulness of fine needle aspiration cytology in diagnosis of soft tissue tumors and its correlation with histopathological features.","authors":"Madhuri Dindalkoppa, Prajna K Shetty, U S Dinesh, Shruti Vimal, Anita P Javalgi","doi":"10.25259/Cytojournal_263_2024","DOIUrl":"10.25259/Cytojournal_263_2024","url":null,"abstract":"<p><strong>Objective: </strong>Fine needle aspiration cytology (FNAC) is a standard diagnostic tool and has several advantages which are specific to soft tissue tumors (STT). STT arises from non-epithelial and extra-skeletal tissue of the body, excluding the reticuloendothelial system, glia, and supporting tissues of organs. Primary STTs are very rare and encompass a wide range of different tumor types; therefore, the classification and diagnosis remain complex. If the tumor is diagnosed as benign, surgery may not be necessary. However, in the case of malignancy, a cytological diagnosis allows for the initiation of palliative treatment. This study was conducted to evaluate the role of FNAC in the diagnosis of STT by sub classifying them based on their cytology features and finally correlating their FNAC findings with histopathological results with special reference to immunohistochemistry (IHC) in diagnostic challenging cases.</p><p><strong>Material and methods: </strong>It was a hospital-based retrospective study conducted in a tertiary care center, over a period of 2 years, i.e., from July 2016 to May 2018. After obtaining approval from the ethics committee of the institution, the study was carried out. All STT cases subjected to FNAC followed by incisional, excisional, or core needle biopsy or complete resection for histopathological examination were studied. The slides of these patients were retrieved and reviewed to establish a proper diagnosis. IHC was carried out in most cases whenever there was a diagnostic dilemma.</p><p><strong>Results: </strong>In our study, among 50 patients who presented with STT, 40 were benign, and 10 were malignant. The median age of incidence was 41, and male-to-female ratio was 0.85:1. The most common site was the trunk. There were four discordant cases, and the final evaluation of all results showed sensitivity, specificity, positive predictive value of tests, and negative predictive value of tests of FNAC as 100%, 76.92%, 92.5%, and 100%, respectively.</p><p><strong>Conclusion: </strong>In STT, most were benign tumors, with lipomas being the most common among them. While benign and malignant were easy to diagnose, intermediate spindle cell tumors were often missed on cytology. These intermediate tumors represent the diagnostic \"grey zone.\" With increasing experience, STT can be diagnosed more accurately. FNAC is therefore a standard pre-operative diagnostic tool and a reliable alternative to open biopsy for diagnosing STT.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"1"},"PeriodicalIF":2.2,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147311615","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}
CytojournalPub Date : 2025-12-29eCollection Date: 2025-01-01DOI: 10.25259/Cytojournal_176_2025
Shuanzeng Wei
{"title":"Molecular cytopathology: The future of pathology?","authors":"Shuanzeng Wei","doi":"10.25259/Cytojournal_176_2025","DOIUrl":"10.25259/Cytojournal_176_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"106"},"PeriodicalIF":3.1,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151105","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}