Cytojournal最新文献

{"title":"Upregulation of phosphatase and tensin homolog deleted on chromosome ten inhibits lung cancer cell proliferation by suppressing the oncogene polo-like kinase 1 and inducing autophagy.","authors":"Weizhou Jiang, Pei Wang, Limin Huang","doi":"10.25259/Cytojournal_146_2024","DOIUrl":"10.25259/Cytojournal_146_2024","url":null,"abstract":"<p><strong>Objective: </strong>Lung cancer is one of the main causes of cancer-related mortality globally, and it poses considerable therapeutic challenges. Polo-like kinase 1 (PLK1) exhibits upregulation in lung cancer, and PLK1 silencing promotes autophagy in lung cancer cells, which inhibits tumor progression. The phosphatase and tensin homolog deleted on chromosome ten (PTEN) acts as a tumor suppressor gene. This study aimed to investigate whether PTEN regulates autophagy and inhibits lung cancer-cell proliferation by suppressing PLK1.</p><p><strong>Material and methods: </strong>In this study, we evaluated cell proliferation by silencing or overexpressing PLK1 and PTEN in A549 cells through 5-ethynyl-2'-deoxyuridine labeling and cloning experiments. The autophagy levels were detected through transmission electron microscopy, real-time quantitative polymerase chain reaction, and Western blot. Finally, the results of <i>in vitro</i> experiment were further verified using an <i>in vivo</i> xenograft tumor animal model.</p><p><strong>Results: </strong>The upregulation of PTEN suppressed PLK1 expression in lung cancer cells and reduced their proliferation rate. In addition, the overexpression of PTEN has been associated with the growth of lung cancer tumors. In parallel, the levels of autophagy of lung cancer cells rose in response to PTEN upregulation <i>in vivo</i> and <i>in vitro</i>.</p><p><strong>Conclusion: </strong>This study revealed that PTEN promotes the autophagy of lung cancer cells and inhibits cell proliferation and tumor growth by suppressing PLK1 expression. This finding provides a new strategy for lung cancer treatment by utilizing the autophagy-regulating effect of PTEN to inhibit lung cancer growth by targeting PLK1.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"10"},"PeriodicalIF":2.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434129","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":"Silencing fatty acid-binding protein 4 improved sepsis-induced myocardial dysfunction through anti-apoptotic and antioxidant effects by mammalian target of rapamycin signaling pathway.","authors":"Zhilei Qiu, Kexing Zhou, Qinyao Qi, Wei Chen","doi":"10.25259/Cytojournal_157_2024","DOIUrl":"10.25259/Cytojournal_157_2024","url":null,"abstract":"<p><strong>Objective: </strong>One of the main complications of sepsis that is linked to poor clinical outcomes and high mortality is sepsis-induced myocardial dysfunction (SIMD). Fatty acid-binding protein 4 (FABP4) is a protein that is expressed in macrophages and adipose tissue and is involved in inflammation and apoptosis in various pathological processes. The purpose of this study was to investigate the role of FABP4 in SIMD.</p><p><strong>Material and methods: </strong>The H9c2 cell model of myocardial dysfunction induced by septicemia was established by lipopolysaccharide (LPS). Measurements of cell viability, apoptosis, reactive oxygen species levels, mitochondrial activity, and proinflammatory factor expression were used to assess FABP4's involvement in SIMD. In addition, the expression level of key proteins in the mammalian target of rapamycin (mTOR) signaling pathway was analyzed using Western blot. Finally, the combination of AZD-8055 further demonstrated the possibility of mTOR as a therapeutic target for SIMD.</p><p><strong>Results: </strong>Silencing FABP4 expression drastically increased H9c2 cell viability and mitochondrial function. In addition, by upregulating B-cell lymphoma-2 (Bcl-2) and downregulating Bcl-2 associated X protein, FABP4 silencing improved LPS-induced anti-apoptosis of H9c2 cells. Finally, silencing FABP4 alleviated SIMD through the mTOR signaling pathway. However, the therapeutic effect was inhibited when FABP4 silencing was combined with the mTOR inhibitor AZD-8055.</p><p><strong>Conclusion: </strong>Silencing FABP4 alleviates LPS-induced inflammatory response and apoptosis in H9c2 cells and enhances mitochondrial function through the mTOR signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"8"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434110","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 protein 6 promotes gastric cancer progression: Modulating immune evasion through autophagy and oxidative stress pathways.","authors":"Xinyue Zhang, Di Na","doi":"10.25259/Cytojournal_230_2024","DOIUrl":"10.25259/Cytojournal_230_2024","url":null,"abstract":"<p><strong>Objective: </strong>Immune response is crucial in the development of gastric cancer (GC), and Jumonji domain-containing protein 6 (JMJD6) plays an important role in mediating GC cell behavior. This study aims to elucidate the mechanisms through which JMJD6 affects autophagy and immune evasion in GC cells.</p><p><strong>Material and methods: </strong>Immunocytochemistry was employed to assess JMJD6 and programmed death-ligand 1 (PD-L1) levels in gastric cancer cell line (MKN-45) and gastric epithelial cell line cells. MKN-45 cells with JMJD6 knockdown and overexpression were generated. The effect of JMJD6 on MKN-45 cells was evaluated using cell counting kit-8 assay, cellular fluorescence staining, and Transwell assays. Western blot analysis and immunofluorescence techniques were employed to investigate the regulation of autophagy by JMJD6. Reactive oxygen species (ROS) levels were evaluated by applying ROS fluorescence staining. Meanwhile, the protein and gene expression levels of molecules related to antioxidant stress responses were assessed through immunofluorescence assays and quantitative real-time polymerase chain reactions, respectively.</p><p><strong>Results: </strong>The expression levels of JMJD6 and PD-L1 were elevated in GC cells (<i>P</i> < 0.001). JMJD6 overexpression enhanced MKN-45 cell migration, invasion, and colony formation <i>in vitro</i> (<i>P</i> < 0.001). In MKN-45 cells, the epithelial-mesenchymal transition was promoted by JMJD6 upregulation but was notably inhibited by JMJD6 knockdown (<i>P</i> < 0.001). JMJD6 overexpression increased the expression levels of Sequestosome 1, Microtubule-associated protein 1A/1B-light chain 3 (LC3)II/LC3I, and PD-L1 in MKN-45 cells, and autophagy activation further elevated PD-L1 levels (<i>P</i> < 0.001). In addition, JMJD6 overexpression reduced ROS production and increased the expression of molecules related to antioxidant stress response, with the reverse effects observed on JMJD6 knockdown (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>JMJD6 notably facilitates GC progression and immune evasion by modulating autophagy and oxidative stress pathways.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"6"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434078","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":"Hypoxia-induced S-phase kinase-interacting protein 2 knockdown repressed the progression of melanoma through extracellular signal-regulated kinase 1/2 pathway.","authors":"Yong Hu","doi":"10.25259/Cytojournal_117_2024","DOIUrl":"10.25259/Cytojournal_117_2024","url":null,"abstract":"<p><strong>Objective: </strong>Hypoxia intensely drives the development of malignant tumors, including skin cutaneous melanoma (SKCM). S-phase kinase-interacting protein 2 (SKP2) is known to participate in the progression of human tumors. The purpose of this study is to explore whether SKP2 acts as a hypoxic response gene during SKCM progression.</p><p><strong>Material and methods: </strong>SKP2 expression in SKCM tissues was analyzed using The Cancer Genome Atlas database. Anoxic experiments were conducted to simulate an anoxic environment. 5-Ethynyl-2'-deoxyuridine and colony formation assays were used to evaluate SKCM cell growth. Scratch healing and Transwell assays were applied to measure the migration and invasion abilities of SKCM cells. An immunoblotting assay was used to detect the levels of extracellular signal-regulated kinase (ERK)1/2 pathway proteins. In addition, the ERK-specific agonist LM22B-10 was added to confirm whether the ERK1/2 signaling pathway is required for SKP2-mediated SKCM progression under hypoxic conditions.</p><p><strong>Results: </strong>SKP2 was significantly upregulated in SKCM tissues and closely related to adverse outcomes in patients. Moreover, SKP2 levels increased in SKCM cells under normoxic conditions and further elevated under hypoxic conditions. SKP2 deficiency led to the reduced proliferation, migration, and invasion potential of cells under hypoxic conditions. Mechanically, SKP2 silencing blocked the ERK1/2 pathway in hypoxic cells, and the activation of the ERK1/2 pathway rescued the suppression effect of SKP2 on the hypoxia-induced progression of SKCM.</p><p><strong>Conclusion: </strong>SKP2 deficiency repressed the hypoxic-induced progression of SKCM through the ERK1/2 pathway. This novel discovery regarding the SKP2/ERK1/2 axis might provide new insights into the pathogenesis of SKCM.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"9"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434076","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":"NPC intracellular cholesterol transporter 2 regulates the anti-apoptotic protein baculoviral inhibitor of apoptosis repeat containing 3 and affects drug resistance in gastric cancer.","authors":"Yanan Xu, Yanbo Wang, Wenyue Zhao, Fengli Liu","doi":"10.25259/Cytojournal_116_2024","DOIUrl":"10.25259/Cytojournal_116_2024","url":null,"abstract":"<p><strong>Objective: </strong>Cisplatin (DDP)-based chemotherapy medications are frequently used as the initial line of treatment for cancer patients, including those with stomach cancer. At present, DDP resistance is a frequent problem in chemotherapy for advanced gastric cancer (GC). This study aimed to investigate the function of NPC intracellular cholesterol transporter 2 (NPC2) in GC cells.</p><p><strong>Material and methods: </strong>The expression of NPC2 and baculoviral inhibitor of apoptosis repeat containing 3 (BIRC3) in gastric epithelial cells-1, BGC823, and BGC823/DDP cells was determined by Western blotting and quantitative real-time polymerase chain reaction, respectively. Subsequently, the proliferative capacity and viability of BGC823 cells were assessed by 3-(4,5-dimethylthiazol2-yl)-2.5-diphenyl-2-tetrazolium bromide, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay, and colony-formation assay. Finally, the association of NPC2 and BIRC3 with the nuclear factor kappa-B (NF-κB) pathway was determined by Western Blot.</p><p><strong>Results: </strong>In GC cells, NPC2 transcription increased, and DDP-resistant cells showed higher NPC2 expression levels than their parental cells (<i>P</i> < 0.001). In terms of mechanism, compared with parental cells, overexpressing NPC2, DDP-resistant cells showed resistance to DDP. Knocking down NPC2 increased the apoptotic response of DDP-resistant cells to DDP and blocked the cancer cells resistant to DDP exhibiting BIRC3, thereby promoting GC cell apoptosis (<i>P</i> < 0.001). Importantly, involving NF-κB signaling overturned the NPC2-mediated DDP resistance.</p><p><strong>Conclusion: </strong>NPC2 regulated BIRC3 and affected drug resistance in GC. Therefore, NPC2 and BIRC3 may be new targets for cancer patient treatment following DDP therapy and act as roadblocks to overcome chemotherapy resistance in GC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"7"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434081","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":"Relationship between transmembrane emp24 domain containing 2 expression and tumor stem cell characteristics in oral cancer.","authors":"Yanhui Wu, Shunchu Zhang, Guimei Zou","doi":"10.25259/Cytojournal_132_2024","DOIUrl":"10.25259/Cytojournal_132_2024","url":null,"abstract":"<p><strong>Objective: </strong>Transmembrane Emp24 Domain Containing 2 <b>(</b>TMED2) is a mediator of membrane protein trafficking involved in intracellular protein transport. Recent research suggests that TMED2 plays an important role in the development and metastasis of tumors; however, its exact mechanisms in oral cancer (OC) remain unclear. This study aims to elucidate the role and possible mechanisms of TMED2 in OC.</p><p><strong>Material and methods: </strong>We investigated the impact of TMED2 knockdown on the invasion, migration, and proliferation capabilities of OC cells. Furthermore, we analyzed the <i>in vitro</i> and <i>in vivo</i> interactions between TMED2 and polypeptide-N-acetylgalactosaminyltransferase 7 (GALNT7) as well as explored the regulatory function of TMED2 on GALNT7. The alterations in stem cell markers were assessed using clone formation assays, western blot, and quantitative real-time polymerase chain reaction.</p><p><strong>Results: </strong>The upregulation of TMED2 promoted the proliferation and invasion abilities of OC cells. Further analysis revealed that TMED2 enhanced the stem-like properties and tumorigenicity of OC cells by directly regulating the expression of GALNT7. <i>In vivo</i> and <i>in vitro</i> results suggested that silencing TMED2 expression reduced the incidence of OC.</p><p><strong>Conclusion: </strong>Our data imply that TMED2 stimulates GALNT7 transcription, which in turn amplifies the stem-like characteristics and carcinogenic potential of OC cells. Moreover, the block of TMED2 prevents cancers from growing and spreading <i>in vivo</i>. This finding provides a new therapeutic target for the treatment of OC and highlights the critical role of TMED2 in the condition.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"5"},"PeriodicalIF":2.5,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434107","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":"Fourth Cytopathology Monograph and Atlas Series Book Titled \"Cytopathology of Urine (& The Paris System)\" as Extension of Open Access Charter of Cytopathology Foundation Inc.","authors":"Vinod B Shidham, Shikha Bose, Zubair Baloch, Lester J Layfield","doi":"10.25259/Cytojournal_256_2024","DOIUrl":"10.25259/Cytojournal_256_2024","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"4"},"PeriodicalIF":2.5,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434121","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":"E2F1-mediated <i>ESPL1</i> transcriptional activation predicts poor prognosis and promotes the proliferation of leiomyosarcoma.","authors":"Xiaojuan Yang, Guihua Miao, Qin Wang, Qin Yu, Qinsheng Hu, Gang Tan","doi":"10.25259/Cytojournal_178_2024","DOIUrl":"10.25259/Cytojournal_178_2024","url":null,"abstract":"<p><strong>Objective: </strong>Soft tissue and bone cancers, collectively known as sarcomas, constitute a diverse array of uncommon tumors originating from connective tissues. Among sarcomas, leiomyosarcoma (LMS) is one of the most frequently encountered subtypes. This study aims to investigate the expression, clinical significance, biological regulation, and dysregulation mechanisms of extra spindle pole bodies like 1 (<i>ESPL1</i>), a gene critical for cell cycle regulation in LMS.</p><p><strong>Material and methods: </strong>Bioinformatics analysis was performed using the data from The Cancer Genome Atlas-Sarcoma and Genotype-Tissue Expression datasets. Functional experiments to assess cell proliferation and the cell cycle were performed in LMS cells (SK-LMS-1) after <i>ESPL1</i> knockdown. Bioinformatics analyses were conducted to identify the potential transcriptional regulators of ESPL1. The regulatory relationship between <i>ESPL1</i> and the E2F transcription factor 1 (E2F1) was validated through the various molecular assays.</p><p><strong>Results: </strong><i>ESPL1</i> is significantly overexpressed in LMS compared with normal muscle tissue. High <i>ESPL1</i> expression is associated with a shorter progression-free interval (PFI) in sarcoma patients, particularly in the LMS subset. <i>ESPL1</i> expression might be an independent prognostic factor for poor overall survival and PFI in LMS patients. Functional studies in the LMS cell line SK-LMS-1 demonstrated that <i>ESPL1</i> knockdown slowed cell proliferation and increased G2/M cell cycle arrest, suggesting its crucial role in maintaining LMS cell viability and genomic integrity. Further bioinformatics analysis identified the E2F1 transcription factor as a key regulator of ESPL1 expression in LMS. Mechanistic investigations demonstrated that E2F1 interacts with the <i>ESPL1</i> promoter, leading to transcriptional activation.</p><p><strong>Conclusion: </strong>These findings highlight the ESPL1-E2F1 axis as a potential prognostic biomarker and therapeutic target in LMS.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"3"},"PeriodicalIF":2.5,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434045","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":"Astragalus polysaccharide attenuates retinal ischemia reperfusion-induced microglial activation through sortilin-related vacuolar protein sorting 10 domain containing receptor 2/laminin subunit alpha 1 upregulation.","authors":"Juanjuan Li, Hua Li, Chunling Wei, Chen Chen, Zhikun Zheng","doi":"10.25259/Cytojournal_131_2024","DOIUrl":"10.25259/Cytojournal_131_2024","url":null,"abstract":"<p><strong>Objective: </strong>Microglial activation is a hallmark of pathogenic retinal conditions such as retinal ischemia-reperfusion (RIR). While sortilin-related vacuolar protein sorting 10 domain containing receptor 2 (Sorcs2) and laminin subunit alpha 1 (Lama1) have been implicated in neuroinflammatory processes, their roles in regulating microglial activation in RIR are not reported. The current work studied the potential of Sorcs2 and Lama1 as negative regulators of microglial activation in RIR and assessed the therapeutic potential of Astragalus polysaccharide (AP).</p><p><strong>Material and methods: </strong>Transcriptome profiling was conducted in retinal specimens of RIR group 72 h after RIR induction. Oxygen-glucose deprivation/reperfusion (OGD/R) in rat microglial cells was employed as the cellular induction model of RIR. The functional role of Sorcs2 and Lama1 in dictating microglial activation was investigated <i>in vitro</i> and <i>in vivo</i> using lentivirus-based gene expression. Further, the potential effect of AP on RIR-mediated microglial activation was investigated.</p><p><strong>Results: </strong>Sorcs2 and Lama1 were identified as two downregulated genes in retinal samples following RIR. OGD/R induction triggered pro-inflammatory microglial activation and induced the downregulation of Sorcs2 and Lama1. Sorcs2 or Lama1 overexpression hindered OGD/R-induced microglial activation <i>in vitro</i> and attenuated inflammatory expansion of microglia cells in RIR-induced rat retinal samples. AP treatment was able to neutralize the oxidative stress, promote the expression of Sorcs2 and Lama1, and suppress microglial activation.</p><p><strong>Conclusion: </strong>Our findings pinpoint Sorcs2 and Lama1 as negative regulators of microglial activation in RIR. AP could be employed as an antioxidant to attenuate microglial activation and ameliorate the inflammatory damages in RIR.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"2"},"PeriodicalIF":2.5,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434037","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":"Histopathological findings of 687 thyroid nodules, suspicious for malignancy on ultrasound, with an indeterminate cytopathological diagnosis after the combination of the Bethesda System and <i>BRAF</i> mutation status.","authors":"Xueqin Meng, Ruoqing Hou, Meidi Zhang, Jiaying Chen, Kai Zhang, Jiawei Li","doi":"10.25259/Cytojournal_97_2024","DOIUrl":"10.25259/Cytojournal_97_2024","url":null,"abstract":"<p><strong>Objective: </strong>The conflicting results of the Bethesda system for reporting thyroid cytopathology (BSRTC) and B-Raf proto-oncogene (<i>BRAF)</i> mutation status during pre-operative fine-needle aspiration cytology (FNAC) of thyroid nodules create a dilemma for clinicians in devising appropriate treatment strategies for patients. This study provides a report on the histopathological findings of 687 thyroid nodules with an indeterminate cytological diagnosis after the combination of the BSRTC and <i>BRAF</i> mutation status.</p><p><strong>Material and methods: </strong>The clinical data of patients with thyroid nodules, suspicious of malignancy at ultrasound (US), who underwent US-guided FNAC between December 2020 and March 2023 at our cancer center were reviewed. Patients with an indeterminate diagnosis, that is, conflicting results of the BSRTC and <i>BRAF</i> mutation status after FNAC, were enrolled. The following four combinations of BSRTC and <i>BRAF</i> mutation status were considered indeterminate: (1) Group 1, BSRTC I and positive for a <i>BRAF</i> mutation; (2) Group 2, BSRTC II and positive for a <i>BRAF</i> mutation; (3) Group 3, BSRTC III and positive for a <i>BRAF</i> mutation; and (4) Group 4, BSRTC V and negative for a <i>BRAF</i> mutation. Finally, only patients who underwent surgical treatment at our center were included in the data analysis.</p><p><strong>Results: </strong>Among the 1,044 eligible patients, 687 underwent surgical treatment. Of the 687 patients, 117 were in Group 1, 14 in Group 2, 394 in Group 3, and 162 in Group 4. Histopathological examination showed that 677 (98.5%) patients had papillary thyroid cancer, including 585 with papillary thyroid microcarcinoma, whereas only 10 (1.5%) had benign nodules. The malignancy rates were 98.3%, 100%, 98.7%, and 98.1% for Groups 1 to 4, respectively. Among the 387 patients in category 4A by the thyroid imaging reporting and data system (TI-RADS 4A) through the US, the malignancy rate was 98.4%, and for the 116 nodules <5 mm in diameter in the US, the malignancy rate was 99.1%. When combining TI-RADS 4A and a nodule diameter <5 mm, the malignancy rate was 98.9% (88/89). A total of 179 patients (26.1%) had histopathologically confirmed central cervical lymph node metastasis, and 46 (6.8%) had lateral cervical lymph node metastasis. Two nodules in Group 1, five nodules in Group 3, and three nodules in Group 4 were determined to be benign post-surgery. The benign thyroid nodules included seven dysplastic, one adenomatous, one fibrotic, and one hyperplastic.</p><p><strong>Conclusion: </strong>Thyroid nodules, suspicious of malignancy on US, after the combined interpretation of BSRTC and <i>BRAF</i> mutation status following pre-operative FNAC had a high risk of malignancy. Repeat US-guided FNAC for indeterminate thyroid nodules is highly recommended in clinical practice.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"1"},"PeriodicalIF":2.5,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434125","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}