Discover. Oncology最新文献

{"title":"Integrated single-cell analysis reveals heterogeneity and therapeutic insights in osteosarcoma.","authors":"Dongan He, Xiaoqian Che, Haiming Zhang, Jiandong Guo, Lei Cai, Jian Li, Jinxi Zhang, Xin Jin, Jianfeng Wang","doi":"10.1007/s12672-024-01523-x","DOIUrl":"https://doi.org/10.1007/s12672-024-01523-x","url":null,"abstract":"<p><p>Osteosarcoma (OSA) is a primary bone malignancy characterized by its aggressive nature and high propensity for metastasis. Despite advancements in multimodal therapies, the clinical outcomes for OSA patients remain suboptimal, necessitating deeper molecular insights for improved therapeutic strategies. Here, we employed single-cell RNA sequencing (scRNA-seq) to elucidate the cellular heterogeneity and transcriptional dynamics of OSA tumors. Our study identified eleven distinct tumor cell subpopulations, including osteoblastic, chondroblastic, and myeloid lineages, each exhibiting unique transcriptional profiles associated with disease progression and metastasis. Epithelial-mesenchymal transition (EMT) emerged as a critical process driving aggressive phenotypes, supported by gene set enrichment analyses (GSVA) and transcription factor regulatory network analyses. Integration of copy number variation (CNV) data highlighted genomic alterations in osteoblastic and chondroblastic cells, implicating potential therapeutic targets. Furthermore, immune cell infiltration analyses revealed distinct immune profiles across OSA subtypes, correlating with tumor mutational burden (TMB) and clinical outcomes. Our findings underscore the complexity of OSA biology and provide a foundation for developing personalized treatment strategies targeting tumor heterogeneity and immune interactions.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647625","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":"Circ_0124346 facilitates cell proliferation of pancreatic adenocarcinoma cells by regulating lipid metabolism via miR-223-3p/ACSL3 axis.","authors":"Meng-Lu Shu, Wan-Ting Yang, Hui-Min Li, Cui-Juan Qian, Xiao-Sheng Teng, Jun Yao","doi":"10.1007/s12672-024-01550-8","DOIUrl":"https://doi.org/10.1007/s12672-024-01550-8","url":null,"abstract":"<p><strong>Background: </strong>Both lipid metabolism and cyclic RNAs (circRNAs) have been found to be involved in pancreatic adenocarcinoma (PAAD) progression, but the relationship between lipid metabolism and circRNAs remains unclear.</p><p><strong>Methods: </strong>The expression levels of miR-223-3p, circ_0124346, and acyl-CoA synthetase long chain family member 3 (ACSL3) were determined through qRT-PCR and Western blot analysis. Cell proliferation was evaluated using the CCK-8 and EdU incorporation assays. Cholesterol (CH) and triglyceride (TG) levels were quantified using relevant kits. The relationships between miR-223-3p and circ_0124346 or ACSL3 mRNA were examined by bioinformatics analysis, luciferase reporter, RNA-RNA pull-down, and RIP assays.</p><p><strong>Results: </strong>We observed a significant elevation in circ_0124346 expression in both pancreatic adenocarcinoma (PAAD) tissues and cell lines, and its expression level was shown to be correlated with tumor size. Circ_0124346 stimulated cell proliferation and facilitated lipid synthesis in PAAD cells. Additionally, we found that circ_0124346 functioned as a sponge for miR-223-3p, preventing miR-223-3p's binding to the 3'-UTR of ACSL3 mRNA, which subsequently led to an elevation in ACSL3 expression and promoted lipid synthesis. Accordingly, circ_0124346 knockdown resulted in a significant decrease in lipid synthesis and cell proliferation in PAAD cells, with partial reversal of these effects achieved via inhibiting miR-223-3p or overexpressing ACSL3.</p><p><strong>Conclusion: </strong>Our study demonstrated that circ_0124346 regulates lipid metabolism in PAAD cells via the miR-223-3p/ACSL3 axis, suggesting that targeting circ_0124346 may serve as a potential strategy for treating PAAD and assisting in its diagnosis.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647604","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":"TMSB4X is a regulator of inflammation-associated ferroptosis, and promotes the proliferation, migration and invasion of hepatocellular carcinoma cells.","authors":"Linlin Tang, Yangli Jin, Jinxu Wang, Xiuyan Lu, Mengque Xu, Mingwei Xiang","doi":"10.1007/s12672-024-01558-0","DOIUrl":"https://doi.org/10.1007/s12672-024-01558-0","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis and inflammation are involved in cancer progression. The aim of this study was to identify inflammation-associated ferroptosis regulators in hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>FerrDb database was searched for ferroptosis-related genes. RNA sequencing data and clinicopathologic information of HCC patients were downloaded from the Cancer Genome Atlas (TCGA) database. Weighted gene co-expression network analysis was applied to obtain the genes probably involved in inflammation-associated ferroptosis. Univariate Cox regression analysis was conducted to screen prognostic genes, and 10 machine learning algorithms were combined to find the optimal strategy to evaluate the prognosis of the patients based on the prognosis-related genes. The patients were divided into high risk group and low risk group, and the differentially expressed genes were obtained. Thymosin beta 4 X-linked (TMSB4X) was overexpressed or knocked down in HCC cell lines, and then qPCR, CCK-8, Transwell, flow cytometery assays were performed to detect the change of HCC cells' phenotypes, and Western blot was used to detect the change of ferroptosis markers.</p><p><strong>Results: </strong>157 genes related to inflammation and ferroptosis in HCC were obtained by WGCNA. rLasso algorithm, with the highest C-index, screened out 29 hub genes, and this model showed good efficacy to predict the prognosis of HCC patients. The patients in high risk group and low risk groups showed distinct molecular characteristics. TMSB4X was the most important gene which dominated the classification, and it was highly expressed in HCC samples. TMSB4X promoted the viability, migration and invasion, and repressed ferroptosis of HCC cells.</p><p><strong>Conclusion: </strong>The risk model constructed based on the inflammation-associated ferroptosis regulators is effective to predict the clinical outcome of HCC patients. TMSB4X, involved in inflammation-associated ferroptosis, is a potential biomarker and therapeutic target for HCC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647639","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":"Construction of a novel lipid drop-mitochondria-associated genetic profile for predicting the survival and prognosis of lung adenocarcinoma.","authors":"Ruijuan Cai, Hongsheng Lin, Qianwen Cheng, Qiyuan Mao, Chuchu Zhang, Ying Tan","doi":"10.1007/s12672-024-01526-8","DOIUrl":"https://doi.org/10.1007/s12672-024-01526-8","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is one of the most common malignant tumors. Although several treatments have been proposed, the long-term prognosis of this cancer is poor. Lipid droplets and mitochondria are important organelles that regulate energy metabolism in cells and are postulated to promote the occurrence and progression of tumors. However, few risk prediction models have been constructed based on lipid drop-mitochondria-related genes (LMRGs).</p><p><strong>Methods: </strong>In this study, we constructed a lipid drop-mitochondrial (LD-M) risk score model based on data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Biological functions and clinical benefits associated with the various risk scores were analyzed using R software, GraphPad Prism 9, and the online database system.</p><p><strong>Results: </strong>An LD-M risk score model comprising ABLIM3, AK4, CAV2, CPS1, CYP24A1, DLGAP5, FGR, and SH3BP5, was developed and its predictive power was validated. The risk score was closely associated with the cell cycle. Immunophenoscore (IPS) and Tumor immune dysfunction and exclusion (TIDE) results demonstrated that the low-risk group was more sensitive to immunotherapy. Drug sensitivity analysis indicated that BMS-754807, ZM447439, SB216763, and other drugs had lower IC50 values in the low-risk group.</p><p><strong>Conclusion: </strong>Our results suggest that the LD-M risk score is an effective prognostic indicator for individualized treatment of LUAD.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647608","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":"Single-cell expression and immune infiltration analysis of polyamine metabolism in breast cancer.","authors":"Xiliang Zhang, Hanjie Guo, Xiaolong Li, Wei Tao, Xiaoqing Ma, Yuxing Zhang, Weidong Xiao","doi":"10.1007/s12672-024-01524-w","DOIUrl":"10.1007/s12672-024-01524-w","url":null,"abstract":"<p><p>Breast cancer is one of the most threatening women health diseases worldwide and its molecular heterogeneity offers a range of response to therapy. The role of polyamine metabolism is receiving increasing attention. Polyamine metabolism not only plays an important role in the occurrence and development of breast cancer, but also interacts with tumor immune microenvironment. In this work, we applied single-cell RNA-sequencing (scRNA-seq) and systems immunological approaches to interrogate immune cell infiltration gene-to-gene co-expressions in the bulk tumor transcriptomes of breast cancer. We acquired breast cancer sample data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), evaluated the infiltration status of 22 immune cell types using CIBERSORTx tool, respectively. By leveraging the Retrospective Breast sample of various technologies including gene expression and methylation, we identified 46 breast cancer proliferation-associated co-expression modules using weighted gene coexpression network analysis (WGCNA) approach along with machine learning models which in turn delineated single cell level expressions features that these selected module possessed. We observed substantial cellular heterogeneity in the breast cancer microenvironment, where lineage-specific gene expression patterns were highly associated with tumor progression. Moreover, we also identified the gene modules correlated with immune cell infiltration level that could function as regulators in response to tumors for immune therapy. Moreover, risk scores were correlated with immune cell function in different patient groups defined by high- and low-risk. The findings of this study shed a new light upon molecular classification prognostic assessment and personalized treatment in breast cancer.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643917","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":"Single-cell data revealed the regulatory mechanism of TNK cell heterogeneity in liver metastasis from gastric cancer.","authors":"Jun Gao, Yujuan Liu, Lu Tao, Peng Zeng, Guiying Ye, Ying Zheng, Nai Zhang","doi":"10.1007/s12672-024-01528-6","DOIUrl":"10.1007/s12672-024-01528-6","url":null,"abstract":"<p><strong>Aim: </strong>The present work set out to classify cell subpopulations related to liver metastasis from gastric cancer (GC) and the mechanisms of their interactions with other immune cell subpopulations.</p><p><strong>Background: </strong>GC is characterized by a high degree of heterogeneity and liver metastasis. Exploring the mechanism of liver metastasis of GC from the perspective of heterogeneity of the tumor microenvironment (TME) might help improve the efficacy of GC treatment.</p><p><strong>Objective: </strong>Based on the cellular subpopulation characteristics of GC with liver metastasis, the regulatory mechanisms contributing to GC progression were analyzed, with special focuses on the roles of signaling pathways, transcription factors (TFs) and ligand-receptor pairs.</p><p><strong>Methods: </strong>The GSE163558 dataset was downloaded from the Gene Expression Omnibus (GEO) database to collect single-cell transcriptomic data of GC patients and their metastasis groups for cell clustering and relevant analyses. Differentially expressed genes (DEGs) in the GC and GC liver metastasis groups were screened and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. SCENIC analysis was used to mine TFs that affected cellular subpopulations during liver metastasis from GC. The relative expression levels of TFs in GC were determined using qRT-PCR. Transwell and wound healing assays were utilized to verify the regulation of the TFs on the migration and invasion of GC cells. Interaction network between the cellular subpopulations was developed applying CellChat.</p><p><strong>Results: </strong>Single-cell clustering was performed to group six major cell subpopulations, namely, Myeloid cells, B cells, Mast cells, Epithelial cells, Fibroblasts, and TNK cells, among which the number of TNK cells was significantly increased in the GC liver metastasis group. Differentially enriched pathways of TNK cells between GC and GC liver metastasis groups mainly included IL-17 and Pi3k-Akt signaling pathways. TNK cell subsets could be further categorized into CD8 T cells, Exhausted T cells, NK cells, NKT cells, and Treg cells, with the GC liver metastasis group showing significantly more CD8 T cells and NKT cells. FOS and JUNB were the TFs of TNK cell marker genes that contributed to liver metastasis from GC and the invasion and migration of GC cell lines. Significant differences in immune cell communication ligand-receptor pairs existed between the GC and GC liver metastasis groups.</p><p><strong>Conclusion: </strong>This study revealed the critical role of TNK cell subsets in GC with liver metastasis applying single-cell transcriptomics analysis. The findings provided an important theoretical basis for developing novel therapies to inhibit liver metastasis from GC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643915","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":"MicroRNA-mediated autophagy and drug resistance in cancer: mechanisms and therapeutic strategies.","authors":"Jinxing Wei, Xianghui Wang, Duo Yu, Yanyang Tu, Yaoyu Yu","doi":"10.1007/s12672-024-01525-9","DOIUrl":"10.1007/s12672-024-01525-9","url":null,"abstract":"<p><p>This paper provides an exhaustive overview of the intricate interplay between microRNAs (miRNAs) and autophagy in the context of human cancers, underscoring the pivotal role these non-coding RNAs play in modulating autophagic pathways and their implications for cancer development, progression, and resistance to therapy. MiRNAs, as critical regulators of gene expression post-transcription, influence various biological processes, including autophagy, a catabolic mechanism essential for cellular homeostasis, stress response, and survival. The review meticulously delineates the mechanisms through which miRNAs impact autophagy by targeting specific genes and signaling pathways, thereby affecting cancer cell proliferation, metastasis, and response to chemotherapy. It highlights several miRNAs with dual roles, acting either as oncogenes or tumor suppressors based on the cellular context and the specific autophagic pathways they regulate. The paper further explores the therapeutic potential of targeting miRNA-autophagy axis, offering insights into novel strategies for cancer treatment through modulation of this axis. Emphasizing the complexity of the miRNA-autophagy relationship, the review calls for more in-depth studies to unravel the nuanced regulatory networks between miRNAs and autophagy in cancer, which could pave the way for the development of innovative therapeutic interventions and diagnostic tools.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643911","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":"SLITRK2 as a prognostic and immunological biomarker in gastric cancer.","authors":"Huiqiong Zhu, Hailin Xiong, Xuli Guo, Haojie Liao, Shuyi Zhang","doi":"10.1007/s12672-024-01534-8","DOIUrl":"10.1007/s12672-024-01534-8","url":null,"abstract":"<p><strong>Background: </strong>SLIT and NTRK-like protein 2 (SLITRK2) encodes a transmembrane protein that regulates neurite outgrowth. Some studies have demonstrated that SLITRK2 overexpressed in glioma. But the expression pattern, prognostic value and immunologic function of SLITRK2 in tumors remains unknown.</p><p><strong>Methods: </strong>The expression pattern of SLITRK2 among pan-cancers was examined through the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx). We analyzed the association between SLITRK2 expression level and tumor stage among pan-cancers. Kaplan-Meier survival analysis was utilized to investigate the prognostic relevance of SLITRK2 across 33 different types of cancers. Moreover, the correlations among SLITRK2 expression, immune cell infiltration, immunomodulatory related genes, tumor mutation burden (TMB), microsatellite instability (MSI) were evaluated. The relationship between SLITRK2 expression and crucial genes mutations was also illustrated. By using tissue microarray (TMA), the expression of SLITRK2 in 89 paired gastric cancer (GC) tissues was investigated.</p><p><strong>Results: </strong>Our study indicated that SLITRK2 expression varied across cancers. Elevated SLITRK2 expression was positively related to advanced tumor stage, poor overall survival (OS) and reduced disease-free survival (DFS). Bioinformatic analyses underscore SLITRK2's role in immune response, with its expression significantly tied to immune cell infiltration and marker expression. Based on TMA data, SLITRK2 expression level was positively associated with differentiation, lymph node metastasis, AJCC stage, TNM stage, and poor survival outcome in GC patients.</p><p><strong>Conclusion: </strong>Our findings provided that SLITRK2 may function as a biomarker by regulating immune cell infiltration. In addition, we verified that high SLITRK2 expression was correlated with poor prognosis in GC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643932","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":"Correlation between thyroid dysfunction and efficacy of immune checkpoint inhibitors in patients with advanced solid tumors.","authors":"Cheng Zhao","doi":"10.1007/s12672-024-01546-4","DOIUrl":"10.1007/s12672-024-01546-4","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitors (ICIs) are currently the first line of tumor immunotherapy for the treatment of a wide range of tumors. However, the main side effect of immune checkpoint inhibitors is that they cause immune-related adverse events (irAEs) in patients. The relationship between the occurrence of immune side effects in patients and efficacy is controversial. The objective of this study was to confirm the relationship between patients who develop thyroid dysfunction after immune checkpoint inhibitors and efficacy.</p><p><strong>Methods: </strong>This study was a retrospective real-world clinical study, and a total of 50 patients with advanced tumors treated with immune checkpoint inhibitors at Anqing People's Hospital from 2020.8 to 2022.5 were retrospectively collected. Among them, 30 patients with hypothyroidism and 20 patients with normal or hyperthyroidism occurred, and the treatment effects and prognostic differences between the two groups were compared.</p><p><strong>Finding: </strong>After PD1 treatment in all patients, there were 10 cases of partial remission(PR), 18 cases of stable disease(SD) and 2 cases of progressive disease(PD) in patients who developed hypothyroidism, with a disease control rate(DCR) of 93.3% and objective remission rate(ORR) of 33.3%. There were 0 complete remission (CR) patient, 3 PR patients, 11 SD patients, 6 PD patients, 70.0% DCR and 15.0% ORR in patients who did not develop hypothyroidism. The DCR and ORR of patients who developed hypothyroidism were better than those of non-hypothyroid patients, and the difference was statistically significant (P < 0.05). Kaplan-Meier survival analysis showed that progression-free survival (PFS) reached 9.2 months (95% CI 7.726-10.779) in patients who developed hypothyroidism and did not hypothyroidism patients have a PFS of 7.3 months (95% CI 5.604-8.505), with a statistically significant difference (P = 0.0341 < 0.05). Further subgroup analysis revealed that among patients who developed hypothyroidism, PFS was 3.3 months (95% CI 0.630-5.440) in patients with cholangiocarcinoma, 6.89 months (95% CI 5.604-8.505) in patients with non-small cell lung cancer, > 12 months in patients with hepatocellular carcinoma, and 11.05 months (95% CI 9.308-12.792) in patients with esophageal cancer months and PFS for patients with gastric cancer was 9.74 months (95% CI 6.979-12.502).</p><p><strong>Interpretation: </strong>When patients with advanced tumors were treated with immune checkpoint inhibitors, DCR and ORR were higher in patients who developed hypothyroidism, and patients had better PFS. The benefits were greater in patients with gastric, esophageal, and hepatocellular carcinomas.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643909","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":"Research trends, hotspots and future directions of tertiary lymphoid structures in cancer: a comprehensive informatics analysis and visualization study.","authors":"Chengdong Yu, Jiawei Xu, Siyi Xu, Lei Tang, Qinyuan Han, Zhengkui Sun","doi":"10.1007/s12672-024-01556-2","DOIUrl":"10.1007/s12672-024-01556-2","url":null,"abstract":"<p><p>Many studies have reported the presence of tertiary lymphoid structures (TLSs) in cancer, but the research progress of TLSs in cancer has not been systematically analyzed. Therefore, we analyzed the global scientific knowledge in the field using informatics methods. The results showed that TLSs in cancer have received increasing attention since the 21st century, with an annual publication growth rate of 27.86%. Unsupervised hierarchical clustering based on machine learning further categorized the research features into four clusters, with the cluster related to immunotherapy being considered an emerging cluster. TLSs and immunotherapy were identified as the top two hotspots with the highest occurrence frequency and total link strength. The Walktrap algorithm indicated that \"TLSs, carcinoma, prognostic value\" and \"high endothelial venules, germinal-centers, node-like structures\" are important to TLSs but remain underexplored, representing promising research directions. These findings suggest that cancer-related TLSs have brought new insights into antitumor immunity, and targeting TLSs has the potential to transform the landscape of antitumor immunotherapy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643913","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}