Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.2881
Chun-Yao Cheng, Wen-Rui Hao, Tzu-Hurng Cheng
In this editorial we comment on the article published in a recent issue of the World Journal of Gastrointestinal Oncology . Characterized by high mortality rates and geographical variations in its incidence, esophageal cancer poses a major global health challenge. This editorial article synthesizes insights from the review of esophageal cancer conducted by Qu et al , which highlights the importance of tailored screening and treatment strategies. Key themes include the effect of regional disparities on screening protocols, advancements in early detection methodologies, and therapeutic management disparities between different regions. By embracing personalized approaches grounded in regional nuances and technological innovation, the article advocates for comprehensive and collaborative efforts to improve patient outcomes in esophageal cancer care.
{"title":"Esophageal cancer: A global challenge requiring tailored strategies","authors":"Chun-Yao Cheng, Wen-Rui Hao, Tzu-Hurng Cheng","doi":"10.4251/wjgo.v16.i7.2881","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.2881","url":null,"abstract":"In this editorial we comment on the article published in a recent issue of the World Journal of Gastrointestinal Oncology . Characterized by high mortality rates and geographical variations in its incidence, esophageal cancer poses a major global health challenge. This editorial article synthesizes insights from the review of esophageal cancer conducted by Qu et al , which highlights the importance of tailored screening and treatment strategies. Key themes include the effect of regional disparities on screening protocols, advancements in early detection methodologies, and therapeutic management disparities between different regions. By embracing personalized approaches grounded in regional nuances and technological innovation, the article advocates for comprehensive and collaborative efforts to improve patient outcomes in esophageal cancer care.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141646837","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.2925
Ki Bae Kim, D. Shin, K. E. Yeob, S. Y. Kim, J. Han, Seon Mee Park, Jong Heon Park, Jong Hyock Park
BACKGROUND Little is known about disparities in diagnosis and treatment among colorectal cancer (CRC) patients with and without disabilities. AIM To investigate the patterns of diagnosis, treatment, and survival for people with and without disabilities who had CRC. METHODS We performed a retrospective analysis using the Korean National Health Insurance Service database, disability registration data, and Korean Central Cancer Registry data. The analysis included 21449 patients with disabilities who were diagnosed with CRC and 86492 control patients diagnosed with CRC. RESULTS The overall distribution of CRC stage was not affected by disability status. Subjects with disabilities were less likely than those without disabilities to undergo surgery [adjusted odds ratio (aOR): 0.85; 95% confidence interval (95%CI): 0.82-0.88], chemotherapy (aOR: 0.84; 95%CI: 0.81-0.87), or radiotherapy (aOR: 0.90; 95%CI: 0.84-0.95). The rate of no treatment was higher in patients with disabilities than in those without disabilities (aOR: 1.48; 95%CI: 1.41-1.55). The overall mortality rate was higher in patients with disabilities [adjusted hazard ratio (aHR): 1.24; 95%CI: 1.22-1.28], particularly severe disabilities (aHR: 1.57; 95%CI: 1.51-1.63), than in those without disabilities. CONCLUSION Patients with severe disabilities tended to have a late or unknown diagnosis. Patients with CRC and disabilities had lower rates of treatment with almost all modalities compared with those without disabilities. During the follow-up period, the mortality rate was higher in patients with disabilities than in those without disabilities. The diagnosis and treatment of CRC need improvement in patients with disabilities.
{"title":"Disparities in the diagnosis and treatment of colorectal cancer among patients with disabilities","authors":"Ki Bae Kim, D. Shin, K. E. Yeob, S. Y. Kim, J. Han, Seon Mee Park, Jong Heon Park, Jong Hyock Park","doi":"10.4251/wjgo.v16.i7.2925","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.2925","url":null,"abstract":"BACKGROUND\u0000 Little is known about disparities in diagnosis and treatment among colorectal cancer (CRC) patients with and without disabilities.\u0000 AIM\u0000 To investigate the patterns of diagnosis, treatment, and survival for people with and without disabilities who had CRC.\u0000 METHODS\u0000 We performed a retrospective analysis using the Korean National Health Insurance Service database, disability registration data, and Korean Central Cancer Registry data. The analysis included 21449 patients with disabilities who were diagnosed with CRC and 86492 control patients diagnosed with CRC.\u0000 RESULTS\u0000 The overall distribution of CRC stage was not affected by disability status. Subjects with disabilities were less likely than those without disabilities to undergo surgery [adjusted odds ratio (aOR): 0.85; 95% confidence interval (95%CI): 0.82-0.88], chemotherapy (aOR: 0.84; 95%CI: 0.81-0.87), or radiotherapy (aOR: 0.90; 95%CI: 0.84-0.95). The rate of no treatment was higher in patients with disabilities than in those without disabilities (aOR: 1.48; 95%CI: 1.41-1.55). The overall mortality rate was higher in patients with disabilities [adjusted hazard ratio (aHR): 1.24; 95%CI: 1.22-1.28], particularly severe disabilities (aHR: 1.57; 95%CI: 1.51-1.63), than in those without disabilities.\u0000 CONCLUSION\u0000 Patients with severe disabilities tended to have a late or unknown diagnosis. Patients with CRC and disabilities had lower rates of treatment with almost all modalities compared with those without disabilities. During the follow-up period, the mortality rate was higher in patients with disabilities than in those without disabilities. The diagnosis and treatment of CRC need improvement in patients with disabilities.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141646483","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3364
Shuang Liu, Liu-Xiang Chen, L. Ye, Bing Hu
The publication by Qu et al provided a comprehensive discussion about the epidemiology, etiology, histopathology, early detection, and endoscopic treatment of esophageal carcinoma (EC) and summarized the progress in the advanced technologies for screening and endoscopic resection for EC. In this editorial, we will provide deeper insight into the challenges that hinder practical application of these advanced technologies along with the role of these technologies in upper endoscopy quality. More efforts need to be made to overcome the challenges and add the value of these technologies in upper endoscopy quality. Clinical outcomes of management strategies after noncurative endoscopic dissection for early EC patients need further investigation. The experiences with noncurative endoscopic resection of other organs may have certain implications for noncurative resection of early EC.
{"title":"Challenges in early detection and endoscopic resection of esophageal cancer: There is a long way to go","authors":"Shuang Liu, Liu-Xiang Chen, L. Ye, Bing Hu","doi":"10.4251/wjgo.v16.i7.3364","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3364","url":null,"abstract":"The publication by Qu et al provided a comprehensive discussion about the epidemiology, etiology, histopathology, early detection, and endoscopic treatment of esophageal carcinoma (EC) and summarized the progress in the advanced technologies for screening and endoscopic resection for EC. In this editorial, we will provide deeper insight into the challenges that hinder practical application of these advanced technologies along with the role of these technologies in upper endoscopy quality. More efforts need to be made to overcome the challenges and add the value of these technologies in upper endoscopy quality. Clinical outcomes of management strategies after noncurative endoscopic dissection for early EC patients need further investigation. The experiences with noncurative endoscopic resection of other organs may have certain implications for noncurative resection of early EC.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141645890","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3032
Han-Xuan Liu, Jie Feng, Jing-Jing Jiang, Wan-Jun Shen, Yu Zheng, Gang Liu, Xiang-Yang Gao
BACKGROUND Colorectal cancer (CRC) prognosis prediction is currently a major challenge. Epigenetic regulation has been widely reported for its role in cancer development. AIM To construct a robust prognostic signature, we used developed and validated across datasets. METHODS After constructing the signature, the prognostic value of the signature was evaluated in the TCGA cohort and six independent datasets (GSE17526, GSE17537, GSE33113, GSE37892, GSE39048 and GSE39582). The clinical, genomic and transcriptomic features related to the signature were identified. The correlations of the signature score with immune cell infiltration and cell-cell interactions were analyzed. The correlations between the signature score and the sensitivity to different drugs were also predicted. RESULTS In the TCGA cohort, patients in the low-risk group according to the signature score had longer survival than those in the high-risk group, and this finding was validated in the validation datasets. The signature was a prognostic factor independent of age and sex and was correlated with stage and PD-1 /PD-L1 expression. Area under the receiving operating characteristic curve was 0.72. Genomic association analyses revealed that samples from high-risk patients exhibited chromosomal instability. Transcriptomic analyses revealed that the signature score was significantly associated with multiple cellular pathways. Bulk RNA-seq and single-cell sequencing data revealed that the signature reflected differences in infiltrating immune cell-tumor cell interactions, especially for macrophages. The signature also predicted the putative drug sensitivity of CRC samples. CONCLUSION The signature is a valuable biomarker for predicting CRC prognosis and reflects multiple features of CRC, especially macrophage infiltration in the microenvironment.
{"title":"Integrated single-cell and bulk RNA sequencing revealed an epigenetic signature predicts prognosis and tumor microenvironment colorectal cancer heterogeneity","authors":"Han-Xuan Liu, Jie Feng, Jing-Jing Jiang, Wan-Jun Shen, Yu Zheng, Gang Liu, Xiang-Yang Gao","doi":"10.4251/wjgo.v16.i7.3032","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3032","url":null,"abstract":"BACKGROUND\u0000 Colorectal cancer (CRC) prognosis prediction is currently a major challenge. Epigenetic regulation has been widely reported for its role in cancer development.\u0000 AIM\u0000 To construct a robust prognostic signature, we used developed and validated across datasets.\u0000 METHODS\u0000 After constructing the signature, the prognostic value of the signature was evaluated in the TCGA cohort and six independent datasets (GSE17526, GSE17537, GSE33113, GSE37892, GSE39048 and GSE39582). The clinical, genomic and transcriptomic features related to the signature were identified. The correlations of the signature score with immune cell infiltration and cell-cell interactions were analyzed. The correlations between the signature score and the sensitivity to different drugs were also predicted.\u0000 RESULTS\u0000 In the TCGA cohort, patients in the low-risk group according to the signature score had longer survival than those in the high-risk group, and this finding was validated in the validation datasets. The signature was a prognostic factor independent of age and sex and was correlated with stage and PD-1 /PD-L1 expression. Area under the receiving operating characteristic curve was 0.72. Genomic association analyses revealed that samples from high-risk patients exhibited chromosomal instability. Transcriptomic analyses revealed that the signature score was significantly associated with multiple cellular pathways. Bulk RNA-seq and single-cell sequencing data revealed that the signature reflected differences in infiltrating immune cell-tumor cell interactions, especially for macrophages. The signature also predicted the putative drug sensitivity of CRC samples.\u0000 CONCLUSION\u0000 The signature is a valuable biomarker for predicting CRC prognosis and reflects multiple features of CRC, especially macrophage infiltration in the microenvironment.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141644925","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3193
Hui Yang, Xiao-Wei Chen, Xue-Jie Song, Hai-Yang Du, Fu-Chun Si
BACKGROUND Esophageal carcinoma (EC) is one of the most prevalent cancers in human populations worldwide. Baitouweng decoction is one of the most important Chinese medicine formulas, with the potential to treat cancer. AIM To investigate the role and mechanism of Baitouweng decoction on EC cells. METHODS Differentially expressed genes (DEGs) in EC tissues and normal tissues were screened by the cDNA microarray technique and by bioinformatics methods. The target genes of microRNAs were predicted based on the TargetScan database and verified by dual luciferase gene reporter assay. We used Baitouweng decoction to intervene EC cells, and detected the activity of EC9706 and KYSE150 cells by the MTT method. Cell cycle and apoptosis were measured by flow cytometry. The expression of BUB1 mRNA and miR-495-3p was measured by qRT-PCR. The protein levels of BUB1, STAT3, p-STAT3, CCNB1, CDK1, Bax, Caspase3, and Caspase9 were measured by Western blot analysis. The migration and invasion abilities of the cells were measured by wound-healing assay and Transwell invasion assay, respectively. RESULTS DEGs identified are involved in biological processes, signaling pathways, and network construction, which are mainly related to mitosis. BUB1 was the key hub gene, and it is also a target gene of miR-495-3p. Baitouweng decoction could upregulate miR-495-3p and inhibit BUB1 expression. In vitro experiments showed that Baitouweng decoction significantly inhibited the migration and invasion of EC cells and induced apoptosis and G2/M phase arrest. After treatment with Baitouweng decoction, the expression of Bax, Caspase 3, and Caspase 9 in EC cells increased significantly, while the expression of BUB1, CCNB1, and CDK1 decreased significantly. Moreover, the STAT3 signaling pathway may play an important role in this process. CONCLUSION Baitouweng decoction has a significant inhibitory effect on EC cell growth. BUB1 is a potential therapeutic target for EC. Further analysis showed that Baitouweng decoction may inhibit the growth of EC cells by upregulating miR-495-3p targeting the BUB1-mediated STAT3 signal pathway.
{"title":"Baitouweng decoction suppresses growth of esophageal carcinoma cells through miR-495-3p/BUB1/STAT3 axis","authors":"Hui Yang, Xiao-Wei Chen, Xue-Jie Song, Hai-Yang Du, Fu-Chun Si","doi":"10.4251/wjgo.v16.i7.3193","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3193","url":null,"abstract":"BACKGROUND\u0000 Esophageal carcinoma (EC) is one of the most prevalent cancers in human populations worldwide. Baitouweng decoction is one of the most important Chinese medicine formulas, with the potential to treat cancer.\u0000 AIM\u0000 To investigate the role and mechanism of Baitouweng decoction on EC cells.\u0000 METHODS\u0000 Differentially expressed genes (DEGs) in EC tissues and normal tissues were screened by the cDNA microarray technique and by bioinformatics methods. The target genes of microRNAs were predicted based on the TargetScan database and verified by dual luciferase gene reporter assay. We used Baitouweng decoction to intervene EC cells, and detected the activity of EC9706 and KYSE150 cells by the MTT method. Cell cycle and apoptosis were measured by flow cytometry. The expression of BUB1 mRNA and miR-495-3p was measured by qRT-PCR. The protein levels of BUB1, STAT3, p-STAT3, CCNB1, CDK1, Bax, Caspase3, and Caspase9 were measured by Western blot analysis. The migration and invasion abilities of the cells were measured by wound-healing assay and Transwell invasion assay, respectively.\u0000 RESULTS\u0000 DEGs identified are involved in biological processes, signaling pathways, and network construction, which are mainly related to mitosis. BUB1 was the key hub gene, and it is also a target gene of miR-495-3p. Baitouweng decoction could upregulate miR-495-3p and inhibit BUB1 expression. In vitro experiments showed that Baitouweng decoction significantly inhibited the migration and invasion of EC cells and induced apoptosis and G2/M phase arrest. After treatment with Baitouweng decoction, the expression of Bax, Caspase 3, and Caspase 9 in EC cells increased significantly, while the expression of BUB1, CCNB1, and CDK1 decreased significantly. Moreover, the STAT3 signaling pathway may play an important role in this process.\u0000 CONCLUSION\u0000 Baitouweng decoction has a significant inhibitory effect on EC cell growth. BUB1 is a potential therapeutic target for EC. Further analysis showed that Baitouweng decoction may inhibit the growth of EC cells by upregulating miR-495-3p targeting the BUB1-mediated STAT3 signal pathway.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141648676","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3011
Jiarong Shang, Jin Zhu, Lu Bai, Delida Kulabiek, Xiao-Xue Zhai, Xia Zheng, Jun Qian
BACKGROUND Adipocytes, especially adipocytes within tumor tissue known as cancer-associated adipocytes, have been increasingly recognized for their pivotal role in the tumor microenvironment of gastric cancer (GC). Their influence on tumor progression and patient prognosis has sparked significant interest in recent research. The main objectives of this study were to investigate adipocyte infiltration, assess its correlation with clinical pathological features, develop a prognostic prediction model based on independent prognostic factors, evaluate the impact of adipocytes on immune cell infiltration and tumor invasiveness in GC, and identify and validate genes associated with high adipocyte expression, exploring their potential diagnostic and prognostic value. AIM To explore the relationship between increased adipocytes within tumor tissue and prognosis in GC patients as well as the associated mechanisms and potential biomarkers, using public databases and clinical data. METHODS Using mRNA microarray datasets from the Gene Expression Omnibus database and clinical samples from Jiangsu Provincial Hospital, survival and regression analyses were conducted to determine the relevant prognostic factors in GC. Feature gene selection was performed using least absolute shrinkage and selection operator and support vector machine recursive feature elimination algorithms, followed by differential gene expression analysis, gene ontology, pathway analysis, and Gene Set Enrichment Analysis. Immune cell infiltration was analyzed using the CIBERSORT algorithm. RESULTS Tumor adipocyte infiltration correlated with poor prognosis in GC, leading to the development of a highly accurate and discriminative prognostic prediction model. Key genes, ADH1B , SFRP1 , PLAC9 , and FABP4 , were identified as associated with high adipocyte expression in GC. The diagnostic and prognostic potential of these identified genes was validated using independent datasets. Downregulation of immune cells was observed in GC with high adipocyte expression. CONCLUSION GC with high intratumoral adipocyte expression demonstrated aggressive tumor biology and a poorer prognosis. The genes ADH1B , SFRP1 , PLAC9 , and FABP4 have been identified as holding diagnostic and prognostic significance in GC. These findings strongly support the use of adipocyte expression as a valuable indicator of tumor invasiveness and anticipated patient outcomes in GC.
{"title":"Adipocytes impact on gastric cancer progression: Prognostic insights and molecular features","authors":"Jiarong Shang, Jin Zhu, Lu Bai, Delida Kulabiek, Xiao-Xue Zhai, Xia Zheng, Jun Qian","doi":"10.4251/wjgo.v16.i7.3011","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3011","url":null,"abstract":"BACKGROUND\u0000 Adipocytes, especially adipocytes within tumor tissue known as cancer-associated adipocytes, have been increasingly recognized for their pivotal role in the tumor microenvironment of gastric cancer (GC). Their influence on tumor progression and patient prognosis has sparked significant interest in recent research. The main objectives of this study were to investigate adipocyte infiltration, assess its correlation with clinical pathological features, develop a prognostic prediction model based on independent prognostic factors, evaluate the impact of adipocytes on immune cell infiltration and tumor invasiveness in GC, and identify and validate genes associated with high adipocyte expression, exploring their potential diagnostic and prognostic value.\u0000 AIM\u0000 To explore the relationship between increased adipocytes within tumor tissue and prognosis in GC patients as well as the associated mechanisms and potential biomarkers, using public databases and clinical data.\u0000 METHODS\u0000 Using mRNA microarray datasets from the Gene Expression Omnibus database and clinical samples from Jiangsu Provincial Hospital, survival and regression analyses were conducted to determine the relevant prognostic factors in GC. Feature gene selection was performed using least absolute shrinkage and selection operator and support vector machine recursive feature elimination algorithms, followed by differential gene expression analysis, gene ontology, pathway analysis, and Gene Set Enrichment Analysis. Immune cell infiltration was analyzed using the CIBERSORT algorithm.\u0000 RESULTS\u0000 Tumor adipocyte infiltration correlated with poor prognosis in GC, leading to the development of a highly accurate and discriminative prognostic prediction model. Key genes, ADH1B , SFRP1 , PLAC9 , and FABP4 , were identified as associated with high adipocyte expression in GC. The diagnostic and prognostic potential of these identified genes was validated using independent datasets. Downregulation of immune cells was observed in GC with high adipocyte expression.\u0000 CONCLUSION\u0000 GC with high intratumoral adipocyte expression demonstrated aggressive tumor biology and a poorer prognosis. The genes ADH1B , SFRP1 , PLAC9 , and FABP4 have been identified as holding diagnostic and prognostic significance in GC. These findings strongly support the use of adipocyte expression as a valuable indicator of tumor invasiveness and anticipated patient outcomes in GC.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141646859","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3321
Da-Ya Zhang, Fei-Hu Bai
BACKGROUND The immune microenvironment (IME) in hepatocellular carcinoma (HCC) plays a pivotal role in determining patient outcomes and responses to treatment. This area is witnessing rapid growth in research interest. However, there is a lack of comprehensive bibliometric analyses that dissect trends and potential focal points in this field. AIM To explore the evolution of research on the IME in HCC from January 1, 2004, to December 31, 2023, using bibliometric methodologies. METHODS English articles and reviews concerning the IME of HCC were retrieved from the Web of Science Core Collection with a search date of December 31, 2023. The R package Bibliometrix was employed to compute basic bibliometric characteristics, illustrate collaborations among countries and authors, and create a three-field diagram illustrating the connections between authors, affiliations, and keywords. Analyses of country and institutional co-authorship, as well as keyword co-occurrence, were conducted using VOSviewer. Additionally, CiteSpace was utilized for the cite burst analysis of keywords and cited literature. RESULTS The study encompassed 3125 documents in the research areas related to HCC of IME, revealing a substantial and continuous increase in the annual publication trend over time. China and Fudan University emerged as leading contributors, with 2103 and 165 publications, respectively. Frontiers in immunology was the most prolific journal in this domain. Among the top ten researchers in the field, eight are based in China. Key research terms identified include tumour microenvironment, expression, immunotherapy, and prognosis. CONCLUSION The relationship between HCC and IME is receiving increasing attention, and related research is in a highly developed stage. Key focus areas, including IME and immune checkpoint inhibitors, immunotherapy are poised to be central to future research endeavors, offering promising pathways for further exploration.
背景 肝细胞癌（HCC）的免疫微环境（IME）在决定患者预后和治疗反应方面起着关键作用。这一领域的研究兴趣正在迅速增长。然而，目前还缺乏全面的文献计量分析来剖析该领域的发展趋势和潜在焦点。目的 采用文献计量学方法，探讨自 2004 年 1 月 1 日至 2023 年 12 月 31 日期间有关 HCC IME 的研究进展。方法 从检索日期为 2023 年 12 月 31 日的 Web of Science 核心文库中检索有关 HCC IME 的英文文章和综述。采用 R 软件包 Bibliometrix 计算基本文献计量学特征，说明国家和作者之间的合作情况，并创建一个三域图，说明作者、所属机构和关键词之间的联系。使用 VOSviewer 对国家和机构共同作者以及关键词共同出现情况进行了分析。此外，还利用 CiteSpace 对关键词和被引文献进行了引文突发分析。结果 研究涵盖了与 IME 的 HCC 相关研究领域的 3125 篇文献，发现随着时间的推移，年发表量呈持续大幅增长趋势。中国和复旦大学分别以 2103 篇和 165 篇论文位居前列。免疫学前沿》是该领域发表论文最多的期刊。在该领域排名前十的研究人员中，有八位来自中国。关键研究术语包括肿瘤微环境、表达、免疫疗法和预后。结论 HCC与IME之间的关系正受到越来越多的关注，相关研究正处于高度发展阶段。包括 IME 和免疫检查点抑制剂、免疫疗法在内的关键重点领域将成为未来研究工作的核心，为进一步探索提供了前景广阔的途径。
{"title":"Research trends and hotspots in the immune microenvironment related to hepatocellular carcinoma: A bibliometric and visualization study","authors":"Da-Ya Zhang, Fei-Hu Bai","doi":"10.4251/wjgo.v16.i7.3321","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3321","url":null,"abstract":"BACKGROUND\u0000 The immune microenvironment (IME) in hepatocellular carcinoma (HCC) plays a pivotal role in determining patient outcomes and responses to treatment. This area is witnessing rapid growth in research interest. However, there is a lack of comprehensive bibliometric analyses that dissect trends and potential focal points in this field.\u0000 AIM\u0000 To explore the evolution of research on the IME in HCC from January 1, 2004, to December 31, 2023, using bibliometric methodologies.\u0000 METHODS\u0000 English articles and reviews concerning the IME of HCC were retrieved from the Web of Science Core Collection with a search date of December 31, 2023. The R package Bibliometrix was employed to compute basic bibliometric characteristics, illustrate collaborations among countries and authors, and create a three-field diagram illustrating the connections between authors, affiliations, and keywords. Analyses of country and institutional co-authorship, as well as keyword co-occurrence, were conducted using VOSviewer. Additionally, CiteSpace was utilized for the cite burst analysis of keywords and cited literature.\u0000 RESULTS\u0000 The study encompassed 3125 documents in the research areas related to HCC of IME, revealing a substantial and continuous increase in the annual publication trend over time. China and Fudan University emerged as leading contributors, with 2103 and 165 publications, respectively. Frontiers in immunology was the most prolific journal in this domain. Among the top ten researchers in the field, eight are based in China. Key research terms identified include tumour microenvironment, expression, immunotherapy, and prognosis.\u0000 CONCLUSION\u0000 The relationship between HCC and IME is receiving increasing attention, and related research is in a highly developed stage. Key focus areas, including IME and immune checkpoint inhibitors, immunotherapy are poised to be central to future research endeavors, offering promising pathways for further exploration.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141648991","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.2894
Nabil Eid, Fabian Davamani
Macroautophagy (hereafter referred to as autophagy) is a prosurvival mechanism for the clearance of damaged cellular components, specifically related to exposure to various stressors such as starvation, excessive ethanol intake, and chemotherapy. This editorial reviews and comments on an article by Zhao et al , to be published in World J Gastrointestinal Oncology in 2024. Based on various molecular biology methodologies, they found that human β-defensin-1 reduced the proliferation of colon cancer cells, which was associated with the inhibition of the mammalian target of rapamycin, resulting in autophagy activation. The activation of autophagy is evidenced by increased levels of Beclin1 and LC3II/I proteins and mediated by the upregulation of long non-coding RNA TCONS_00014506. Our study discusses the impact of autophagy activation and mechanisms of autophagy, including autophagic flux, on cancer cells. Additionally, we emphasize the importance of describing the detailed methods for isolating long noncoding RNAs TCONS_00014506. Our review will benefit the scientific community and improve the overall clarity of the paper.
{"title":"Human β-defensin-1 activates autophagy in human colon cancer cells via regulation of long non-coding RNA TCONS_00014506","authors":"Nabil Eid, Fabian Davamani","doi":"10.4251/wjgo.v16.i7.2894","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.2894","url":null,"abstract":"Macroautophagy (hereafter referred to as autophagy) is a prosurvival mechanism for the clearance of damaged cellular components, specifically related to exposure to various stressors such as starvation, excessive ethanol intake, and chemotherapy. This editorial reviews and comments on an article by Zhao et al , to be published in World J Gastrointestinal Oncology in 2024. Based on various molecular biology methodologies, they found that human β-defensin-1 reduced the proliferation of colon cancer cells, which was associated with the inhibition of the mammalian target of rapamycin, resulting in autophagy activation. The activation of autophagy is evidenced by increased levels of Beclin1 and LC3II/I proteins and mediated by the upregulation of long non-coding RNA TCONS_00014506. Our study discusses the impact of autophagy activation and mechanisms of autophagy, including autophagic flux, on cancer cells. Additionally, we emphasize the importance of describing the detailed methods for isolating long noncoding RNAs TCONS_00014506. Our review will benefit the scientific community and improve the overall clarity of the paper.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141647894","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3270
Tong-Yan An, Quan-Man Hu, Peng Ni, Yan-Qiao Hua, Di Wang, Guang-Cai Duan, Shuai-Yin Chen, Bin Jia
BACKGROUND Helicobacter pylori (H. pylori ) colonizes the human gastric mucosa and is implicated in the development of gastric cancer (GC). The tumor microenvironment is characterized by hypoxia, where hypoxia-inducible factor-1α (HIF-1α) plays a key role as a transcription factor, but the mechanisms underlying H. pylori -induced HIF-1α expression and carcinogenesis remain unclear. AIM To explore the underlying mechanism of H. pylori -induced HIF-1α expression in promoting the malignant biological behavior of gastric epithelial cells (GES-1). METHODS The study was conducted with human GES-1 cells in vitro . Relative protein levels of methyltransferase-like protein 14 (METTL14), HIF-1α, main proteins of the PI3K/AKT pathway, epithelial-mesenchymal transition (EMT) biomarkers, and invasion indicators were detected by Western blot. Relative mRNA levels of METTL14 and HIF-1α were detected by quantitative reverse transcription-polymerase chain reaction. mRNA stability was evaluated using actinomycin D, and the interaction between METTL14 and HIF-1α was confirmed by immunofluorescence staining. Cell proliferation and migration were evaluated by cell counting kit-8 assay and wound healing assay, respectively. RESULTS H. pylori promoted HIF-1α expression and activated the PI3K/AKT pathway. Notably, METTL14 was downregulated in H. pylori -infected gastric mucosal epithelial cells and positively regulated HIF-1α expression. Functional experiments showed that the overexpression of HIF-1α or knockdown of METTL14 enhanced the activity of the PI3K/AKT pathway, thereby driving a series of malignant transformation, such as EMT and cell proliferation, migration, and invasion. By contrast, the knockdown of HIF-1α or overexpression of METTL14 had an opposite effect. CONCLUSION H. pylori- induced underexpression of METTL14 promotes the translation of HIF-1α and accelerates tumor progression by activating the PI3K/AKT pathway. These results provide novel insights into the carcinogenesis of GC.
{"title":"N6-methyladenosine modification of hypoxia-inducible factor-1α regulates Helicobacter pylori-associated gastric cancer via the PI3K/AKT pathway","authors":"Tong-Yan An, Quan-Man Hu, Peng Ni, Yan-Qiao Hua, Di Wang, Guang-Cai Duan, Shuai-Yin Chen, Bin Jia","doi":"10.4251/wjgo.v16.i7.3270","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3270","url":null,"abstract":"BACKGROUND\u0000 Helicobacter pylori (H. pylori ) colonizes the human gastric mucosa and is implicated in the development of gastric cancer (GC). The tumor microenvironment is characterized by hypoxia, where hypoxia-inducible factor-1α (HIF-1α) plays a key role as a transcription factor, but the mechanisms underlying H. pylori -induced HIF-1α expression and carcinogenesis remain unclear.\u0000 AIM\u0000 To explore the underlying mechanism of H. pylori -induced HIF-1α expression in promoting the malignant biological behavior of gastric epithelial cells (GES-1).\u0000 METHODS\u0000 The study was conducted with human GES-1 cells in vitro . Relative protein levels of methyltransferase-like protein 14 (METTL14), HIF-1α, main proteins of the PI3K/AKT pathway, epithelial-mesenchymal transition (EMT) biomarkers, and invasion indicators were detected by Western blot. Relative mRNA levels of METTL14 and HIF-1α were detected by quantitative reverse transcription-polymerase chain reaction. mRNA stability was evaluated using actinomycin D, and the interaction between METTL14 and HIF-1α was confirmed by immunofluorescence staining. Cell proliferation and migration were evaluated by cell counting kit-8 assay and wound healing assay, respectively.\u0000 RESULTS\u0000 H. pylori promoted HIF-1α expression and activated the PI3K/AKT pathway. Notably, METTL14 was downregulated in H. pylori -infected gastric mucosal epithelial cells and positively regulated HIF-1α expression. Functional experiments showed that the overexpression of HIF-1α or knockdown of METTL14 enhanced the activity of the PI3K/AKT pathway, thereby driving a series of malignant transformation, such as EMT and cell proliferation, migration, and invasion. By contrast, the knockdown of HIF-1α or overexpression of METTL14 had an opposite effect.\u0000 CONCLUSION\u0000 H. pylori- induced underexpression of METTL14 promotes the translation of HIF-1α and accelerates tumor progression by activating the PI3K/AKT pathway. These results provide novel insights into the carcinogenesis of GC.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141647880","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}
Pub Date : 2024-07-15DOI: 10.4251/wjgo.v16.i7.3082
Huiqin Shi, Shu Huang, Xinyue Ma, Zhenju Tan, Rui Luo, Bei Luo, Wei Zhang, Lei Shi, Xiao-Lin Zhong, Muhan Lü, Xia Chen, Xiaowei Tang
BACKGROUND Hepatocellular carcinoma (HCC) is a malignant tumor that has a high incidence and mortality worldwide. Despite extensive studies, the detailed molecular mechanism of HCC development remains unclear. Studies have shown that the occurrence and development of HCC are closely related to abnormal gene expression. BCAR3 has been shown to be overexpressed in a variety of malignant tumors. However, the role of BCAR3 in HCC remains unclear. AIM To investigate the expression of BCAR3 and BCAR3 -related competing endogenous RNAs (ceRNAs) in HCC and their clinical significance, in order to provide new ideas for the diagnosis and treatment of HCC. METHODS The data of HCC were obtained from the Cancer Genome Atlas database and The Genotype Tissue Expression, including transcriptome data and clinical information. Multiple common databases, including UALCAN, Timer 2.0, cBioPortal, LinkedOmics, starBase, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, were used to analyse the expression of BCAR3 , prognostic value, genetic alteration, co-expressed genes, differentially expressed genes, BCAR3 gene-related ceRNAs and functional enrichment analysis in HCC patients. Kaplan-Meier analysis, univariate and multivariate Cox regression analysis were used to analyze survival prognosis and the Spearman test was used to measure correlations between BCAR3 and immune functions. And R language package was used to analyze the correlation between BCAR3 and immune invasion of HCC. RESULTS Our study indicated that BCAR3 was differentially expressed in various tumor tissues. The over-expression of BCAR3 gene was an unfavorable prognostic indicator for HCC patients, and associated with unfavorable cytogenetic risk and gene mutations. Moreover, most immune cells were positively correlated with BCAR3 (P < 0.05). According to the results of functional enrichment analysis, BCAR3 was involved in the positive regulation of epidermal growth factor receptor signaling pathway and ERBB signaling pathway, and was related to DNA replication and GTPase regulator activity. Finally, our study found that based on RAB30-DT and miR-19b-3p pathways, targeting BCAR3 might promote the occurrence and development of HCC. CONCLUSION Collectively, this study indicated that the BCAR3 gene was involved in the occurrence and development of HCC, and it might be a new biomarker and therapeutic target for HCC, but the specific mechanism remains to be further verified.
{"title":"BCAR3 and BCAR3-related competing endogenous RNA expression in hepatocellular carcinoma and their prognostic value","authors":"Huiqin Shi, Shu Huang, Xinyue Ma, Zhenju Tan, Rui Luo, Bei Luo, Wei Zhang, Lei Shi, Xiao-Lin Zhong, Muhan Lü, Xia Chen, Xiaowei Tang","doi":"10.4251/wjgo.v16.i7.3082","DOIUrl":"https://doi.org/10.4251/wjgo.v16.i7.3082","url":null,"abstract":"BACKGROUND\u0000 Hepatocellular carcinoma (HCC) is a malignant tumor that has a high incidence and mortality worldwide. Despite extensive studies, the detailed molecular mechanism of HCC development remains unclear. Studies have shown that the occurrence and development of HCC are closely related to abnormal gene expression. BCAR3 has been shown to be overexpressed in a variety of malignant tumors. However, the role of BCAR3 in HCC remains unclear.\u0000 AIM\u0000 To investigate the expression of BCAR3 and BCAR3 -related competing endogenous RNAs (ceRNAs) in HCC and their clinical significance, in order to provide new ideas for the diagnosis and treatment of HCC.\u0000 METHODS\u0000 The data of HCC were obtained from the Cancer Genome Atlas database and The Genotype Tissue Expression, including transcriptome data and clinical information. Multiple common databases, including UALCAN, Timer 2.0, cBioPortal, LinkedOmics, starBase, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, were used to analyse the expression of BCAR3 , prognostic value, genetic alteration, co-expressed genes, differentially expressed genes, BCAR3 gene-related ceRNAs and functional enrichment analysis in HCC patients. Kaplan-Meier analysis, univariate and multivariate Cox regression analysis were used to analyze survival prognosis and the Spearman test was used to measure correlations between BCAR3 and immune functions. And R language package was used to analyze the correlation between BCAR3 and immune invasion of HCC.\u0000 RESULTS\u0000 Our study indicated that BCAR3 was differentially expressed in various tumor tissues. The over-expression of BCAR3 gene was an unfavorable prognostic indicator for HCC patients, and associated with unfavorable cytogenetic risk and gene mutations. Moreover, most immune cells were positively correlated with BCAR3 (P < 0.05). According to the results of functional enrichment analysis, BCAR3 was involved in the positive regulation of epidermal growth factor receptor signaling pathway and ERBB signaling pathway, and was related to DNA replication and GTPase regulator activity. Finally, our study found that based on RAB30-DT and miR-19b-3p pathways, targeting BCAR3 might promote the occurrence and development of HCC.\u0000 CONCLUSION\u0000 Collectively, this study indicated that the BCAR3 gene was involved in the occurrence and development of HCC, and it might be a new biomarker and therapeutic target for HCC, but the specific mechanism remains to be further verified.","PeriodicalId":23762,"journal":{"name":"World Journal of Gastrointestinal Oncology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141648469","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}
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