Mincheol Chae, Jae-Ho Lee, Jong Ho Park, Dong Yoon Keum, Hanna Jung, Youngok Lee, Deok Heon Lee
Background: TRF1, TRF2, and TERT (Telomerase reverse transcriptase) are telomere-associated factors that regulate telomere length. Genetic changes in these genes may be associated with cancer pathogenesis; however, this relationship has not yet been comprehensively elucidated in lung cancer. Aim: : Exploring the clinicopathologic and prognostic values of TRF1, TRF2, and TERT mRNA expression in non-small cell lung cancers (NSCLC). Methods: : The clinical significance of TRF1, TRF2, and TERT expression in 141 patients with NSCLC was investigated. Additionally, these findings were supported by the open big data from The Cancer Genome Atlas (TCGA). Results: : TRF1 and TRF2 expression levels tended to be associated with smoking, and TERT expression was positively correlated with age. The survival analysis showed that TRF1 expression predicted a better prognosis for squamous cell carcinoma (SCC), whereas TRF2 expression was associated with a shorter survival in adenocarcinoma. TCGA data also showed a better prognosis for SCC with TRF1 expression. However, the TRF2 results were not in agreement with our data. Conclusions: : We present the clinical and prognostic values of TRF1, TRF2, and TERT expression in NSCLC tissues and TCGA. Our findings suggest that TRF1 expression is a possible prognostic marker for NSCLC, particularly SCC.
{"title":"Different Role of TRF1 and TRF2 Expression in Non-Small Cell Lung Cancers","authors":"Mincheol Chae, Jae-Ho Lee, Jong Ho Park, Dong Yoon Keum, Hanna Jung, Youngok Lee, Deok Heon Lee","doi":"10.2147/ott.s461430","DOIUrl":"https://doi.org/10.2147/ott.s461430","url":null,"abstract":"<strong>Background:</strong> TRF1, TRF2, and TERT (Telomerase reverse transcriptase) are telomere-associated factors that regulate telomere length. Genetic changes in these genes may be associated with cancer pathogenesis; however, this relationship has not yet been comprehensively elucidated in lung cancer.<br/><strong>Aim:</strong> : Exploring the clinicopathologic and prognostic values of TRF1, TRF2, and TERT mRNA expression in non-small cell lung cancers (NSCLC).<br/><strong>Methods:</strong> : The clinical significance of TRF1, TRF2, and TERT expression in 141 patients with NSCLC was investigated. Additionally, these findings were supported by the open big data from The Cancer Genome Atlas (TCGA).<br/><strong>Results:</strong> : TRF1 and TRF2 expression levels tended to be associated with smoking, and TERT expression was positively correlated with age. The survival analysis showed that TRF1 expression predicted a better prognosis for squamous cell carcinoma (SCC), whereas TRF2 expression was associated with a shorter survival in adenocarcinoma. TCGA data also showed a better prognosis for SCC with TRF1 expression. However, the TRF2 results were not in agreement with our data.<br/><strong>Conclusions:</strong> : We present the clinical and prognostic values of TRF1, TRF2, and TERT expression in NSCLC tissues and TCGA. Our findings suggest that TRF1 expression is a possible prognostic marker for NSCLC, particularly SCC.<br/><br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"67 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141252973","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}
Hangsheng Zhou, Jiandong Gui, Lijie Zhu, Yuanyuan Mi
Abstract: Methylation-mediated gene silencing is closely related to the occurrence and development of human tumors. The euchromatic histone lysine methyltransferase 2 (EHMT2, also known as G9a) is highly expressed in many tumors and is generally considered to be an oncogene, which is associated with the poor outcome of many tumors. Combined immunotherapy and immune checkpoint blockade therapy also have good efficacy and certain safety. However, there are still many difficulties in the drugs targeting G9a, and the combined effect and safety of G9a with many drugs is still under study. This article aims to summarize the role and mechanism of G9a and its inhibitors in tumors in the past two years, and to understand the application prospect of G9a from the perspective of diagnosis and treatment.
{"title":"The Role and Mechanism of the Histone Methyltransferase G9a in Tumors: Update","authors":"Hangsheng Zhou, Jiandong Gui, Lijie Zhu, Yuanyuan Mi","doi":"10.2147/ott.s451108","DOIUrl":"https://doi.org/10.2147/ott.s451108","url":null,"abstract":"<strong>Abstract:</strong> Methylation-mediated gene silencing is closely related to the occurrence and development of human tumors. The euchromatic histone lysine methyltransferase 2 (EHMT2, also known as G9a) is highly expressed in many tumors and is generally considered to be an oncogene, which is associated with the poor outcome of many tumors. Combined immunotherapy and immune checkpoint blockade therapy also have good efficacy and certain safety. However, there are still many difficulties in the drugs targeting G9a, and the combined effect and safety of G9a with many drugs is still under study. This article aims to summarize the role and mechanism of G9a and its inhibitors in tumors in the past two years, and to understand the application prospect of G9a from the perspective of diagnosis and treatment.<br/><br/><strong>Keywords:</strong> cancer, G9a, methyltransferase, function, mechanism<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"76 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141188504","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}
Purpose: The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is an effective first-line therapy for patients with common EGFR mutation-positive non-small cell lung cancer (NSCLC). However, almost all patients become resistant to treatment. In some patients, emergence of tertiary EGFR mutations is implicated as a resistance mechanism. This study describes patients with NSCLC who acquired the rare EGFR mutations, L718Q or G724S, following EGFR TKI treatment. Patients and Methods: This was a retrospective, observational study undertaken in France from Feb–Nov 2021, in patients with EGFR mutation-positive NSCLC with an acquired L718Q or G724S mutation. Primary objectives were description of tumor characteristics, progression, and progression under treatment. Results: Nine eligible patients were identified. Acquired resistance to initial EGFR TKI treatment was associated with T790M emergence in six patients, who then received osimertinib monotherapy. Overall, eight patients received osimertinib monotherapy treatment at some point (average treatment duration: 18.3 months). Following the emergence of L718Q or G724S, patients received chemotherapy (n = 4; two of whom subsequently received afatinib), nivolumab (n = 2), afatinib (n = 2), or immunochemotherapy (n = 1). In the four patients who received afatinib after identification of L718Q or G724S, 2 achieved a partial response, one had stable disease and one had progressive disease. Treatment duration was 1.6– 31.7 months. In patients with controlled disease (n = 3), progression-free survival was 6.1– 31.7 months. Two of these patients had previously received osimertinib. Conclusion: Currently, there is no consensus regarding the treatment of EGFR mutation-positive NSCLC following emergence of the osimertinib resistance mutations, L718Q or G724S. Afatinib appears to be a promising treatment option in this setting.
{"title":"Characterization of Patients with EGFR Mutation-Positive NSCLC Following Emergence of the Osimertinib Resistance Mutations, L718Q or G724S: A Multicenter Retrospective Observational Study in France","authors":"Mateo Sanchis-Borja, Florian Guisier, Aurélie Swalduz, Hubert Curcio, Victor Basse, Christophe Maritaz, Christos Chouaid, Jean-Bernard Auliac","doi":"10.2147/ott.s448909","DOIUrl":"https://doi.org/10.2147/ott.s448909","url":null,"abstract":"<strong>Purpose:</strong> The third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimertinib, is an effective first-line therapy for patients with common <em>EGFR</em> mutation-positive non-small cell lung cancer (NSCLC). However, almost all patients become resistant to treatment. In some patients, emergence of tertiary <em>EGFR</em> mutations is implicated as a resistance mechanism. This study describes patients with NSCLC who acquired the rare <em>EGFR</em> mutations, L718Q or G724S, following EGFR TKI treatment.<br/><strong>Patients and Methods:</strong> This was a retrospective, observational study undertaken in France from Feb–Nov 2021, in patients with <em>EGFR</em> mutation-positive NSCLC with an acquired L718Q or G724S mutation. Primary objectives were description of tumor characteristics, progression, and progression under treatment.<br/><strong>Results:</strong> Nine eligible patients were identified. Acquired resistance to initial EGFR TKI treatment was associated with T790M emergence in six patients, who then received osimertinib monotherapy. Overall, eight patients received osimertinib monotherapy treatment at some point (average treatment duration: 18.3 months). Following the emergence of L718Q or G724S, patients received chemotherapy (n = 4; two of whom subsequently received afatinib), nivolumab (n = 2), afatinib (n = 2), or immunochemotherapy (n = 1). In the four patients who received afatinib after identification of L718Q or G724S, 2 achieved a partial response, one had stable disease and one had progressive disease. Treatment duration was 1.6– 31.7 months. In patients with controlled disease (n = 3), progression-free survival was 6.1– 31.7 months. Two of these patients had previously received osimertinib.<br/><strong>Conclusion:</strong> Currently, there is no consensus regarding the treatment of <em>EGFR</em> mutation-positive NSCLC following emergence of the osimertinib resistance mutations, L718Q or G724S. Afatinib appears to be a promising treatment option in this setting.<br/><br/><strong>Keywords:</strong> osimertinib, afatinib, real-world evidence, tertiary <em>EGFR</em> mutations<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"15 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141165649","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}
Sijia Yang, Ang Li, Lihong Lv, Jinxin Duan, Zhihua Zheng, Wenfeng Zhuo, Jun Min, Jinxing Wei
Background: Nicotinamide (NAM+) regulates redox and metabolic activities in the mitochondria. The intention of the research was to identify key genes that relate to nicotinamide in hepatocellular carcinoma (HCC). Methods: Relevant clinical information were collected as well as RNA-seq data using the Cancer Genome Atlas (TCGA) database. Differential analysis was used to discover the genes that were differently expressed. On the key genes associated with NAM, functional enrichment analysis was carried out. Next, receiver operating characteristic (ROC) and prognosis Kaplan-Meier (K-M) curve analyses were used to evaluate the importance of important gene expression, respectively. The immune cell signatures were estimated using the CIBERSORT algorithm. Finally, the anticancer impact of NAM on HCC was experimentally confirmed, and important genes NADSYN1 and NT5C were validated at the protein level in clinical specimens. Results: Six prognostic key genes (NAXE, NADSYN1, NT5C, NT5C3A, PNP and NT5E) were identified. There is an association between the level of key gene expression and the clinical prognosis. Four key genes (NAXE, NADSYN1, NT5C and NT5C3A) have statistical significance of survival prognosis. Finally, the expression of NAM-related genes and the inhibitory effect of NAM on HCC were verified by experiments. Conclusion: The study first found some Nicotinamide metabolism-related differentially expressed genes (NMRDEGs) that are related to HCC can contribute to predicting survival and monitoring the treatment.
背景：烟酰胺（NAM+）调节线粒体中的氧化还原和代谢活动。该研究旨在确定肝细胞癌（HCC）中与烟酰胺相关的关键基因：方法：利用癌症基因组图谱（TCGA）数据库收集相关临床信息和RNA-seq数据。差异分析用于发现表达不同的基因。对与 NAM 相关的关键基因进行了功能富集分析。然后，分别使用接收者操作特征（ROC）和预后卡普兰-梅耶（K-M）曲线分析来评估重要基因表达的重要性。使用 CIBERSORT 算法估算了免疫细胞特征。最后，实验证实了NAM对HCC的抗癌作用，并从蛋白水平验证了临床标本中的重要基因NADSYN1和NT5C：结果：发现了六个预后关键基因（NAXE、NADSYN1、NT5C、NT5C3A、PNP 和 NT5E）。关键基因的表达水平与临床预后有关。4个关键基因（NAXE、NADSYN1、NT5C和NT5C3A）对生存预后有统计学意义。最后，通过实验验证了NAM相关基因的表达以及NAM对HCC的抑制作用：该研究首次发现了一些与HCC相关的烟酰胺代谢相关差异表达基因（NMRDEGs），有助于预测生存率和监测治疗效果。
{"title":"Identification and Validation of Nicotinamide Metabolism-Related Gene Signatures as a Novel Prognostic Model for Hepatocellular Carcinoma","authors":"Sijia Yang, Ang Li, Lihong Lv, Jinxin Duan, Zhihua Zheng, Wenfeng Zhuo, Jun Min, Jinxing Wei","doi":"10.2147/ott.s464709","DOIUrl":"https://doi.org/10.2147/ott.s464709","url":null,"abstract":"<strong>Background:</strong> Nicotinamide (NAM+) regulates redox and metabolic activities in the mitochondria. The intention of the research was to identify key genes that relate to nicotinamide in hepatocellular carcinoma (HCC).<br/><strong>Methods:</strong> Relevant clinical information were collected as well as RNA-seq data using the Cancer Genome Atlas (TCGA) database. Differential analysis was used to discover the genes that were differently expressed. On the key genes associated with NAM, functional enrichment analysis was carried out. Next, receiver operating characteristic (ROC) and prognosis Kaplan-Meier (K-M) curve analyses were used to evaluate the importance of important gene expression, respectively. The immune cell signatures were estimated using the CIBERSORT algorithm. Finally, the anticancer impact of NAM on HCC was experimentally confirmed, and important genes NADSYN1 and NT5C were validated at the protein level in clinical specimens.<br/><strong>Results:</strong> Six prognostic key genes (NAXE, NADSYN1, NT5C, NT5C3A, PNP and NT5E) were identified. There is an association between the level of key gene expression and the clinical prognosis. Four key genes (NAXE, NADSYN1, NT5C and NT5C3A) have statistical significance of survival prognosis. Finally, the expression of NAM-related genes and the inhibitory effect of NAM on HCC were verified by experiments.<br/><strong>Conclusion:</strong> The study first found some Nicotinamide metabolism-related differentially expressed genes (NMRDEGs) that are related to HCC can contribute to predicting survival and monitoring the treatment.<br/><br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"23 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141165644","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}
Jian Zhou, Housheng Zheng, Huiru Zhang, Wenqiang Yu, Baoer Li, Liang Ye, Lu Wang
Objective: MCM5 is a DNA licensing factor involved in cell proliferation and has been previously established as an excellent biomarker in a number of malignancies. Nevertheless, the role of MCM5 in GBM has not been fully clarified. The present study aimed to investigate the potential roles of MCM5 in the treatment of GBM and to elucidate its underlying mechanism, which is beneficial for developing new therapeutic strategies and predicting prognosis. Methods: Firstly, we obtained transcriptomic and proteomic data from the TCGA and CPTAC databases on glioma patients. Employing the DeSeq2 R package, we then identified genes with joint differential expression in GBM tissues subjected to chemotherapy. To develop a prognostic risk score model, we performed univariate and multivariate Cox regression analyses. In vitro knockdown and overexpression of MCM5 were used to further investigate the biological functions of GBM cells. Additionally, we also delved into the upstream regulation of MCM5, revealing associations with several transcription factors. Finally, we investigated differences in immune cell infiltration and drug sensitivity across diverse risk groups identified in the prognostic risk model. Results: In this study, the chemotherapy-treated GBM samples exhibited consistent alterations in 46 upregulated and 94 downregulated genes at both the mRNA and protein levels. Notably, MCM5 emerged as a gene with prognostic significance as well as potential therapeutic relevance. In vitro experiments subsequently validated the role of increased MCM5 expression in promoting GBM cell proliferation and resistance to TMZ. Correlations with transcription factors such as CREB1, CTCF, NFYB, NRF1, PBX1, TEAD1, and USF1 were discovered during upstream regulatory analysis, enriching our understanding of MCM5 regulatory mechanisms. The study additionally delves into immune cell infiltration and drug sensitivity, providing valuable insights for personalized treatment approaches. Conclusion: This study identifies MCM5 as a key player in GBM, demonstrating its prognostic significance and potential therapeutic relevance by elucidating its role in promoting cell proliferation and resistance to chemotherapy.
Keywords: glioblastoma, minichromosome maintenance protein 5, chemotherapeutic drug resistance
{"title":"MCM5 is a Novel Therapeutic Target for Glioblastoma","authors":"Jian Zhou, Housheng Zheng, Huiru Zhang, Wenqiang Yu, Baoer Li, Liang Ye, Lu Wang","doi":"10.2147/ott.s457600","DOIUrl":"https://doi.org/10.2147/ott.s457600","url":null,"abstract":"<strong>Objective:</strong> MCM5 is a DNA licensing factor involved in cell proliferation and has been previously established as an excellent biomarker in a number of malignancies. Nevertheless, the role of MCM5 in GBM has not been fully clarified. The present study aimed to investigate the potential roles of MCM5 in the treatment of GBM and to elucidate its underlying mechanism, which is beneficial for developing new therapeutic strategies and predicting prognosis.<br/><strong>Methods:</strong> Firstly, we obtained transcriptomic and proteomic data from the TCGA and CPTAC databases on glioma patients. Employing the DeSeq2 R package, we then identified genes with joint differential expression in GBM tissues subjected to chemotherapy. To develop a prognostic risk score model, we performed univariate and multivariate Cox regression analyses. In vitro knockdown and overexpression of MCM5 were used to further investigate the biological functions of GBM cells. Additionally, we also delved into the upstream regulation of MCM5, revealing associations with several transcription factors. Finally, we investigated differences in immune cell infiltration and drug sensitivity across diverse risk groups identified in the prognostic risk model.<br/><strong>Results:</strong> In this study, the chemotherapy-treated GBM samples exhibited consistent alterations in 46 upregulated and 94 downregulated genes at both the mRNA and protein levels. Notably, MCM5 emerged as a gene with prognostic significance as well as potential therapeutic relevance. In vitro experiments subsequently validated the role of increased MCM5 expression in promoting GBM cell proliferation and resistance to TMZ. Correlations with transcription factors such as CREB1, CTCF, NFYB, NRF1, PBX1, TEAD1, and USF1 were discovered during upstream regulatory analysis, enriching our understanding of MCM5 regulatory mechanisms. The study additionally delves into immune cell infiltration and drug sensitivity, providing valuable insights for personalized treatment approaches.<br/><strong>Conclusion:</strong> This study identifies MCM5 as a key player in GBM, demonstrating its prognostic significance and potential therapeutic relevance by elucidating its role in promoting cell proliferation and resistance to chemotherapy.<br/><br/><strong>Keywords:</strong> glioblastoma, minichromosome maintenance protein 5, chemotherapeutic drug resistance<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"60 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140927974","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}
Retraction for the article Long Noncoding RNA NEAT1 Promotes Cell Proliferation And Invasion And Suppresses Apoptosis In Hepatocellular Carcinoma By Regulating miRNA-22-3p/akt2 In Vitro And In Vivo
{"title":"Long Noncoding RNA NEAT1 Promotes Cell Proliferation and Invasion and Suppresses Apoptosis in Hepatocellular Carcinoma by Regulating miRNA-22-3p/akt2 in vitro and in vivo [Retraction]","authors":"Xichang Zhou, Xiang Wang, Yizhou Zhou, Long Cheng, Youwei Zhang, Yangmei Zhang","doi":"10.2147/ott.s476432","DOIUrl":"https://doi.org/10.2147/ott.s476432","url":null,"abstract":"Retraction for the article Long Noncoding RNA NEAT1 Promotes Cell Proliferation And Invasion And Suppresses Apoptosis In Hepatocellular Carcinoma By Regulating miRNA-22-3p/akt2 In Vitro And In Vivo","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"33 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140887807","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}
Baicheng Li, Zhao Chen, Guangzhi Wang, Yaqing Liu, Shili Ning
Abstract: Primary cancer of the ileum is rare, and when it occurs in conjunction with primary colon cancer, it becomes even more infrequent and challenging to diagnose prior to surgical intervention. Primary small bowel cancers can be overlooked and may be misidentified as small bowel mesenchymal tumours or advanced metastases from colon cancer. We present an exceedingly uncommon case of ruptured primary ileal cancer combined with primary descending colon cancer presenting with gastrointestinal bleeding. Based on our understanding, instances of dual tumours concurrently occurring are exceedingly infrequent. In this patient, there was a preoperative suspicion of bleeding from colon cancer in the descending region. However, intraoperative exploration revealed that the location of the bleeding was a terminal ileal mass. Following the surgical intervention, the patient recovered satisfactorily. Intraoperative exploration of the entire gastrointestinal tract is therefore necessary in patients with gastrointestinal haemorrhage, especially in those who require urgent surgery without adequate preoperative investigations. If a mass is detected at the end of the ileum, intraoperative pathology should be performed if feasible. Subsequently, if the diagnosis reveals an adenocarcinoma, terminal ileocolic resection and right hemicolectomy are necessary for appropriate resection.
Keywords: multiple primary malignant neoplasms, gut bleeding, adenocarcinoma of the small bowel, descending colon cancer, gastrointestinal tumours, case report
{"title":"Synchronous Multiple Primary Malignant Adenocarcinoma of the Descending Colon and Fungating Bleeding Adenocarcinoma of the Terminal Ileum Presenting Massive Rectal Bleeding: A Trap for the Unwary","authors":"Baicheng Li, Zhao Chen, Guangzhi Wang, Yaqing Liu, Shili Ning","doi":"10.2147/ott.s453682","DOIUrl":"https://doi.org/10.2147/ott.s453682","url":null,"abstract":"<strong>Abstract:</strong> Primary cancer of the ileum is rare, and when it occurs in conjunction with primary colon cancer, it becomes even more infrequent and challenging to diagnose prior to surgical intervention. Primary small bowel cancers can be overlooked and may be misidentified as small bowel mesenchymal tumours or advanced metastases from colon cancer. We present an exceedingly uncommon case of ruptured primary ileal cancer combined with primary descending colon cancer presenting with gastrointestinal bleeding. Based on our understanding, instances of dual tumours concurrently occurring are exceedingly infrequent. In this patient, there was a preoperative suspicion of bleeding from colon cancer in the descending region. However, intraoperative exploration revealed that the location of the bleeding was a terminal ileal mass. Following the surgical intervention, the patient recovered satisfactorily. Intraoperative exploration of the entire gastrointestinal tract is therefore necessary in patients with gastrointestinal haemorrhage, especially in those who require urgent surgery without adequate preoperative investigations. If a mass is detected at the end of the ileum, intraoperative pathology should be performed if feasible. Subsequently, if the diagnosis reveals an adenocarcinoma, terminal ileocolic resection and right hemicolectomy are necessary for appropriate resection.<br/><br/><strong>Keywords:</strong> multiple primary malignant neoplasms, gut bleeding, adenocarcinoma of the small bowel, descending colon cancer, gastrointestinal tumours, case report<br/>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"43 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835843","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":"Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis [Retraction]","authors":"Mengyan Zhang, Weiguo Zhu, Mansour Haeryfar, Sumei Jiang, Xiang Jiang, Wei Chen, Jiancheng Li","doi":"10.2147/ott.s474055","DOIUrl":"https://doi.org/10.2147/ott.s474055","url":null,"abstract":"Retraction for the article Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"30 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140617206","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}
Zhilin Sha, Qingxiang Gao, Lei Wang, Ni An, Yingjun Wu, Dong Wei, Tong Wang, Chen Liu, Yang Shen
Background: Colorectal cancer (CRC) is one of the deadliest causes of death by cancer worldwide. Liver metastasis (LM) is the main cause of death in patients with CRC. Therefore, identification of patients with the greatest risk of liver metastasis is critical for early treatment and reduces the mortality of patients with colorectal cancer liver metastases. Methods: Initially, we characterized cell composition through single-cell transcriptome analysis. Subsequently, we employed copy number variation (CNV) and pseudotime analysis to delineate the cellular origins of LM and identify LM-related epithelial cells (LMECs). The LM-index was constructed using machine learning algorithms to forecast the relative abundance of LMECs, reflecting the risk of LM. Furthermore, we analyzed drug sensitivity and drug targeted gene expression in LMECs and patients with a high risk of LM. Finally, functional experiments were conducted to determine the biological roles of metastasis-related gene in vitro. Results: Single-cell RNA sequencing analysis revealed different immune landscapes between primary CRC and LM tumor. LM originated from chromosomal variants with copy number loss of chr1 and chr6p and copy number gain of chr7 and chr20q. We identified the LMECs cluster and found LM-associated pathways such as Wnt/beta-catenin signaling and KRAS signaling. Subsequently, we identified ten metastasis-associated genes, including SOX4, and established the LM-index, which correlates with poorer prognosis, higher stage, and advanced age. Furthermore, we screened two drugs as potential candidates for treating LM, including Linsitinib_1510, Lapatinib_1558. Immunohistochemistry results demonstrated significantly elevated SOX4 expression in tumor samples compared to normal samples. Finally, in vitro experiments verified that silencing SOX4 significantly inhibited tumor cell migration and invasion. Conclusion: This study reveals the possible cellular origin and driving factors of LM in CRC at the single cell level, and provides a reference for early detection of CRC patients with a high risk of LM.
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Fang Ren, Christina Shrestha, Huirong Shi, Fangfang Sun, Minghui Zhang, Yuan Cao, Gailing Li
Retraction for the article Targeting of KDM5A by miR-421 in Human Ovarian Cancer Suppresses the Progression of Ovarian Cancer Cells
撤回《miR-421 在人类卵巢癌中靶向 KDM5A 可抑制卵巢癌细胞的进展》一文的决定
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