Aberrant glycosylation in tumor cells is a hallmark during carcinogenesis. KRAS gene mutations are the most well-known oncogenic abnormalities but their association with glycan alterations in pancreatic ductal adenocarcinoma (PDAC) is largely unknown. We employed patient-derived 3D organoids to culture pure live PDAC cells, excluding contamination by fibroblasts and immune cells, to gasp the comprehensive cancer cell surface glycan expression profile using lectin microarray and transcriptomic analyses. Surgical specimens from 24 PDAC patients were digested and embedded into a 3D culture system. Surface-bound glycans of 3D organoids were analyzed by high-density, 96-lectin microarrays. KRAS mutation status and expression of various glycosyltransferases were analyzed by RNA-seq. We successfully established 16 3D organoids: 14 PDAC, 1 intraductal papillary mucinous neoplasm (IPMN), and 1 normal pancreatic duct. KRAS was mutated in 13 (7 G12V, 5 G12D, 1 Q61L) and wild in 3 organoids (1 normal duct, 1 IPMN, 1 PDAC). Lectin reactivity of AAL (Aleuria aurantia) and AOL (Aspergillus oryzae) with binding activity to α1-3 fucose was higher in organoids with KRAS mutants than those with KRAS wild-type. FUT6 (α1-3fucosyltransferase 6) and FUT3 (α1-3/4 fucosyltransferase 3) expression was also higher in KRAS mutants than wild-type. Meanwhile, mannose-binding lectin (rRSL [Ralstonia solanacearum] and rBC2LA [Burkholderia cenocepacia]) signals were higher while those of galactose-binding lectins (rGal3C and rCGL2) were lower in the KRAS mutants. We demonstrated here that PDAC 3D-cultured organoids with KRAS mutations were dominantly covered in increased fucosylated glycans, pointing towards novel treatment targets and/or tumor markers.
{"title":"Aberrant Glycosylation in Pancreatic Ductal Adenocarcinoma 3D Organoids Is Mediated by KRAS Mutations","authors":"Hiromitsu Nakahashi, Tatsuya Oda, Osamu Shimomura, Yoshimasa Akashi, Kazuhiro Takahashi, Yoshihiro Miyazaki, Tomoaki Furuta, Yukihito Kuroda, Pakavarin Louphrasitthiphol, Bryan J. Mathis, Hiroaki Tateno","doi":"10.1155/2024/1529449","DOIUrl":"https://doi.org/10.1155/2024/1529449","url":null,"abstract":"Aberrant glycosylation in tumor cells is a hallmark during carcinogenesis. KRAS gene mutations are the most well-known oncogenic abnormalities but their association with glycan alterations in pancreatic ductal adenocarcinoma (PDAC) is largely unknown. We employed patient-derived 3D organoids to culture pure live PDAC cells, excluding contamination by fibroblasts and immune cells, to gasp the comprehensive cancer cell surface glycan expression profile using lectin microarray and transcriptomic analyses. Surgical specimens from 24 PDAC patients were digested and embedded into a 3D culture system. Surface-bound glycans of 3D organoids were analyzed by high-density, 96-lectin microarrays. KRAS mutation status and expression of various glycosyltransferases were analyzed by RNA-seq. We successfully established 16 3D organoids: 14 PDAC, 1 intraductal papillary mucinous neoplasm (IPMN), and 1 normal pancreatic duct. KRAS was mutated in 13 (7 G12V, 5 G12D, 1 Q61L) and wild in 3 organoids (1 normal duct, 1 IPMN, 1 PDAC). Lectin reactivity of AAL (<i>Aleuria aurantia</i>) and AOL (<i>Aspergillus oryzae</i>) with binding activity to <i>α</i>1-3 fucose was higher in organoids with KRAS mutants than those with KRAS wild-type. <i>FUT6</i> (<i>α</i>1-3fucosyltransferase 6) and <i>FUT3</i> (<i>α</i>1-3/4 fucosyltransferase 3) expression was also higher in KRAS mutants than wild-type. Meanwhile, mannose-binding lectin (rRSL [<i>Ralstonia solanacearum</i>] and rBC2LA [<i>Burkholderia cenocepacia</i>]) signals were higher while those of galactose-binding lectins (rGal3C and rCGL2) were lower in the KRAS mutants. We demonstrated here that PDAC 3D-cultured organoids with KRAS mutations were dominantly covered in increased fucosylated glycans, pointing towards novel treatment targets and/or tumor markers.","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140146455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shital K. Barman, Monokesh K. Sen, David A. Mahns, Ming J. Wu, Chandra S. Malladi
Zinc dyshomeostasis is manifested in breast and prostate cancer cells. This study attempted to uncover the molecular details prodded by the change of extracellular zinc by employing a panel of normal and cancerous breast and prostate cell lines coupled with the top-down proteomics with two-dimensional gel electrophoresis followed by liquid chromatography-tandem mass spectrometry. The protein samples were generated from MCF-7 breast cancer cells, MCF10A normal breast cells, PC3 prostate cancer cells, and RWPE-1 normal prostate cells with or without exogenous zinc exposure in a time course (T0 and T120). By comparing the cancer cells vs respective normal epithelial cells without zinc treatment (T0), differentially expressed proteins (23 upregulated and 18 downregulated in MCF-7 cells; 14 upregulated and 30 downregulated in PC3 cells) were identified, which provides insights into the intrinsic differences of breast and prostate cancer cells. The dynamic protein landscapes in the cancer cells prodded by the extracellular zinc treatment reveal the potential roles of the identified zinc-responsive proteins (e.g., triosephosphate isomerase, S100A13, tumour proteins hD53 and hD54, and tumour suppressor prohibitin) in breast and prostate cancers. This study, for the first time, simultaneously investigated the two kinds of cancer cells related to zinc dyshomeostasis, and the findings shed light on the molecular understanding of the breast and prostate cancer cells in response to extracellular zinc variation.
{"title":"Molecular Insights into the Breast and Prostate Cancer Cells in Response to the Change of Extracellular Zinc","authors":"Shital K. Barman, Monokesh K. Sen, David A. Mahns, Ming J. Wu, Chandra S. Malladi","doi":"10.1155/2024/9925970","DOIUrl":"https://doi.org/10.1155/2024/9925970","url":null,"abstract":"Zinc dyshomeostasis is manifested in breast and prostate cancer cells. This study attempted to uncover the molecular details prodded by the change of extracellular zinc by employing a panel of normal and cancerous breast and prostate cell lines coupled with the top-down proteomics with two-dimensional gel electrophoresis followed by liquid chromatography-tandem mass spectrometry. The protein samples were generated from MCF-7 breast cancer cells, MCF10A normal breast cells, PC3 prostate cancer cells, and RWPE-1 normal prostate cells with or without exogenous zinc exposure in a time course (<i>T</i><sub>0</sub> and <i>T</i><sub>120</sub>). By comparing the cancer cells vs respective normal epithelial cells without zinc treatment (<i>T</i><sub>0</sub>), differentially expressed proteins (23 upregulated and 18 downregulated in MCF-7 cells; 14 upregulated and 30 downregulated in PC3 cells) were identified, which provides insights into the intrinsic differences of breast and prostate cancer cells. The dynamic protein landscapes in the cancer cells prodded by the extracellular zinc treatment reveal the potential roles of the identified zinc-responsive proteins (e.g., triosephosphate isomerase, S100A13, tumour proteins hD53 and hD54, and tumour suppressor prohibitin) in breast and prostate cancers. This study, for the first time, simultaneously investigated the two kinds of cancer cells related to zinc dyshomeostasis, and the findings shed light on the molecular understanding of the breast and prostate cancer cells in response to extracellular zinc variation.","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139462322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Osteosarcoma is a rare malignant tumor that commonly occurs in children. Anticancer drugs, for example, cisplatin, aid in postsurgery recovery but induce side effects such as renal damage, affecting the life prognosis of patients. Decursin which is one of the bioactive components has been reported for its anti-inflammatory, antioxidant, and antitumor effects, but the effect on osteosarcoma is unexplained. In this study, the research theme was to examine the sensitizing effect of decursin and its influence on cisplatin-induced nephrotoxicity. The cell viability and half maximal inhibitory concentration (IC50), apoptosis induction, and effect on cell cycle and Akt pathways were examined. In vivo, we examine the effects of decursin on tumors and mice bodies. Additionally, the effects of the cisplatin-decursin combination were evaluated in vitro and in vivo. Decursin suppressed cell viability and induced apoptosis via the cell cycle. Decursin also inhibited the Akt pathway by suppressing the phosphorylation of Akt. It enhanced apoptosis induction and lowered cell viability in combination with cisplatin. The increasing tumor volume was suppressed in the decursin-administrated group with further suppression in combination with cisplatin compared to sole cisplatin administration. The decrease in renal function and renal epithelial cell damage caused by cisplatin was improved by the combinatorial treatment with decursin. Therefore, decursin demonstrated an antitumor effect on the osteosarcoma cells and a renal protective effect in combination with cisplatin. Therefore, decursin is a prospective therapeutic agent against osteosarcoma.
{"title":"A Natural Organic Compound “Decursin” Has Both Antitumor and Renal Protective Effects: Treatment for Osteosarcoma","authors":"Daichi Hayashi, Toshiharu Shirai, Ryu Terauchi, Shinji Tsuchida, Naoki Mizoshiri, Yuki Mori, Seiji Shimomura, Osam Mazda, Kenji Takahashi","doi":"10.1155/2023/5445802","DOIUrl":"https://doi.org/10.1155/2023/5445802","url":null,"abstract":"Osteosarcoma is a rare malignant tumor that commonly occurs in children. Anticancer drugs, for example, cisplatin, aid in postsurgery recovery but induce side effects such as renal damage, affecting the life prognosis of patients. Decursin which is one of the bioactive components has been reported for its anti-inflammatory, antioxidant, and antitumor effects, but the effect on osteosarcoma is unexplained. In this study, the research theme was to examine the sensitizing effect of decursin and its influence on cisplatin-induced nephrotoxicity. The cell viability and half maximal inhibitory concentration (IC50), apoptosis induction, and effect on cell cycle and Akt pathways were examined. In vivo, we examine the effects of decursin on tumors and mice bodies. Additionally, the effects of the cisplatin-decursin combination were evaluated in vitro and in vivo. Decursin suppressed cell viability and induced apoptosis via the cell cycle. Decursin also inhibited the Akt pathway by suppressing the phosphorylation of Akt. It enhanced apoptosis induction and lowered cell viability in combination with cisplatin. The increasing tumor volume was suppressed in the decursin-administrated group with further suppression in combination with cisplatin compared to sole cisplatin administration. The decrease in renal function and renal epithelial cell damage caused by cisplatin was improved by the combinatorial treatment with decursin. Therefore, decursin demonstrated an antitumor effect on the osteosarcoma cells and a renal protective effect in combination with cisplatin. Therefore, decursin is a prospective therapeutic agent against osteosarcoma.","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138631346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective. The bromodomain-containing 4 (BRD4) is a member of the bromodomain and extra terminal domain (BET) family, which is an important epigenetic reader. It is currently a promising oncology target. In some tumors, BET bromodomain inhibitors have demonstrated promising results. Proteolysis-targeting methods (PROTAC), which rapidly and effectively degrade BRD4, have displayed considerable potential in the treatment of tumors in recent years. The purpose of this study is to examine the potential impact of BRD4 PROTAC compounds ARV-825 on oncogene BRD4-NUT fused protein in NUT carcinoma. Methods. The effectiveness of ARV-825 was evaluated at the cellular level using the cell counting kit 8 test, wound healing, cell transfection, western blotting analysis, and RNA sequencing. The effectiveness of ARV-825 was also examined in vivo using a xenograft model. Results. The BRD4-NUT fusion gene was overexpressed in 3T3 cells, and the pathogenic fusion gene was simulated. The results showed that the overexpression of BRD4-NUT could promote the proliferation and migration of 3T3 cells, but the expression of BRD4 protein was degraded after the addition of the novel cereblon-based PROTAC compound ARV-825 against BRD4, resulting in inhibition of BRD4-NUT 3T3 cell proliferation and migration. Further RNA-seq analysis showed that overexpression of BRD4-NUT was accompanied by increased expression of gene (e.g., Myc, E2F, TRAFs, Wnt, Gadd45g, and Sox6) with significantly enriched pathway (e.g., small cell lung cancer, NF-kappa B signaling pathway, and breast cancer), promoted cell cycle from G 1 phase to S phase, and increased cell proliferation and migration, activated the antiapoptosisi signal, led to abnormal cell growth, and ultimately led to tumorigenesis. The addition of ARV-825 effectively rescued this process and effectively inhibited cell vitality, proliferation, and migration. In vivo studies demonstrated that treatment with ARV-825 greatly suppressed tumor growth without causing harmful side effects and downregulated the BRD4-NUT expression level. Conclusion. Through the induction of BRD4 protein degradation, ARV-825 can successfully limit BRD4-NUT 3T3 cell proliferation in vitro and in vivo. These findings suggested that the BRD4 inhibitor ARV-825 would be an effective therapeutic strategy for treating NUT carcinoma that with the genetic feature of BRD4-NUT fusion event.
目标。bromodomain-containing 4 (BRD4)是bromodomain and extra terminal domain (BET)家族的一员，是一个重要的表观遗传读本。目前它是一个很有前途的肿瘤靶点。在某些肿瘤中，BET溴结构域抑制剂已显示出良好的效果。Proteolysis-targeting methods (PROTAC)能够快速有效地降解BRD4，近年来在肿瘤治疗中显示出相当大的潜力。本研究的目的是研究BRD4 PROTAC化合物ARV-825对NUT癌中致癌基因BRD4-NUT融合蛋白的潜在影响。方法。通过细胞计数试剂盒8测试、伤口愈合、细胞转染、western blotting分析和RNA测序，在细胞水平上评估ARV-825的有效性。ARV-825的有效性也通过异种移植模型在体内进行了检验。结果。BRD4-NUT融合基因在3T3细胞中过表达，模拟致病性融合基因。结果表明，过表达BRD4- nut可促进3T3细胞的增殖和迁移，但添加基于小脑的新型PROTAC化合物ARV-825抑制BRD4后，BRD4蛋白的表达被降解，从而抑制BRD4- nut 3T3细胞的增殖和迁移。进一步的RNA-seq分析表明，BRD4-NUT过表达伴随着Myc、E2F、TRAFs、Wnt、Gadd45g、Sox6等基因的表达增加，且通路(如小细胞肺癌、NF-kappa B信号通路、乳腺癌)显著富集，促进细胞周期从g1期进入S期，增加细胞增殖和迁移，激活抗凋亡信号，导致细胞异常生长，最终导致肿瘤发生。ARV-825的加入有效地挽救了这一过程，并有效地抑制了细胞活力、增殖和迁移。体内研究表明，用ARV-825治疗可显著抑制肿瘤生长而无不良副作用，并下调BRD4-NUT表达水平。结论。ARV-825通过诱导BRD4蛋白降解，成功地在体外和体内限制了BRD4- nut 3T3细胞的增殖。这些发现提示BRD4抑制剂ARV-825将是治疗具有BRD4-NUT融合事件遗传特征的NUT癌的有效治疗策略。
{"title":"ARV-825 Showed Antitumor Activity against BRD4-NUT Fusion Protein by Targeting the BRD4","authors":"Liu Yang, Yue Jing, Xia Xia, Xiushan Yin","doi":"10.1155/2023/9904143","DOIUrl":"https://doi.org/10.1155/2023/9904143","url":null,"abstract":"<i>Objective</i>. The bromodomain-containing 4 (BRD4) is a member of the bromodomain and extra terminal domain (BET) family, which is an important epigenetic reader. It is currently a promising oncology target. In some tumors, BET bromodomain inhibitors have demonstrated promising results. Proteolysis-targeting methods (PROTAC), which rapidly and effectively degrade BRD4, have displayed considerable potential in the treatment of tumors in recent years. The purpose of this study is to examine the potential impact of BRD4 PROTAC compounds ARV-825 on oncogene BRD4-NUT fused protein in NUT carcinoma. <i>Methods</i>. The effectiveness of ARV-825 was evaluated at the cellular level using the cell counting kit 8 test, wound healing, cell transfection, western blotting analysis, and RNA sequencing. The effectiveness of ARV-825 was also examined in vivo using a xenograft model. <i>Results</i>. The BRD4-NUT fusion gene was overexpressed in 3T3 cells, and the pathogenic fusion gene was simulated. The results showed that the overexpression of BRD4-NUT could promote the proliferation and migration of 3T3 cells, but the expression of BRD4 protein was degraded after the addition of the novel cereblon-based PROTAC compound ARV-825 against BRD4, resulting in inhibition of BRD4-NUT 3T3 cell proliferation and migration. Further RNA-seq analysis showed that overexpression of BRD4-NUT was accompanied by increased expression of gene (e.g., Myc, E2F, TRAFs, Wnt, Gadd45g, and Sox6) with significantly enriched pathway (e.g., small cell lung cancer, NF-kappa B signaling pathway, and breast cancer), promoted cell cycle from G 1 phase to S phase, and increased cell proliferation and migration, activated the antiapoptosisi signal, led to abnormal cell growth, and ultimately led to tumorigenesis. The addition of ARV-825 effectively rescued this process and effectively inhibited cell vitality, proliferation, and migration. In vivo studies demonstrated that treatment with ARV-825 greatly suppressed tumor growth without causing harmful side effects and downregulated the BRD4-NUT expression level. <i>Conclusion</i>. Through the induction of BRD4 protein degradation, ARV-825 can successfully limit BRD4-NUT 3T3 cell proliferation in vitro and in vivo. These findings suggested that the BRD4 inhibitor ARV-825 would be an effective therapeutic strategy for treating NUT carcinoma that with the genetic feature of BRD4-NUT fusion event.","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"78 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138631263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-01eCollection Date: 2023-01-01DOI: 10.1155/2023/9807856
Journal Of Oncology
[This retracts the article DOI: 10.1155/2022/2043880.].
[这收回了文章DOI:10.1155/2022/2043880.]。
{"title":"Retracted: IL2RB Is a Prognostic Biomarker Associated with Immune Infiltrates in Pan-Cancer.","authors":"Journal Of Oncology","doi":"10.1155/2023/9807856","DOIUrl":"10.1155/2023/9807856","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2022/2043880.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9807856"},"PeriodicalIF":0.0,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10632053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72014450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-11eCollection Date: 2023-01-01DOI: 10.1155/2023/9894235
Journal Of Oncology
[This retracts the article DOI: 10.1155/2021/1262291.].
[这收回了DOI:10.1155/2021/1262291的文章。]。
{"title":"Retracted: Mst2 Overexpression Inhibits Thyroid Carcinoma Growth and Metastasis by Disrupting Mitochondrial Fitness and Endoplasmic Reticulum Homeostasis.","authors":"Journal Of Oncology","doi":"10.1155/2023/9894235","DOIUrl":"10.1155/2023/9894235","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2021/1262291.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9894235"},"PeriodicalIF":0.0,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49690996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-11eCollection Date: 2023-01-01DOI: 10.1155/2023/9814758
Journal Of Oncology
[This retracts the article DOI: 10.1155/2021/5212721.].
[这收回了文章DOI:10.1155/2021/5212721.]。
{"title":"Retracted: Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress.","authors":"Journal Of Oncology","doi":"10.1155/2023/9814758","DOIUrl":"10.1155/2023/9814758","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2021/5212721.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9814758"},"PeriodicalIF":0.0,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49690997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-11eCollection Date: 2023-01-01DOI: 10.1155/2023/9803262
Journal Of Oncology
[This retracts the article DOI: 10.1155/2021/5070099.].
[这收回了文章DOI:10.1155/2021/5070099.]。
{"title":"Retracted: Development and Validation of a Novel Mitophagy-Related Gene Prognostic Signature for Hepatocellular Carcinoma Based on Immunoscore Classification of Tumor.","authors":"Journal Of Oncology","doi":"10.1155/2023/9803262","DOIUrl":"10.1155/2023/9803262","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2021/5070099.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9803262"},"PeriodicalIF":0.0,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49690995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-10eCollection Date: 2023-01-01DOI: 10.1155/2023/9870174
Nan Zhang, Yuxin Zuo, Yu Peng, Lielian Zuo
[This corrects the article DOI: 10.1155/2021/6461552.].
[这更正了文章DOI:10.1155/2021/6461552.]。
{"title":"Corrigendum to \"Function of N6-Methyladenosine Modification in Tumors\".","authors":"Nan Zhang, Yuxin Zuo, Yu Peng, Lielian Zuo","doi":"10.1155/2023/9870174","DOIUrl":"https://doi.org/10.1155/2023/9870174","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2021/6461552.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9870174"},"PeriodicalIF":0.0,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10581853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49678628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-14eCollection Date: 2023-01-01DOI: 10.1155/2023/9807575
Journal Of Oncology
[This retracts the article DOI: 10.1155/2022/2967981.].
[这收回了DOI:10.1155/2022/2967981的文章。]。
{"title":"Retracted: Preventive Effect of Intensive Nursing Intervention of Deep Vein Thrombosis of Lower Extremities in Elderly Patients with Gastrointestinal Tumors after Surgery.","authors":"Journal Of Oncology","doi":"10.1155/2023/9807575","DOIUrl":"https://doi.org/10.1155/2023/9807575","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2022/2967981.].</p>","PeriodicalId":16619,"journal":{"name":"Journal of Oncology","volume":"2023 ","pages":"9807575"},"PeriodicalIF":0.0,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10513809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41124264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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