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Radiotherapy and Anrotinib in Malignant Glomus Tumor of the Bladder: A Case Report and Literature Review. 放疗和安罗替尼治疗恶性膀胱结节瘤:病例报告与文献综述
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2024-02-07 DOI: 10.1089/cbr.2023.0151
Jing Ai, Shuang Zhang, Yimeng Qian, Lin Kang, Litao Zhang, Jing Zhao
{"title":"Radiotherapy and Anrotinib in Malignant Glomus Tumor of the Bladder: A Case Report and Literature Review.","authors":"Jing Ai, Shuang Zhang, Yimeng Qian, Lin Kang, Litao Zhang, Jing Zhao","doi":"10.1089/cbr.2023.0151","DOIUrl":"10.1089/cbr.2023.0151","url":null,"abstract":"<p><p><b><i>Background:</i></b> Malignant glomus tumors (MGTs) are rare malignancies, which grow rapidly and are aggressive. Surgical resection has been regarded as the standard management, but treatment options for those unresectable tumors are limited, resulting in a high recurrence rate and poor prognosis. <b><i>Case Description:</i></b> An 85-year-old man presented with gross hematuria and was diagnosed with MGTs of bladder. The patient achieved long-term local control after multimodal therapy comprising radiotherapy, iodine-125 seeds brachytherapy, transcatheter arterial chemoembolization, and antiangiogenic targeted therapy. <b><i>Conclusion:</i></b> MGTs occurring in the bladder are clinically rare and refractory. The case presented here highlights the importance of multidisciplinary diagnosis and treatment, providing evidence that radiotherapy and antiangiogenic therapy may play an important role in unresectable bladder MGT.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"318-321"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139698975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Prognostic Model for Prostate Cancer Patients Based on Two DNA Damage Response Mutation-Related Immune Genes. 基于两个 DNA 损伤反应突变相关免疫基因的前列腺癌患者预后模型
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2023-08-22 DOI: 10.1089/cbr.2023.0033
Jian Wang, Li Jiang, Zhenhua Shang, Zhaohua Ye, Dan Yuan, Xin Cui
{"title":"A Prognostic Model for Prostate Cancer Patients Based on Two DNA Damage Response Mutation-Related Immune Genes.","authors":"Jian Wang, Li Jiang, Zhenhua Shang, Zhaohua Ye, Dan Yuan, Xin Cui","doi":"10.1089/cbr.2023.0033","DOIUrl":"10.1089/cbr.2023.0033","url":null,"abstract":"<p><p><b><i>Background:</i></b> DNA damage response (DDR) mutation-related genes and composition of immune cells are core factors affecting the effectiveness of immune checkpoint inhibitor therapy. The aim of this study is to combine DDR with immune-related genes to screen the prognostic signature for prostate cancer (PCa). <b><i>Methods:</i></b> Gene expression profile and somatic mutation were downloaded from The Cancer Genome Atlas (TCGA). DDR-related genes were obtained from published study. After identification of prognostic-related DDR genes, samples were divided into mutation and nonmutation groups. Differentially expressed genes between these two groups were screened, followed by selection of immune-related DDR genes. Univariate and multivariate Cox analyses were performed to screen genes for constructing prognostic model. Nomogram model was also developed. The expression level of signature was detected by quantitative real-time PCR (qPCR). <b><i>Results:</i></b> Two genes (<i>MYBBP1A</i> and <i>PCDHA9</i>) were screened to construct the prognostic model, and it showed good risk prediction of PCa prognosis. Survival analysis showed that patients in high-risk group had worse overall survival than those in low-risk group. Cox analyses indicated that risk score could be used as an independent prognostic factor for PCa. qPCR results indicated that <i>MYBBP1A</i> was upregulated, whereas <i>PCDHA9</i> was downregulated in PCa cell lines. <b><i>Conclusions:</i></b> A prognostic model based on DDR mutation-related genes for PCa was established, which serves as an effective tool for prognostic differentiation in patients with PCa.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"306-317"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10414408","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}
引用次数: 0
LncRNA SNHG6 Promotes Wilms' Tumor Progression Through Regulating miR-429/FRS2 Axis. LncRNA SNHG6通过调控miR-429/FRS2轴促进Wilms'肿瘤进展
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2021-01-22 DOI: 10.1089/cbr.2020.3705
Yingjie Wang, Junli Liu, Qiying Yao, Yuchuan Wang, Zhengjuan Liu, Li Zhang
{"title":"LncRNA SNHG6 Promotes Wilms' Tumor Progression Through Regulating miR-429/FRS2 Axis.","authors":"Yingjie Wang, Junli Liu, Qiying Yao, Yuchuan Wang, Zhengjuan Liu, Li Zhang","doi":"10.1089/cbr.2020.3705","DOIUrl":"10.1089/cbr.2020.3705","url":null,"abstract":"<p><p><b><i>Background:</i></b> Long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) has been reported to be an oncogene in a variety of cancers. However, the role of SNHG6 and its associated mechanisms in Wilms' tumor progression remain largely unknown. <b><i>Methods:</i></b> The expression of SNHG6, microRNA-429 (miR-429), and FGF receptor substrates 2 (FRS2) messenger RNA (mRNA) was detected by quantitative real-time polymerase chain reaction. Cell proliferation was analyzed through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and plate colony assay. The apoptosis was assessed by flow cytometry. Cell glycolytic metabolism was analyzed through detecting the lactate dehydrogenase activity, glucose uptake, lactate production, and ATP level. The target relationship between miR-429 and SNHG6 or FRS2 was predicted by miRcode or Starbase and then validated by dual-luciferase reporter assay and RNA pull-down assay. Murine xenograft model was established to validate the function of SNHG6 <i>in vivo</i>. <b><i>Results:</i></b> The level of SNHG6 was elevated in Wilms' tumor tissues and cells, and SNHG6 played an oncogenic role to promote the proliferation and glycolysis and restrain the apoptosis of Wilms' tumor cells. MiR-429 was identified as a target of SNHG6, and miR-429 interference partly reversed the inhibitory effects induced by SNHG6 silencing on the malignant behaviors of Wilms' tumor cells. FRS2 mRNA bound to miR-429 in Wilms' tumor cells. SNHG6 upregulated the expression of FRS2 through acting as a sponge of miR-429. MiR-429-induced influences in Wilms' tumor cells were largely counteracted by the overexpression of FRS2. SNHG6 silencing suppressed the Wilms' tumor growth through miR-429/FRS2 axis <i>in vivo</i>. <b><i>Conclusion:</i></b> SNHG6 accelerated Wilms' tumor progression through regulating miR-429/FRS2 signaling <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"264-275"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38852930","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}
引用次数: 0
Promising Therapeutic Targets in Kidney Renal Clear Cell Carcinoma: PLXNA1 and PLXNB3. 肾脏透明细胞癌的有望治疗靶点:PLXNA1 和 PLXNB3。
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2021-12-01 DOI: 10.1089/cbr.2021.0336
Can-Xuan Li, Dan Long, Quan Meng
{"title":"Promising Therapeutic Targets in Kidney Renal Clear Cell Carcinoma: <i>PLXNA1</i> and <i>PLXNB3</i>.","authors":"Can-Xuan Li, Dan Long, Quan Meng","doi":"10.1089/cbr.2021.0336","DOIUrl":"10.1089/cbr.2021.0336","url":null,"abstract":"<p><p><b><i>Aims:</i></b> This study sets out to identify dysregulated plexins and investigate their roles in KIRC through an integrated bioinformatics approach. <b><i>Methods:</i></b> RNA-sequencing data and clinicopathological information of KIRC, extracted from The Cancer Genome Atlas (TCGA) database, were used to perform comprehensive bioinformatics analysis. <b><i>Results:</i></b> Almost all plexin gene family members were dysregulated in KIRC. Univariate and multivariate Cox regression analyses revealed that <i>PLXNA1/B3</i> were independent prognostic factors of overall survival in patients with KIRC. Mechanically, <i>PLXNA1/B3</i> may promote ccRCC progression through several cancer-related signaling pathways, tumor immunity, and angiogenesis. Drug sensitivity analysis suggested that vemurafenib was the potential drug for <i>PLXNA1/B3</i>. <b><i>Conclusion:</i></b> Herein, we found that <i>PLXNA1/B3</i> were independent prognostic factors, making them attractive new targets for KIRC treatment.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"276-290"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39949920","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}
引用次数: 0
IL-6 Accelerates the Proliferation and Metastasis of Pancreatic Cancer Cells via the miR-455-5p/IGF-1R Axis. IL-6 通过 miR-455-5p/IGF-1R 轴加速胰腺癌细胞的增殖和转移
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-05-01 Epub Date: 2022-12-30 DOI: 10.1089/cbr.2022.0045
Yuting Zhang, Huan He, Lanying He, Bing Shi
{"title":"IL-6 Accelerates the Proliferation and Metastasis of Pancreatic Cancer Cells via the miR-455-5p/IGF-1R Axis.","authors":"Yuting Zhang, Huan He, Lanying He, Bing Shi","doi":"10.1089/cbr.2022.0045","DOIUrl":"10.1089/cbr.2022.0045","url":null,"abstract":"<p><p><b><i>Background:</i></b> Pancreatic cancer (PaC) is a highly malignant gastrointestinal tumor with invasive and metastatic characteristics. Interleukin-6 (IL-6), a negative prognostic marker, contributes to PaC progression. However, the mechanism of IL-6 in PaC is not yet fully understood. <b><i>Methods:</i></b> miR-455-5p levels were first tested by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in PaC tissues or cells. Subsequently, PaC cell-related functions were identified through CCK-8, Transwell, and Western blotting. Changes in miR-455-5p and IGF-1R expression were confirmed using RT-qPCR and Western blotting. miR-455-5p methylation was assessed by bisulfite sequencing PCR. <b><i>Results:</i></b> The authors discovered that miR-455-5p was expressed at low levels in PaC tissues and cells, and miR-455-5p expression was observably reduced by IL-6 in PaC cells. In addition, IL-6 dramatically induces miR-455-5p methylation in PaC cells. Functionally, the data revealed that IL-6 could facilitate the malignant properties of PaC cells, including proliferation, epithelial-mesenchymal transition, and metastasis. The authors found that miR-455-5p could suppress the progression of PaC cells by downregulating IGF-1R in PaC cells. Mechanistically, IL-6 downregulated miR-455-5p and upregulated IGF-1R, and miR-455-5p reduced IGF-1R expression through targeted binding. <b><i>Conclusions:</i></b> The authors demonstrated that the miR-455-5p/IGF-1R axis is necessary for the induction of IL-6 in PaC progression. The results here may provide a theoretical basis for the application of the IL-6/miR-455-5p/IGF-1R axis in the clinical therapy of PaC.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"255-263"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10459928","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}
引用次数: 0
Knockdown of lncRNA SNHG20 Suppressed the Proliferation of Cholangiocarcinoma by Sponging miR-520f-3p. 敲除lncRNA SNHG20可通过疏导miR-520f-3p抑制胆管癌的增殖
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-04-01 Epub Date: 2020-09-09 DOI: 10.1089/cbr.2020.4042
Canghai Guan, Yuqiao Zhao, Weina Wang, Zengtao Hu, Lang Liu, Wenzhi Li, Xingming Jiang
{"title":"Knockdown of lncRNA SNHG20 Suppressed the Proliferation of Cholangiocarcinoma by Sponging miR-520f-3p.","authors":"Canghai Guan, Yuqiao Zhao, Weina Wang, Zengtao Hu, Lang Liu, Wenzhi Li, Xingming Jiang","doi":"10.1089/cbr.2020.4042","DOIUrl":"10.1089/cbr.2020.4042","url":null,"abstract":"<p><p><b><i>Objective:</i></b> A large number of studies had found that small nucleolar RNA host gene 20 (SNHG20) was a long noncoding RNA (lncRNA) that played important regulatory functions in numerous tumors. Nevertheless, the expression and pathophysiological role of SNHG20 in cholangiocarcinoma (CCA) are currently unclear. The objective of this study is to reveal the clinical significance and pathophysiological function of SNHG20 in CCA. <b><i>Methods:</i></b> The tumor tissues and adjacent normal tissues of CCA were obtained to determine the expression and clinical significance of SNHG20, and the targets of related genes were predicted through bioinformatics analysis. The function and regulatory mechanism of SNHG20 in CCA were evaluated by transfection, CCK-8 experiment, and luciferase reporter assay. <b><i>Result:</i></b> In CCA, SNHG20 was highly expressed. Overexpressed SNHG20 was markedly interrelated with the lymph node invasion and TNM stage. In addition, it could be used as indicator to evaluate the prognosis of patients. SNHG20 sponging miR-520f-3p could accelerate the proliferation of CCA tumor cells. MiR-520f-3p acted as a tumor suppressor in CCA and could also serve as a prognostic indicator. Abolition of miR-520f-3p caused an antagonistic effect and diminished the impacts of SNHG20 knockdown. SNHG20 combined with miR-520f-3p could better predict the prognosis of CCA patients. <b><i>Conclusion:</i></b> These data confirmed the knockdown SNHG20 expression in CCA could inhibit the proliferation by means of sponging miR-520f-3p.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"178-187"},"PeriodicalIF":3.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38360965","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}
引用次数: 0
Knockdown of BUB1B Inhibits the Proliferation, Migration, and Invasion of Colorectal Cancer by Regulating the JNK/c-Jun Signaling Pathway. 敲除BUB1B通过调节JNK/c-Jun信号通路抑制癌症的增殖、迁移和侵袭。
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-04-01 Epub Date: 2023-09-29 DOI: 10.1089/cbr.2023.0070
Qingjun Zeng, Sanjun Zhang, Linfang He, Qingyan Fu, Li Liao, Linjie Chen, Xiang Ding
{"title":"Knockdown of <i>BUB1B</i> Inhibits the Proliferation, Migration, and Invasion of Colorectal Cancer by Regulating the JNK/c-Jun Signaling Pathway.","authors":"Qingjun Zeng, Sanjun Zhang, Linfang He, Qingyan Fu, Li Liao, Linjie Chen, Xiang Ding","doi":"10.1089/cbr.2023.0070","DOIUrl":"10.1089/cbr.2023.0070","url":null,"abstract":"<p><p><b><i>Background:</i></b> Colorectal cancer (CRC) ranks as the third most common cancer, accounting for a significant number of cancer-related deaths worldwide every year. Yet, the molecular mechanisms responsible for the progression of this malignancy are not fully understood. Numerous studies indicate that BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) plays a role in the progression of various malignant tumors. However, the specific biological functions and the detailed mechanisms of how BUB1B influences CRC are still not completely known. This study aimed to explore the expression and role of BUB1B in CRC. <b><i>Materials and Methods:</i></b> To achieve this, the expression levels of BUB1B in human CRC tissues and cell lines were examined using real-time polymerase chain reaction and Western blotting. The role and associated mechanisms of BUB1B in CRC cell progression were assessed both <i>in vitro</i> and <i>in vivo</i> using RNA interference. <b><i>Results:</i></b> The findings of this study revealed an elevated expression of <i>BUB1B</i> in both CRC tissues and cell lines. The silencing of <i>BUB1B</i> in CRC cell lines notably inhibited cell proliferation, migration, and invasion, leading to cell cycle arrest and apoptosis. In addition, the knockdown of <i>BUB1B</i> inhibited the JNK/c-Jun signaling pathway, increased the expression of proapoptotic proteins, and decreased the expression of antiapoptotic proteins. The effects of BUB1B knockdown on CRC cell progression were reversed by the JNK activator PAF(C-16). <b><i>Conclusions:</i></b> In summary, the suppression of BUB1B hindered malignant tumor progression and heightened apoptosis and cell cycle arrest in CRC cells via the JNK/c-Jun pathway. Importantly, the removal of <i>BUB1B</i> expression curtailed tumor growth in human CRC xenografts in nude mice, suggesting its potential as a promising therapeutic target for CRC patients. ClinicalTrials.gov ID: No.2019 K-C086.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"236-246"},"PeriodicalIF":3.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41152919","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}
引用次数: 0
Noninvasive Assessment of HER2 Expression Status in Gastric Cancer Using 18F-FDG Positron Emission Tomography/Computed Tomography-Based Radiomics: A Pilot Study. 使用基于 18F-FDG 正电子发射断层成像/计算机断层扫描的放射组学对胃癌中 HER2 表达状态进行无创评估:一项试点研究。
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-04-01 Epub Date: 2024-01-09 DOI: 10.1089/cbr.2023.0162
Xiaojing Jiang, Tianyue Li, Jianfang Wang, Zhaoqi Zhang, Xiaolin Chen, Jingmian Zhang, Xinming Zhao
{"title":"Noninvasive Assessment of HER2 Expression Status in Gastric Cancer Using <sup>18</sup>F-FDG Positron Emission Tomography/Computed Tomography-Based Radiomics: A Pilot Study.","authors":"Xiaojing Jiang, Tianyue Li, Jianfang Wang, Zhaoqi Zhang, Xiaolin Chen, Jingmian Zhang, Xinming Zhao","doi":"10.1089/cbr.2023.0162","DOIUrl":"10.1089/cbr.2023.0162","url":null,"abstract":"<p><p><b><i>Purpose:</i></b> Immunohistochemistry (IHC) is the main method to detect human epidermal growth factor receptor 2 (HER2) expression levels. However, IHC is invasive and cannot reflect HER2 expression status in real time. The aim of this study was to construct and verify three types of radiomics models based on <sup>18</sup>F-fuorodeoxyglucose (<sup>18</sup>F-FDG) positron emission tomography/computed tomography (PET/CT) imaging and to evaluate the predictive ability of these radiomics models for the expression status of HER2 in patients with gastric cancer (GC). <b><i>Patients and Methods:</i></b> A total of 118 patients with GC were enrolled in this study. <sup>18</sup>F-FDG PET/CT imaging was performed prior to surgery. The LIFEx software package was applied to extract PET and CT radiomics features. The minimum absolute contraction and selection operator (least absolute shrinkage and selection operator [LASSO]) algorithm was used to select the best radiomics features. Three machine learning methods, logistic regression (LR), support vector machine (SVM), and random forest (RF) models, were constructed and verified. The Synthetic Minority Oversampling Technique (SMOTE) was applied to address data imbalance. <b><i>Results:</i></b> In the training and test sets, the area under the curve (AUC) values of the LR, SVM, and RF models were 0.809, 0.761, 0.861 and 0.628, 0.993, 0.717, respectively, and the Brier scores were 0.118, 0.214, and 0.143, respectively. Among the three models, the LR and RF models exhibited extremely good prediction performance. The AUC values of the three models significantly improved after SMOTE balanced the data. <b><i>Conclusions:</i></b> <sup>18</sup>F-FDG PET/CT-based radiomics models, especially LR and RF models, demonstrate good performance in predicting HER2 expression status in patients with GC and can be used to preselect patients who may benefit from HER2-targeted therapy.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"169-177"},"PeriodicalIF":3.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139405395","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}
引用次数: 0
Curcumol Inhibits the Progression of Hepatocellular Carcinoma by Regulating the Expression of hsa_circ_0028861. 姜黄醇通过调节 hsa_circ_0028861 的表达抑制肝细胞癌的进展
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-04-01 Epub Date: 2024-01-05 DOI: 10.1089/cbr.2023.0061
Yinbing Wu, Huafei Tang, Quanxing Liao, Yinuo Tu, Shuxian Fang, Jinfu He, Shuzhong Cui
{"title":"Curcumol Inhibits the Progression of Hepatocellular Carcinoma by Regulating the Expression of hsa_circ_0028861.","authors":"Yinbing Wu, Huafei Tang, Quanxing Liao, Yinuo Tu, Shuxian Fang, Jinfu He, Shuzhong Cui","doi":"10.1089/cbr.2023.0061","DOIUrl":"10.1089/cbr.2023.0061","url":null,"abstract":"<p><p><b><i>Background:</i></b> Hsa_circ_0028861, a newly discovered serum exosome circular RNA (circRNA), is greatly reduced in the serum of patients with hepatocellular carcinoma (HCC). However, the exact role of hsa_circ_0028861 in the progression of liver cancer is still unknown. <b><i>Materials and Methods:</i></b> Thirty patients with HCC were enrolled in this study. Hsa_circ_0028861 expression was explored via real-time polymerase chain reaction (PCR) assay. The influence of curcumol on HCC cells were tested using CCK-8 assay, 5-ethynyl-2'-deoxyuridine (EdU) staining, cell wound healing assay, and migration assay, respectively. The related mechanism was determined by Western blot. A xenograft tumor model was constructed, and mice were administrated with curcumol. <b><i>Results:</i></b> The expression of hsa_circ_0028861 in tumor tissues was elevated of patients with HCC and in HCC cells. Curcumol treatment decreased the expression of hsa_circ_0028861 in HCC cells. Curcumol treatment could largely suppress the viability, proliferation, and migration of HCC cells by reducing hsa_circ_0028861 expression and mediating the epithelial-mesenchymal transition (EMT) process. Curcumol also effectively restrained tumor growth in the HCC mice model. <b><i>Conclusions:</i></b> Curcumol exerted an inhibitory role in HCC progression by downregulating hsa_circ_0028861 expression and mediating the EMT process, which provides evidence for screening new therapeutic targets and drug therapies for HCC treatment.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"203-210"},"PeriodicalIF":3.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139106943","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}
引用次数: 0
Predicting the Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer Using Soluble Immune Checkpoints. 利用可溶性免疫检查点预测局部晚期直肠癌新辅助放化疗的疗效。
IF 3.4 4区 医学
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-04-01 Epub Date: 2023-11-20 DOI: 10.1089/cbr.2023.0134
Aziz Ari, Husnu Sevik, Mert Mahsuni Sevinc, Cihad Tatar, Kenan Buyukasik, Aziz Ahmet Surel, Ufuk Oguz Idiz
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