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  • 1
    In: BMJ Open, BMJ, Vol. 12, No. 4 ( 2022-04), p. e055273-
    Abstract: Oesophageal squamous cell carcinoma (OSCC) is one of the most commonly occurring devastating tumours worldwide, including in China. To date, the standard care of patients with stage IV OSCC is systemic chemotherapy and palliative care, which results in poor prognosis. However, no consensus has been established regarding the role of radiotherapy in targeting the primary tumour in patients with stage IVa OSCC. Thus, the aim of this study is to assess the effectiveness of primary radiotherapy combined with S-1 and nedaplatin (NPD) chemotherapy in the patients with stage IV OSCC. Methods and analysis The study is a multicentre, open-label, randomised controlled trial. A total of 180 eligible patients with stage IV OSCC will be randomised into a study group (90 patients) and a control group (90 patients). Patients in the study group will receive radiotherapy to the primary tumour at a dose of 50.4 Gy combined with 4–6 cycles of S-1 and NPD chemotherapy. In the control group, patients will only receive 4–6 cycles of S-1 and NPD chemotherapy. The primary and secondary outcomes will be measured. The differences between the two groups will be statistically analysed with regard to overall survival, the progression-free survival and safety. All outcomes will be ascertained before treatment, after treatment and after the follow-up period. The results of this study will provide evidence on the role of radiotherapy in patients with stage IV OSCC in China, which will show new options for patients with advanced oesophageal cancer. Ethics and dissemination This study was approved by the Institutional Ethics Committee of The First Hospital Affiliated of Zhengzhou University (approval number: SS-2018–04). Trial registration The trial has been registered at the Chinese Clinical Trial Registry (ChiCTR1800015765) on 1 November 2018; retrospectively registered, http://www.chictr.org.cn/index.aspx .
    Type of Medium: Online Resource
    ISSN: 2044-6055 , 2044-6055
    Language: English
    Publisher: BMJ
    Publication Date: 2022
    detail.hit.zdb_id: 2599832-8
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  • 2
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2020
    In:  Cell Death & Disease Vol. 11, No. 3 ( 2020-03-06)
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 11, No. 3 ( 2020-03-06)
    Abstract: Colorectal cancer (CRC) is a global healthcare problem. Radioresistance is a huge setback for CRC radiotherapy. In this text, the roles and molecular mechanisms of long non-coding RNA HOTAIR in CRC tumorigenesis and radioresistance were further investigated. ATG12 mRNA, HOTAIR, and microRNA-93 (miR-93) levels were measured by quantitative reverse transcription polymerase chain reaction (RT-qPCR) assay. Protein levels of LC3 I, LC3 II, p62, ATG12, cleaved caspase 3, Bax, and Bcl-2 were detected by western blotting assay in cells and were examined by immunohistochemistry (IHC) assay in tissues. Cell survival fractions, viability, and apoptotic rates were determined by clonogenic survival assay, CCK-8 assay, and flow cytometry analysis, respectively. The relationships of HOTAIR, miR-93, and ATG12 were tested by bioinformatics analysis and luciferase reporter assay. Mouse xenograft tumor models were established to investigate the influence of HOTAIR knockdown on CRC radioresistance in vivo. We found that HOTAIR expression was markedly upregulated in plasma from CRC patients after radiotherapy and CRC cells after irradiation. HOTAIR knockdown, miR-93 overexpression, or ATG12 silencing weakened cell viability, induced cell apoptosis, inhibited cell autophagy, and enhanced cell radiosensitivity in CRC. HOTAIR exerted its functions by downregulating miR-93. Moreover, HOTAIR functioned as a molecular sponge of miR-93 to regulate ATG12 expression. ATG12 protein expression was markedly upregulated and associated with miR-93 and HOTAIR expression in CRC tissues. Furthermore, HOTAIR knockdown enhanced radiosensitivity of CRC xenograft tumors by regulating miR-93/ATG12 axis. In conclusion, HOTAIR knockdown potentiated radiosensitivity through regulating miR-93/ATG12 axis in CRC, further elucidating the roles and molecular basis of HOTAIR in CRC radioresistance.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2541626-1
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  • 3
    In: SSRN Electronic Journal, Elsevier BV
    Type of Medium: Online Resource
    ISSN: 1556-5068
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
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  • 4
    In: Thoracic Cancer, Wiley, Vol. 13, No. 7 ( 2022-04), p. 934-946
    Abstract: Circular RNAs (circRNAs) are implicated in the progression and radiosensitivity of human cancers, including esophageal carcinoma (ESCA). In this study, we aimed to explore the functions of circRNA 5‐aminoimidazole‐4‐carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase (circATIC) in ESCA progression. Methods CircATIC expression, miR‐10b‐3p and Rh family C glycoprotein (RHCG) were examined via quantitative real‐time polymerase chain reaction (qRT‐PCR), western blot assay or immunohistochemistry (IHC) assay. 5′‐ethynyl‐2′‐deoxyuridine (EdU), wound‐healing, transwell, and cell colony formation assays and flow cytometry analysis were conducted to evaluate cell proliferation, migration, invasion, radiosensitivity and apoptosis, respectively. Dual‐luciferase reporter assay and RNA pulldown assay were conducted to analyze the relationships among circATIC, miR‐10b‐3p and RHCG. A murine xenograft model assay was performed to explore the functions of circATIC in tumor formation and radiosensitivity in vivo. Results CircATIC was decreased in ESCA. CircATIC overexpression suppressed cell proliferation, migration and invasion and promoted radiosensitivity and apoptosis in ESCA cells in vitro and repressed tumor formation and radioresistance in vivo. Functionally, circATIC served as the sponge for miR‐10b‐3p, which directly targeted RHCG. MiR‐10b‐3p elevation reversed circATIC‐mediated effect on ESCA cell progression. Moreover, miR‐10b‐3p inhibition suppressed cell growth and metastasis and enhanced radiosensitivity in ESCA cells by targeting RHCG. Conclusions Overexpression of circATIC hampered ESCA progression and promoted radiosensitivity depending on the regulation of miR‐10b‐3p and RHCG.
    Type of Medium: Online Resource
    ISSN: 1759-7706 , 1759-7714
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2559245-2
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  • 5
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 247, No. 8 ( 2022-04), p. 658-671
    Abstract: LncRNA expression can be conducive to gastric cancer (GC) prognosis. The objective of this study is to ascertain five specific lncRNAs involved in tumor progression of GC and their role as prognostic markers to diagnose clinical stage-wise GC. High-throughput RNA sequencing data were obtained from The Cancer Genome Atlas (TCGA) database and performed genome-wide lncRNA expression analysis using edgeR package, Bioconductor.org , and R-statistical computing to analyze differentially expressed lncRNA analysis. Cutoff parameters were FDR 〈 0.05 and |Log2FC| 〉 2. Total 351 tumor samples with differentially expressed lncRNAs were divided into group-1 lncRNAs such as AC019117.2 and LINC00941, and group-2 lncRNAs such as LINC02410, AC012317.2, and AC141273.1 by 2:1. The Spearman correlation coefficients ( p 〈 0.05) and correlation test function (cor.test ()) were performed for lncRNAs as per clinical stage. Cytoscape software was used to construct lncRNA–mRNA interaction networks. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway ( p 〈 0.05) analysis were conducted using the clusterProfiler package. Kaplan–Meier survival analysis was performed to determine the overall survival of patients based on the expression of five lncRNAs in different clinical stages of GC. AC019117.2 and LINC00941 of group 1 inferred a positive correlation with clinical stages of stage I to stage IV, and their expressions were higher in tumor tissues than normal tissues. On the contrary, LINC02410, AC012317.2, and AC141273.1 of group 2 exhibited a negative correlation with clinical stage, and they exhibited more expression in normal tissues compared to tumor tissues. GO and KEGG pathway analysis reported that AC019117.2 may interact with LINC00941 via ITGA3 and trophoblast glycoprotein (TPBG) to foster tumor progression. Tumor-specific group-1 lncRNAs were conducive to the poor overall survival and exhibited a positive correlation with the clinical stages of stage I to stage IV in GC as per the lncRNA–mRNA networking analysis. These five lncRNAs could be considered as clinically useful lncRNA-based prognostic markers to predict clinical stage-wise GC progression.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2022
    detail.hit.zdb_id: 2020856-X
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2022
    In:  Neurotoxicity Research Vol. 40, No. 5 ( 2022-10), p. 1292-1303
    In: Neurotoxicity Research, Springer Science and Business Media LLC, Vol. 40, No. 5 ( 2022-10), p. 1292-1303
    Type of Medium: Online Resource
    ISSN: 1029-8428 , 1476-3524
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2074876-0
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  • 7
    Online Resource
    Online Resource
    Wiley ; 2022
    In:  European Journal of Neuroscience Vol. 56, No. 4 ( 2022-08), p. 4275-4286
    In: European Journal of Neuroscience, Wiley, Vol. 56, No. 4 ( 2022-08), p. 4275-4286
    Abstract: Homologous to the E6‐associated protein carboxyl terminus domain containing 3 (HECTD3) has been reported to play a role in carcinogenesis. Here, we explored the role of HECTD3 in regulating the radiation resistance of glioma, and the underlying mechanism. HECTD3 expressions in glioma tissues were assessed using Western blotting, quantitative reverse transcription (qRT)‐polymerase chain reaction (PCR) and immunohistochemistry. Glioma cells were exposed to 2‐, 4‐, 6‐ or 8‐Gy X‐ray to mimic the radiation treatment. Cell count kit‐8 (CCK‐8), clone formation assay, flow cytometry assay, transwell chambers and animal assay were used to test cell viability, apoptosis, migration, invasiveness and tumourigenesis, respectively. HECTD3 expression was increased in glioma tissues, especially from patients with radiation resistance. Knockdown of HECTD3 promoted cell apoptosis and inhibited cell viability under the condition of 8‐Gy X‐ray, as well as suppressed cell migration and invasiveness. In mechanism, HECTD3 positively regulated ZEB1 (zinc finger E‐box binding hemeobox 1) expression through regulating the ubiquitination of liver kinase B1 (LKB1) protein. Overexpression of ZEB1 significantly abolished the effects of HECTD3 downregulation in inhibiting the radiation resistance and migration of glioma cells. Moreover, downregulation of HECTD3 further enhanced the anti‐tumour effect of X‐ray on glioma growth in vivo. In conclusion, HECTD3 was overexpressed in glioma patients with radiation resistance. Knockdown of HECTD3 sensitized glioma cells to radiation and inhibited cell migration by downregulating ZEB1 expression via regulating the ubiquitination of LKB1 protein. This study reveals that HECTD3 might be a potent target to enhance the radiation sensitivity of glioma.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 8
    In: Radiation Research, Radiation Research Society, ( 2023-07-14)
    Abstract: To investigate the effect of Temozolomide combined with intensity modulated radiation therapy on serum factor, immune function and clinical efficacy in postoperative glioma patients. One hundred twenty-four patients with high-grade glioma admitted to the First Affiliated Hospital of Zhengzhou University from December 2019 to December 2020 were selected and randomly divided into the study group and the control group, with 62 cases in each group. The control group was given intensity modulated radiation therapy alone, and the study group was given Temozolomide combined with intensity modulated radiation therapy. The clinical efficacy, serum factor, immune function and adverse reactions were observed and compared. The overall response rate of the study group was 95.16%, which is higher than 83.87% in the control group, and the differences were significant (P & lt; 0.05); After the treatment, the serum VEGF, EGF and HGF indicators and diverse immune function indicators were superior to those in the control group, and the differences indicated significance (P & lt; 0.05); the incidence of adverse reactions in the study group was 37.10%, which is higher than 25.81% in the control group, but the differences showed no significance (P & gt; 0.05). Temozolomide combined with intensity modulated radiation therapy could improve the level of serum factor in postoperative glioma patients, strengthen the immune function of the patients, and effectively facilitate the clinical comprehensive efficacy without increasing adverse reactions.
    Type of Medium: Online Resource
    ISSN: 1938-5404 , 0033-7587
    RVK:
    Language: English
    Publisher: Radiation Research Society
    Publication Date: 2023
    detail.hit.zdb_id: 2135113-2
    detail.hit.zdb_id: 80322-4
    SSG: 11
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  • 9
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2021
    In:  Radiation Oncology Vol. 16, No. 1 ( 2021-11-07)
    In: Radiation Oncology, Springer Science and Business Media LLC, Vol. 16, No. 1 ( 2021-11-07)
    Abstract: Boron neutron capture therapy (BNCT) was first proposed as early as 1936, and research on BNCT has progressed relatively slowly but steadily. BNCT is a potentially useful tool for cancer treatment that selectively damages cancer cells while sparing normal tissue. BNCT is based on the nuclear reaction that occurs when 10 B capture low-energy thermal neutrons to yield high-linear energy transfer (LET) α particles and recoiling 7 Li nuclei. A large number of 10 B atoms have to be localized within the tumor cells for BNCT to be effective, and an adequate number of thermal neutrons need to be absorbed by the 10 B atoms to generate lethal 10 B (n, α) 7 Li reactions. Effective boron neutron capture therapy cannot be achieved without appropriate boron carriers. Improvement in boron delivery and the development of the best dosing paradigms for both boronophenylalanine (BPA) and sodium borocaptate (BSH) are of major importance, yet these still have not been optimized. Here, we present a review of this treatment modality from the perspectives of radiation oncology, biology, and physics. This manuscript provides a brief introduction of the mechanism of cancer-cell-selective killing by BNCT, radiobiological factors, and progress in the development of boron carriers and neutron sources as well as the results of clinical study.
    Type of Medium: Online Resource
    ISSN: 1748-717X
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2224965-5
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  • 10
    In: Radiation Research, Radiation Research Society, Vol. 200, No. 3 ( 2023-9-22)
    Type of Medium: Online Resource
    ISSN: 0033-7587
    RVK:
    Language: Unknown
    Publisher: Radiation Research Society
    Publication Date: 2023
    detail.hit.zdb_id: 2135113-2
    detail.hit.zdb_id: 80322-4
    SSG: 11
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