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Genes & Diseases 2024年第2期11卷 550-553页

作者： Jing Tang Yue Li Jiazhu Wu Haorui Shen Hua Yin Jinhua Liang Li Wang Jianyong Li Yi Xia Wei Xu Department of Hematology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjingJiangsu 210029China Key Laboratory of Hematology of Nanjing Medical University NanjingJiangsu 210029China Collaborative Innovation Center for Cancer Personalized Medicine NanjingJiangsu 210029China

PR/SET domain 1(PRDM1)gene is located on chromosome 6q21,encoding the B lymphocyte-induced maturation protein 1(BLIMP1).1 It is reported that loss of PRDM1 function is exacerbated in activated B-cell-like(ABC)-diffuse large B cell lymphoma(DLBCL)and associated with inferior survival.However,it remains unclear what leads to PRDM1 inactivation and the drug resistance mechanism caused by abnormal inactivation of PRDM1.We investigated the contribution of PRDM1 gene as a prognosis and potential therapeutic target for ABC-DLBCL patients and further clarified the possible mechanism of PRDM1 abnormal inactivation.We first proposed that tp53 could regulate PRDM1 by histone ubiquitination modification at the post-transcriptional level.

关键词： PRDM1 tp53 therapeutic

Identification of tp53 mutation-associated prognostic genes and investigation of the immune cell infiltration in patients with hepatocellular carcinoma

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Genes & Diseases 2024年第2期11卷 520-523页

作者： Qijun Yang Lianke Gao Yuhan Xu Gaoquan Cao Yingcheng He Wenyige Zhang Xue Zhang Chengfeng Wu Kaili Liao Xiaozhong Wang Department of Clinical Laboratory The Second Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330006China Queen Mary College of Nanchang University NanchangJiangxi 330031China Advanced Manufacturing College of Nanchang University NanchangJiangxi 330031China The Forth Clinical School of Nanchang University The South Road of Bayi SquareNanchangJiangxi 330031China Department of Vascular Surgery The Second Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330006China

Primary liver cancer,which is mainly composed of hepatocellular carcinoma(HcC),is the sixth most common type of cancer worldwide and the thirdmost common cause of cancer mortality.1 The total number of mutations present in tumor specimens is called tumor mutation burden(TMB)and it is an emerging biomarker of immunotherapy response.2 TMB can predict clinical responses to immunotherapy such as ICl(immune checkpoint inhibitor)treatments and higher TMB is related to better survival.3 tp53,a gene encoding a tumor suppressor protein that triggers apoptosis and cell cycle arrest,is one of the most prevalent mutations in 25%-30%of HCC patients.4 Research shows that tp53 mutations in HCC patients are associated with advanced tumor grade and poor prognosis.5 To identify the tp53 mutation-related genes which can predict HCC patients'prognosis and explore the immune cell infiltration,we constructed a risk model based on six tp53 mutation-related genes which can accurately predict patients'prognosis.Besides,six immune cells with a similar expression pattern were identified in The Cancer Genome Atlas(TCGA)and International Cancer Genome Consortium(ICGC)databases.

关键词： tp53 patients hepatocellular

BMSC-derived Exosomes Ameliorate Peritoneal Dialysis-associated Peritoneal Fibrosis via the Mir-27a-3p/tp53 Pathway

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Current Medical Science 2024年第2期44卷 333-345页

作者： Jun-li ZHAO Lin ZHAO Qiu-nan ZHAN Miao LIU Ting ZHANG Wen-wen CHU Department of Nephrology Shanghai University of Medicine&Health Sciences Ailiated Zhoupu HospitalShanghai 201318China Orthopedic Department Guangming Traditional Chinese Medicine Hospital of Pudong New AreaShanghai 201399China

Objective:Peritoneal fibrosis(PF)is the main cause of declining efficiency and ultrafiltration failure of the peritoneum,which restricts the long-term application of peritoneal dialysis(PD).This study aimed to investigate the therapeutic effects and mechanisms of bone marrow mesenchymal stem cells-derived exosomes(BMSC-Exos)on PF in response to PD.Methods:Small RNA sequencing analysis of BMSC-Exos was performed by second-generation sequencing.C57BL/6J mice were infused with 4.25%glucose-based peritoneal dialysis fluid(PDF)for 6 consecutive weeks to establish a PF model.A total of 36 mice were randomly divided into 6 groups:control group,1.5%PDF group,2.5%PDF group,4.25%PDF group,BMSC-Exos treatment group,and BMSC-Exos+tp53 treatment group.Reverse transcription quantitative polymerase chain reaction(RT-qPCR)was performed to measure the expression level of miR-27a-3p in BMSC-Exos and peritoneum of mice treated with different concentrations of PDF.HE and Masson staining were performed to evaluate the extent of PF.The therapeutic potential of BMSC-Exos for PF was examined through pathological examination,RT-qPCR,Western blotting,and peritoneal function analyses.Epithelial-mesenchymal transition(EMT)of HMrSV5 was induced with 4.25%PDF.Cells were divided into control group,4.25%PDF group,BMSC-Exos treatment group,and BMSC-Exos+tp53 treatment group.Cell Counting Kit-8 assay was used to measure cell viability,and transwell migration assay was used to verify the capacity of BMSC-Exos to inhibit EMT in HMrSV5 cells.Results:Small RNA sequencing analysis showed that miR-27a-3p was highly expressed in BMSC-derived exosomes compared to BMSCs.The RT-qPCR results showed that the expression of miR-27a-3p was upregulated in BMSC-Exos,but decreased in PD mice.We found that PF was glucose concentration-dependently enhanced in the peritoneum of the PD mice.Compared with the control mice,the PD mice showed high solute transport and decreased ultrafiltration volume as well as an obvious fibroproliferative response,with markedly increas

关键词： peritoneal fibrosis bone marrow mesenchymal stem cell-derived exosomes miR-27a-3p tp53 epithelialmesenchymal transition

Aberrant epithelial cell interaction promotes esophageal squamous-cell carcinoma development and progression

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Signal Transduction and Targeted Therapy 2024年第1期9卷 279-294页

作者： Liping Chen Shihao Zhu Tianyuan Liu Xuan Zhao Tao Xiang Xiao Hu Chen Wu Dongxin Lin Department of Etiology and Carcinogenesis National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Key Laboratory of Cancer Genomic Biology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjing 211166China CAMS Oxford Institute Chinese Academy of Medical SciencesBeijing 100006China Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South ChinaGuangzhou 510060China

Epithelial-mesenchymal transition(EMT)and proliferation play important roles in epithelial cancer formation and progression,but what molecules and how they trigger EMT is largely unknown.Here we performed spatial transcriptomic and functional analyses on samples of multistage esophageal squamous-cell carcinoma(ESCC)from mice and humans to decipher these critical issues.By investigating spatiotemporal gene expression patterns and cell–cell interactions,we demonstrated that the aberrant epithelial cell interaction via EFNB1-EPHB4 triggers EMT and cell cycle mediated by downstream SRC/ERK/AKT signaling.The aberrant epithelial cell interaction occurs within the basal layer at early precancerous lesions,which expands to the whole epithelial layer and strengthens along the cancer development and progression.Functional analysis revealed that the aberrant EFNB1-EPHB4 interaction is caused by overexpressedΔNP63 due to tp53 mutation,the culprit in human ESCC tumorigenesis.Our results shed new light on the role of tp53-tp63/ΔNP63-EFNB1-EPHB4 axis in EMT and cell proliferation in epithelial cancer formation.

关键词： esophageal tp53 squamous

The Multiple Roles of Autophagy in Neural Function and Diseases

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Neuroscience Bulletin 2024年第3期40卷 363-382页

作者： Yan-Yan Li Zheng-Hong Qin Rui Sheng Department of Pharmacology and Laboratory of Aging and Nervous Diseases Jiangsu Key laboratory of Neuropsychiatric DiseasesCollege of Pharmaceutical Sciences of Soochow UniversitySuzhou 215123China

Autophagy involves the sequestration and delivery of cytoplasmic materials to lysosomes,where proteins,lipids,and organelles are degraded and recycled.According to the way the cytoplasmic components are engulfed,autophagy can be divided into macroautophagy,microautophagy,and chaperone-mediated autophagy.Recently,many studies have found that autophagy plays an important role in neurological diseases,including Alzheimer's disease,Parkinson's disease,Huntington's disease,neuronal excitotoxicity,and cerebral ischemia.Autophagy maintains cell homeostasis in the nervous system via degradation of misfolded proteins,elimination of damaged organelles,and regulation of apoptosis and inflammation.AMPK-mTOR,Beclin 1,tp53,endoplasmic reticulum stress,and other signal pathways are involved in the regulation of autophagy and can be used as potential therapeutic targets for neurological diseases.Here,we discuss the role,functions,and signal pathways of autophagy in neurological diseases,which will shed light on the pathogenic mechanisms of neurological diseases and suggest novel targets for therapies.

关键词： Autophagy Neurodegenerative diseases Cerebral ischemia AMPK mTOR Beclin 1 tp53 Endoplasmic reticulum stress

Mutational landscape of tp53 and CDH1 in gastric cancer

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World Journal of Gastrointestinal Surgery 2024年第2期16卷 276-283页

作者： Hong-Qiao Cai Li-Yue Zhang Li-Ming Fu Bin Xu Yan Jiao Department of Hepatobiliary and Pancreatic Surgery General Surgery CenterThe First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina Department of Critical Care Medicine The First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina Department of Traditional Chinese Medicine The First Hospital of Jilin UniversityChangchun 130021Jilin ProvinceChina

In this editorial we comment on an article published in a recent issue of the World J Gastrointest Surg.A common gene mutation in gastric cancer(GC)is the tp53 mutation.As a tumor suppressor gene,tp53 is implicated in more than half of all tumor occurrences.tp53 gene mutations in GC tissue may be related with clinical pathological aspects.The tp53 mutation arose late in the progression of GC and aided in the final switch to malignancy.CDH1 encodes E-cadherin,which is involved in cell-to-cell adhesion,epithelial structure maintenance,cell polarity,differentiation,and intracellular signaling pathway modulation.CDH1 mutations and functional loss can result in diffuse GC,and CDH1 mutations can serve as independent prognostic indicators for poor prognosis.GC patients can benefit from genetic counseling and testing for CDH1 mutations.Demethylation therapy may assist to postpone the onset and progression of GC.The investigation of tp53 and CDH1 gene mutations in GC allows for the investigation of the relationship between these two gene mutations,as well as providing some basis for evaluating the prognosis of GC patients.

关键词： tp53 CDH1 Gastric cancer Gene mutation Methylation

Insights from TARGET-seq:Inflammation drives tp53-mediated clonal evolution

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The Innovation 2024年第2期5卷 7-8页

作者： Yeqian Zhao Wenxuan Huo Yue Liang Xiaodong Mo Shanshan Pei Yanmin Zhao Bone Marrow Transplantation Center the First Affiliated HospitalZhejiang University School of MedicineHangzhou 310009China Liangzhu Laboratory Zhejiang University Medical CenterHangzhou 311121China Institute of Hematology Zhejiang UniversityHangzhou 311121China Peking University People’s Hospital Peking University Institute of HematologyNational Clinical Research Center for Hematologic DiseaseBeijing 100044China

Approximately 10%–20%myeloproliferative neoplasms(MPNs)can progress into blast-phase MPNs,also termed secondary acute myeloid leukemias(sAMLs),presenting dismal prognoses.sAML exhibits a distinctive clinical and pathological profile compared to de novo AML,marked by a higher incidence of erythroid leukemias and reduced responsive to conventional chemotherapies,resulting in a median survival of approximately 6 months.tp53 alterations are prevalent adverse events in leukemic transformation(LT),occurring in around one-third of sAML subjects.

关键词： tp53 neoplasms alterations

Twenty years of Gendicine?rAd-p53 cancer gene therapy:The first-in-class human cancer gene therapy in the era of personalized oncology

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Genes & Diseases 2024年第4期11卷 234-245页

作者： Li Qi Guiqing Li Peipei Li Hongwei Wang Xiaolong Fang Tongchuan He Jingjing Li Affiliated Hospital of Weifang Medical University School of Clinical MedicineWeifang Medical UniversityWeifangShandong 262700China Jinming Yu Academician Workstation of Oncology Affiliated Hospital of Weifang Medical UniversityWeifangShandong 262700China Decording Therapeutics Corp Shangha 200000China Yangkun Biogroup Co. LtdNanjingJiangsu 210002China The University of Chicago ChicagoIL 60290USA

Genetic mutations in tp53 contribute to human malignancies through various means.To date,there have been a variety of therapeutic strategies targeting p53,including gene therapy to restore normal p53 function,mutant p53 rescue,inhibiting the MDM2-p53 interaction,p53-based vaccines,and a number of other approaches.This review focuses on the functions of tp53 and discusses the aberrant roles of mutant p53 in various types of cancer.Recombinant human p53 adenovirus,trademarked as Gendicine,which is the first anti-tumor gene therapy drug,has made tremendous progress in cancer gene therapy.We herein discuss the biological mechanisms by which Gendicine exerts its effects and describe the clinical re-sponses reported in clinical trials.Notably,the clinical studies suggest that the combination of Gendicine with chemotherapy and/or radiotherapy may produce more pronounced efficacy in slowing tumor growth and progression than gene therapy/chemotherapy alone.Finally,we summarize the methods of administration of recombinant human p53 adenovirus for different cancer types to provide a reference for future clinical trials.

关键词： Gendicine Gene therapy p53 mutation Recombinant p53 adenovirus tp53

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tp53基因异常多发性骨髓瘤治疗进展

中国实用内科杂志 2024年第1期44卷 80-85页

作者：张弛李炳宗昆山市第一人民医院江苏苏州215334 苏州大学附属第二医院血液科江苏苏州215004

多发性骨髓瘤(multiple myeloma,MM)是仅次于白血病的第二大血液系统恶性肿瘤,约占血液系统肿瘤的10%[1]。tp53基因异常在MM患者中的发病率并不低,Li等[2]在大样本患者的分析发现其发生率大约在18%。tp53基因位于17号染色体的短臂端,其... 详细信息

多发性骨髓瘤(multiple myeloma,MM)是仅次于白血病的第二大血液系统恶性肿瘤,约占血液系统肿瘤的10%[1]。tp53基因异常在MM患者中的发病率并不低,Li等[2]在大样本患者的分析发现其发生率大约在18%。tp53基因位于17号染色体的短臂端,其异常包含3种类型:(1)17号染色体短臂的缺失,即del(17p);(2)tp53单等位基因突变;(3)tp53双等位基因失活。其中del(17p)和tp53双等位基因失活已在多个临床试验中被证实预后不佳。

关键词：多发性骨髓瘤 tp53 基因异常

tp53基因突变急性髓系白血病患者临床及分子生物学特征分析

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中国肿瘤临床 2024年第6期51卷 281-286页

作者：徐蕾林国祥徐州医科大学附属淮安医院(淮安市第二人民医院)检验科江苏省淮安市223022 徐州医科大学附属淮安医院(淮安市第二人民医院)血液科江苏省淮安市223022

目的:分析tp53基因突变急性髓系白血病(acute myeloid leukemia,AML)患者临床及分子生物学特征。方法:回顾性分析2017年7月至2023年5月就诊于徐州医科大学附属淮安医院256例初发AML患者临床资料,均行聚合酶链式反应(polymerase chain re... 详细信息

目的:分析tp53基因突变急性髓系白血病(acute myeloid leukemia,AML)患者临床及分子生物学特征。方法:回顾性分析2017年7月至2023年5月就诊于徐州医科大学附属淮安医院256例初发AML患者临床资料,均行聚合酶链式反应(polymerase chain reaction,PCR)结合一代测序技术检测,统计tp53基因突变频率,分析tp53基因突变患者临床、实验室特征、分子学特征、核型特征及总生存期。结果:tp53基因突变频率为7.8%;tp53基因突变组年龄、世界卫生组织(WHO)分型,白细胞(white blood cell,WBC)计数和骨髓原始细胞与tp53基因无突变组具有显著性差异(Ptp53基因突变组中检测出BCR-ABL、NPM1突变、CEBPA突变、RUNX1-RUNX1T1、MLL相关融合基因、FLT3-ITD突变及CBFβ-MYH11突变分子学异常发生率与tp53基因无突变组无显著性差异(P>0.05);tp53基因突变组中单体核型、复杂核型、异常核型、-17/17p-、-7/7q-和-3/3q-检出率与tp53基因无突变组具有显著性差异(Ptp53基因无突变组总生存期显著优于tp53基因突变组患者(Ptp53基因突变均为AML患者的独立影响因素(均Ptp53基因突变AML患者具有一定临床及分子生物学特征,伴有tp53基因突变患者生存预后不佳。

关键词： tp53 基因突变急性髓系白血病核型预后