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Outcome of aggressive B-cell lymphoma with tp53 alterations administered with CAR T-cell cocktail alone or in combination with ASCT

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Signal Transduction and Targeted Therapy 2022年第5期7卷 1681-1691页

作者： Jia Wei Min Xiao Zekai Mao Na Wang Yang Cao Yi Xiao Fankai Meng Weimin Sun Ying Wang Xingcheng Yang Liting Chen Yicheng Zhang Haichuan Zhu Shangkun Zhang Tongcun Zhang Jianfeng Zhou Liang Huang Department of Hematology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030China Immunotherapy Research Center for Hematologic Diseases of Hubei Province WuhanHubei 430030China College of Life Science and Health Wuhan University of Science and TechnologyWuhanHubei 430065China Wuhan Bio-Raid Biotechnology CO. LTDWuhanHubei 430078China

tp53 gene alteration confers inferior prognosis in refractory/relapse aggressive B-cell non-Hodgkin lymphoma(r/r B-NHL).From September 2016 to September 2020,257 r/r B-NHL patients were assessed for eligibility for two trials in our center,assessing anti-CD19 and anti-CD22 chimeric antigen receptor(CAR19/22)T-cell cocktail treatment alone or in combination with autologous stem cell transplantation(ASCT).tp53 alterations were screened in 123 enrolled patients and confirmed in ***19/22 T-cell administration resulted in best objective(ORR)and complete(CRR)response rate of 87.1%and 45.2%in patients with tp53 alterations.

关键词： tp53 alterations lymphoma

Epigenetic regulation of tp53 is involved in prostate cancer radioresistance and DNA damage response signaling

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Signal Transduction and Targeted Therapy 2023年第11期8卷 5404-5416页

作者： Catarina Macedo-Silva Vera Miranda-Gonçalves Nuno Tiago Tavares Daniela Barros-Silva Joana Lencart João Lobo Ângelo Oliveira Margareta PCorreia Lucia Altucci Carmen Jerónimo Cancer Biology&Epigenetics Group Research Center of IPO Porto(CI-IPOP)/CI-IPOP@RISE(Health Research Network)Portuguese Oncology Institute of Porto(IPO-Porto)/Porto Comprehensive Cancer Center Raquel Seruca(Porto.CCC)R.Dr.António Bernardino de Almeida4200-072PortoPortugal Department of Precision Medicine University of Campania“Luigi Vanvitelli”80138NaplesItaly Department of Pathology and Molecular Immunology ICBAS-School of Medicine&Biomedical SciencesUniversity of PortoR.Jorge de Viterbo Ferreira 2284050-313PortoPortugal Medical Physics Radiobiology and Radiation Protection Group-Research Center of IPO Porto(CI-IPOP)/CI-IPOP@RISE(Health Research Network)Portuguese Oncology Institute of Porto(IPO-Porto)/Porto Comprehensive Cancer Center Raquel Seruca(Porto.CCC)R.Dr.António Bernardino de Almeida4200-072PortoPortugal Department of Medical Physics Portuguese Oncology Institute of Porto4200-072PortoPortugal Department of Pathology Portuguese Oncology Institute of PortoPortoPortugal Department of Radiation Oncology Portuguese Oncology Institute of PortoPortoPortugal BIOGEM Molecular Biology and Genetics Research Institute83100AvellinoItaly IEOS Institute of Endocrinology and Oncology80100NaplesItaly

External beam radiotherapy(RT)is a leading first-line therapy for prostate cancer(PCa),and,in recent years,significant advances have been ***,RT resistance can arise and result in long-term recurrence or disease progression in the worst-case ***,making crucial the discovery of new targets for PCa ***,we generated a radioresistant PCa cell line,and found p53 to be highly expressed in radioresistant PCa cells,as well as in PCa patients with recurrent/disease progression submitted to *** dissection revealed that RT could promote p53 expression via epigenetic ***,a decrease of H3K27me3 occupancy at tp53 gene promoter,due to increased KDM6B activity,was observed in radioresistant PCa ***,p53 is essential for efficient DNA damage signaling response and cell recovery upon stress induction by prolonged fractionated ***,KDM6B inhibition by GSK-J4 significantly decreased p53 expression,consequently attenuating the radioresistant phenotype of PCa cells and hampering in vivo 3D tumor ***,this work contributes to improve the understanding of p53 as a mediator of signaling transduction in DNA damage repair,as well as the impact of epigenetic targeting for PCa radiosensitization.

关键词： tp53 damage cancer

tp53 gene mediates distinct dopaminergic neuronal damage in different dopaminergic neurotoxicant models

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Neural Regeneration Research 2017年第9期12卷 1413-1417页

作者： Tao Lu Paul Kim Yu Luo Department of Neurological Surgery Case Western Reserve University Medical Faculty Kunming University of Science and Technology

tp53, a stress response gene, is involved in diverse cell death pathways and its activation is implicated in the pathogenesis of Parkinson＇s disease. However, whether the neuronal tp53 protein plays a direct role in regulating dopaminergic （DA） neuronal cell death or neuronal terminal damage in different neurotoxicant models is unknown. In our recent studies, in contrast to the global inhibition of tp53 function by phar- macological inhibitors and in traditional tp53 knock-out mice, we examined the effects of DA-specific tp53 gene deletion after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and methamphetamine exposure. Our data suggests that the tp53 gene might be involved in both neuronal apoptosis and neuronal termi- nal damage caused by different neurotoxicants. Additional results from other studies also suggest that as a master regulator of many pathways that regulate apoptosis and synaptic terminal damage, it is possible that tp53 may function as a signaling hub to integrate different signaling pathways to mediate distinctive target pathways. tp53 protein as a signaling hub might be able to evaluate the microenvironment of neurons, assess the forms and severities of injury incurred, and determine whether apoptotic cell death or neuro- nal terminal degeneration occurs. Identification of the precise mechanisms activated in distinct neuronal damage caused by different forms and severities of injuries might allow for development of specific tp53 inhibitors or ways to modulate distinct downstream target pathways involved.

关键词： Parkinson's disease tp53 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity apoptosis methamphetamine

Impairment of rigidity sensing caused by mutant tp53 gain of function in osteosarcoma

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Bone Research 2023年第2期11卷 416-426页

作者： Ming Luo Mingyang Huang Ningning Yang Yufan Zhu Peng Huang Zhujun Xu Wengang Wang Lin Cai Department of Orthopedics Zhongnan Hospital of Wuhan UniversityWuhan 430071China Department of Orthopedics The First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052China Department of Emergency The First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052China

Osteosarcoma(OS)is the most common primary malignant pediatric bone tumor and is characterized by high *** have revealed a wide range of phenotypic differences among OS cell lines in terms of their in vivo tumorigenicity and in vitro colony-forming ***,the underlying molecular mechanism of these discrepancies remains *** potential role of mechanotransduction in tumorigenicity is of particular *** this end,we tested the tumorigenicity and anoikis resistance of OS cell lines both in vitro and in *** utilized a sphere culture model,a soft agar assay,and soft and rigid hydrogel surface culture models to investigate the function of rigidity sensing in the tumorigenicity of OS ***,we quantified the expression of sensor proteins,including four kinases and seven cytoskeletal proteins,in OS cell *** upstream core transcription factors of rigidity-sensing proteins were further *** detected anoikis resistance in transformed OS *** mechanosensing function of transformed OS cells was also impaired,with general downregulation of rigidity-sensing *** identified toggling between normal and transformed growth based on the expression pattern of rigidity-sensing proteins in OS *** further uncovered a novel tp53 mutation(R156P)in transformed OS cells,which acquired gain of function to inhibit rigidity sensing,thus sustaining transformed *** findings suggest a fundamental role of rigidity-sensing components in OS tumorigenicity as mechanotransduction elements through which cells can sense their physical *** addition,the gain of function of mutant tp53 appears to serve as an executor for such malignant programs.

关键词： tp53 impaired rigidity

Engineered a dual-targeting HA-tpP/A nanoparticle for combination therapy against KRAS-tp53 co-mutation in gastrointestinal cancers

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Bioactive Materials 2024年第2期32卷 277-291页

作者： Yong Mei Xiaohua Qin Zhenyu Yang Shiyao Song Xiaoting Liu Chong Wu Jieying Qian Xiaowan Huang Yunjiao Zhang Weiling He Department of Gastrointestinal Surgery The First Affiliated HospitalSun Yat-Sen UniversityGuangzhouGuangdong510080China School of Biomedical Science and Engineering School of MedicineSouth China University of TechnologyGuangzhouGuangdong510006China Department of Gastrointestinal Surgery Xiang’an Hospital of Xiamen UniversitySchool of MedicineXiamen UniversityXiamenFujian361000China National Engineering Research Centre for Tissue Restoration and Reconstruction and Key Laboratory of Biomedical Engineering of Guangdong Province South China University of TechnologyGuangzhouGuangdong510006China

KRAS-tp53 co-mutation is strongly associated with poor prognosis and high malignancy in gastrointestinal ***,a novel approach to oncotherapy may lie in combination therapy targeting both KRAS and ***,we present a novel self-assembled nanoparticle(HA-tpP/A)that are functionalized nano-carrier hyaluronic acid(HA)-tpP conjugate(HA-tpP)to degrade mutant p53 proteins(mutp53)and co-deliver AMG510 for treating KRAS-tp53 co-alteration of gastrointestinal cancers by inhibiting the mutant KRAS and mutp53 signaling *** HA-tpP/A nanoparticles led to ubiquitination-dependent proteasomal degradation of mutp53 by targeting damage to ***,these nanoparticles abrogated the gain-of-function(GOF)phenotypes of mutp53 and increased sensitivity to AMG510-induced cell killing,thereby reducing cell proliferation and migration in gastrointestinal cancer with KRAS-tp53 *** co-loaded HA-tpP/A nanoparticles demonstrated remarkable therapeutic efficacy in a tumor-bearing mouse model,particularly in KRAS-tp53 double mutant expressing cancer cells,compared with single drug and combined free drug ***,HA-tpP/A is the first reported nanoparticle with an ability to co-target KRAS-tp53,providing a promising approach for therapy in highly malignant gastrointestinal tumors and potentially expanding clinical indications for AMG510 targeted therapies in gastrointestinal tumors.

关键词： Dual-targeting KRAS tp53 Co-mutation HA-tpP/A nanoparticle Mitochondrial targeting Gastrointestinal cancer

Prognostic value of BCL2 and tp53 genetic alterations for diffuse large B-cell lymphoma patients treated with R-CHOP

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Cancer Biology & Medicine 2022年第6期19卷 893-909页

作者： Yan Qin Haizhu Chen Peng Liu Changgong Zhang Jianliang Yang Lin Gui Xiaohui He Liqiang Zhou Shengyu Zhou Shiyu Jiang Hongxin Jiang Yuankai Shi Department of Medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing Key Laboratory of Clinical Study on Anticancer Molecular Targeted DrugsBeijing 100021China Department of Medical Oncology Suzhou Municipal HospitalAffiliated Suzhou Hospital of Nanjing Medical UniversitySuzhou 215001China

Objective:Limited data about the prognostic significance of BCL2 mutations and BCL2 copy number variations in diffuse large B-cell lymphoma(DLBCL)are *** study aimed to comprehensively describe BCL2 genetic alterations in DLBCL patients,and examine correlation of BCL2,tp53 and other genetic alterations with outcomes in patients treated with ***:Probe capture-based high-resolution sequencing was performed on 191 patients diagnosed with de novo ***,BCL2,and BCL6 protein expressions were detected by ***:The presence of BCL2 alterations significantly correlated with poor progression-free survival(PFS)(5-year PFS:13.7%vs.40.8%;P=0.003)and overall survival(OS)(5-year OS:34.0%vs.70.9%;P=0.036).Importantly,patients who harbored BCL2 gain/amplifications(BCL2GA/AMP)also had a remarkably inferior 5-year PFS(11.1%vs.38.3%;Ptp53 mutations,and International Prognostic Index(IPI)were significantly associated with inferior PFS and *** prognostic models for OS were constructed based on 3 risk factors,including BCL2 alterations(Model 1)or BCL2GA/AMP(Model 2),tp53 mutations,and IPI,to stratify patients into 4 risk groups with different survival ***:This study showed that DLBCL patients treated with R-CHOP,BCL2 alterations,especially BCL2GA/AMP and tp53 mutations were significantly associated with inferior outcomes,which were independent of the *** novel prognostic models we proposed predicted outcomes for DLBCL patients treated with R-CHOP,but further validation of the prognostic models is still warranted.

关键词： BCL2 tp53 genetic alterations diffuse large B-cell lymphoma prognosis

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 Affiliated 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 ***: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 *** 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 *** and Masson staining were performed to evaluate the extent of *** therapeutic potential of BMSC-Exos for PF was examined through pathological examination,RT-qPCR,Western blotting,and peritoneal function ***-mesenchymal transition(EMT)of HMrSV5 was induced with 4.25%*** were divided into control group,4.25%PDF group,BMSC-Exos treatment group,and BMSC-Exos+tp53 treatment *** 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 ***:Small RNA sequencing analysis showed that miR-27a-3p was highly expressed in BMSC-derived exosomes compared to *** RT-qPCR results showed that the expression of miR-27a-3p was upregulated in BMSC-Exos,but decreased in PD *** found that PF was glucose concentration-dependently enhanced in the peritoneum of the PD *** with the control mice,the PD mice showed high solute transport and decreased ultrafiltration volume as well as an obvious f

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

Tissue array for tp53,C-myc,CCND1 gene over-expression in different tumors

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World Journal of Gastroenterology 2008年第47期14卷 7199-7207页

作者： Guo-Yan Liu Qi Luo Bin Xiong Chao Pan Ping Yin Hong-Feng Liao Wei-Chun Zhuang Hong-Zhi Gao Zhongnan Hospital Wuhan UniversityWuhan 430071 China The General Surgery of the AffiliatedZhongshan Hospital of Xiamen University The Digest DiseaseResearch Institution of Xiamen University Xiamen 361004Fujian Province China Department of GeneralHong-Feng Liao Wei-ChunSurgery Affiliated ZhongshanHospital of Xiamen University Digest Disease ResearchInstitute of Xiamen University Xiamen 361004 FujianProvince. China Zhongnan Hospital Wuhan University Wuhan430071 Hubei Proyince China The Second Affiliated Hospital of FujianMedical University Fujian Province China

AIM:To rapidly detect molecular alterations in different malignancies and investigate the possible role of tp53,C-myc,and CCND1 genes in development of tumors in human organs and their adjacent normal tissues,as well as the possible relation between well-and poorly-differentiated ***:A tissue array consisting of seven different tumors was *** tissue array included 120 points of esophagus,120 points of stomach,80 points of rectum,60 points of thyroid gland,100 points of mammary gland,80 points of liver,and 80 points of *** of tp53,C-myc,and CCND1 were determined by RNA in situ hybridization.3' terminal digoxin-labeled anti-sense single stranded oligonucleotide and locked nucleic acid modifying probe were ***:The expression level of tp53 gene was higher in six different carcinoma tissue samples than in paracancerous tissue samples with the exception in colon carcinoma tissue samples(P tp53,CCND1,and C-myc genes appears to play a role in development of human cancer by regulating the expression of ***53,CCND1 and C-myc genes are significantly correlated with the development of different carcinomas.

关键词： tp53 C-myc CCND1 Tissue microarray RNA in situ hybridization

Human endogenous retroviruses as epigenetic therapeutic targets in tp53-mutated diffuse large B-cell lymphoma

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Signal Transduction and Targeted Therapy 2023年第11期8卷 5325-5337页

作者： Ying Fang Mu-Chen Zhang Yang He Chen Li Hai Fang Peng-Peng Xu Shu Cheng Yan Zhao Yan Feng Qian Liu Li Wang Wei-Li Zhao Shanghai Institute of Hematology State Key Laboratory of Medical GenomicsNational Research Center for Translational Medicine at ShanghaiRuijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Network and Information Center Shanghai Jiao Tong UniversityShanghaiChina State Key Laboratory of Microbial Metabolism School of Life Sciences and BiotechnologyShanghai Jiao Tong UniversityShanghaiChina

tp53 mutation(tp53^(mut))occurs in 10–20%of diffuse large B-cell lymphoma(DLBCL)cases and serves as an unfavorable biomarker of DLBCL *** confers resistance to immunochemotherapy,high-dose chemotherapy,autologous stem cell transplantation,and anti-CD19 chimeric antigen receptor T-cell *** targeting of tp53^(mut) remains a significant challenge in DLBCL *** we assessed tp53^(mut) in 667 patients with newly diagnosed DLBCL,including 576 patients treated with immunochemotherapy rituximab,cyclophosphamide,doxorubicin,vincristine,and prednisone(R-CHOP)and 91 patients with decitabine plus R-CHOP(DR-CHOP,NCT02951728 and NCT04025593).tp53^(mut) independently predicted an inferior prognosis in R-CHOP-treated DLBCL,although this could be mitigated by DR-CHOP *** tp53^(mut) patients,multiple viral regulation pathways were repressed,resulting in the inhibition of immune modulation,as revealed by gene set enrichment ***53^(mut) DLBCL exhibited increased methyltransferase SUV39H1 expression and H3K9 trimethylation(H3K9me3),contributing to repression of endogenous retroviruses(ERVs)and immunosuppressive tumor *** tp53^(mut) DLBCL cell lines,decitabine down-regulated SUV39H1,inhibited H3K9me3 occupancy on ERVs,and triggered ERV expression,thereby unleashing interferons program and CD4^(+)T/CD8^(+)T cell *** silencing of SUV39H1 significantly abrogated decitabine-induced H3K9me3 inhibition and ERV *** tp53^(mut) patient-derived xenograft models and tp53^(mut) patients,the anti-tumor effect was improved upon the use of combined treatment of decitabine and doxorubicin via SUV39H1-H3K9me3-ERVs ***,our findings highlight an ERV regulatory circuitry in tp53^(mut) DLBCL and the crucial roles ERVs for epigenetically reprogramming tumor microenvironment for treating tp53^(mut)-driven cancers.

关键词： tp53 endogenous chemotherapy