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乳腺癌组织特异性治疗靶标MED（英文）

Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2019年第5期20卷 381-390页

作者： Marissa LEONARD Xiaoting ZHANG Department of Cancer Biology University of Cincinnati College of Medicine

在这篇综述中,我们讨论了雌激素受体共激活子转录中介体亚基1(MED1)作为独特的组织特异性辅因子在乳腺癌干细胞形成、转移和治疗抗性中的关键作用。此外,我们详细介绍了目前使用最先进的RNA纳米技术靶标MED1的成果,并提出了未来的展望。

关键词：转录中介体亚基1(MED1) 中介体雌激素受体乳腺癌内分泌治疗抗性 RNA纳米技术

Autophagy in neural stem cells and glia for brain health and diseases

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Neural Regeneration Research 2024年第4期19卷 729-736页

作者： Aarti Nagayach Chenran Wang Department of Cancer Biology University of Cincinnati College of Medicine

Autophagy is a multifaceted cellular process that not only maintains the homeostatic and adaptive responses of the brain but is also dynamically involved in the regulation of neural cell generation,maturation,and survival.Autophagy facilities the utilization of energy and the microenvironment for developing neural stem cells.Autophagy arbitrates structural and functional remodeling during the cell differentiation process.Autophagy also plays an indispensable role in the maintenance of stemness and homeostasis in neural stem cells during essential brain physiology and also in the instigation and progression of diseases.Only recently,studies have begun to shed light on autophagy regulation in glia(microglia,astrocyte,and oligodendrocyte)in the brain.Glial cells have attained relatively less consideration despite their unquestioned influence on various aspects of neural development,synaptic function,brain metabolism,cellular debris clearing,and restoration of damaged or injured tissues.Thus,this review composes pertinent information regarding the involvement of autophagy in neural stem cells and glial regulation and the role of this connexion in normal brain functions,neurodevelopmental disorders,and neurodegenerative diseases.This review will provide insight into establishing a concrete strategic approach for investigating pathological mechanisms and developing therapies for brain diseases.

关键词： astrocyte autophagy glia microglia neural stem cells neurodegenerative diseases neurodevelopmental disorders oligodendrocyte

Novel CYP1B1 mutations and a possible prognostic use for surgical management of congenital glaucoma

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International Journal of Ophthalmology(English edition) 2019年第4期12卷 607-614页

作者： Mohamed M.Khafagy Nadia El-Guendy Marwa A Tantawy Mohamed A.Eldaly Hala M.Elhilali Abdel Hady A.Abdel Wahab Ophthalmology department Faculty of Medicine Cairo University cancer biology department National Cancer Institute Cairo University Research department Children's Cancer Hospital

AIM: To identify CYP1B1 gene mutations and evaluate their possible role as a prognostic factor for success rates in the surgical management of Egyptian congenital glaucoma patients.METHODS: Totally 42 eyes of 29 primary congenital glaucoma patients were operated on with combined trabeculotomy/trabeculectomy with mitomycin-C and followed up at 1 d, 1 wk, 1, 6 and 12 mo postoperatively. Genomic DNA was extracted from peripheral blood leukocytes. Coding regions of CYP1B1 gene were amplified using 13 pairs of primers, screened for mutations using single-strand conformation polymorphism followed by sequencing of both strands. Efficacy of the operation was graded as either a success [maintaining intraocular pressure(IOP) less than 21 mm Hg with or without antiglaucoma medication], or a failure(IOP more than 21 mm Hg with topical antiglaucoma medications). RESULTS: Seven novel mutations out of a total of 15 different mutations were found in the CYP1B1 genes of 14 patients(48.2%). The presence of CYP1B1 gene mutations did not correlate with the failure of the surgery(P=0.156, odds ratio=3.611, 95%CI, 0.56 to 22.89); while the positive consanguinity strongly correlated with failure of the initial procedure(P=0.016, odds ratio=11.25, 95%CI, 1.57 to 80.30). However, the Kaplan-Meier survival analysis revealed a significantly lower time of IOP control in the subgroup with mutations in CYP1B1 versus the congenital primary glaucoma group without mutations(log rank test, P=0.015).CONCLUSION: Seven new CYP1B1 mutations are identified in Egyptian patients. Patients harboring confirmed mutations suffered from early failure of the initial surgery. CYP1B1 mutations could be considered as a prognostic factor for surgery in primary congenital glaucoma.

关键词： CYP1B1 mutations primary congenital glaucoma intraocular pressure trabeculotomy/trabeculectomy with mitomycin-C.

Research progress in hepatitis B virus covalently closed circular DNA

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cancer biology & Medicine 2022年第4期19卷 415-431页

作者： Xiaodong Zhang Yufei Wang Guang Yang department of Gastrointestinal cancer biology Liver Cancer CenterTianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin’s Clinical Research Center for CancerTianjin 300060China department of cancer Research College of Life SciencesNankai UniversityTianjin 300071China

Hepatitis B virus(HBV)infections are a global public health issue.HBV covalently closed circular DNA(cccDNA),the template for the transcription of viral RNAs,is a key factor in the HBV replication cycle.Notably,many host factors involved in HBV cccDNA epigenetic modulation promote the development of hepatocellular carcinoma(HCC).The HBV cccDNA minichromosome is a clinical obstacle that cannot be efficiently eliminated.In this review,we provide an update on the advances in research on HBV cccDNA and further discuss factors affecting the modulation of HBV cccDNA.Hepatitis B virus X protein(HBx)contributes to HBV cccDNA transcription and the development of hepatocarcinogenesis through modulating host epigenetic regulatory factors,thus linking the cccDNA to hepatocarcinogenesis.The measurable serological biomarkers of continued transcription of cccDNA,the effects of anti-HBV drugs on cccDNA,and potential therapeutic strategies targeting cccDNA are discussed in detail.Thus,this review describes new insights into HBV cccDNA mechanisms and therapeutic strategies for cleaning cccDNA,which will benefit patients with liver diseases.

关键词： Hepatitis B virus cccDNA HBx hepatocarcinogenesis epigenetic modulation therapy

Highlighted multi-modifications of enzymes:a novel succinylation mediated by histone acetyltransferase 1 in tumors

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cancer biology & Medicine 2022年第2期19卷 133-135页

作者： Xiaodong Zhang Chunyu Hou Guang Yang department of Gastrointestinal cancer biology Liver Cancer CenterTianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin’s Clinical Research Center for CancerTianjin 300060China

Histone acetyltransferase 1 serves as a succinyl transferase in tumors Protein post-translational modification(PTM)as an important research field has attracted increasing attention.Recently,our group has reported that histone acetyltransferase 1(HAT1)succinylated histones and non-histones and promoted tumorigenesis1.HAT1 plays a role in different biological processes,including cell cycle progression,glucose metabolism,histone production,and DNA damage repair2.We found that HAT1 succinylated histone H3 on K122.For a non-histone,HAT1 catalyzed the succinylation of phosphoglycerate mutase 1(PGAM1)on K99 to increase its enzyme activity,promoting glycolysis in cancer cells.Functionally,HAT1-mediated succinylation contributed to tumorigenesis.Our finding provided new insight into the mechanism of how a histone acetyltransferase HAT1 modulated succinylation during cancer development.

关键词： metabolism mediated tumors

Novel oncogenes and tumor suppressor genes in hepatocellular carcinoma

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Liver Research 2021年第4期5卷 195-203页

作者： Fang Wang Peter Breslin S J Wei Qiu department of Surgery and cancer biology Loyola University Chicago Stritch School of MedicineMaywoodILUSA department of Molecular/Cellular Physiology Cancer BiologyCardinal Bernardin Cancer CenterLoyola University Medical Centerand BiologyLoyola University ChicagoChicagoILUSA

Hepatocellular carcinoma(HCC)is a very deadly disease.HCC initiation and progression involve multiple genetic events,including the activation of proto-oncogenes and disruption of the function of specific tumor suppressor genes.Activation of oncogenes stimulates cell growth and survival,while loss-of-function mutations of tumor suppressor genes result in unrestrained cell growth.In this review,we summarize the new findings that identified novel proto-oncogenes and tumor suppressors in HCC over the past five years.These findings may inspire the development of novel therapeutic strategies to improve the outcome of HCC patients.

关键词： Hepatocellular carcinoma(HCC) Oncogene Tumor suppressor Activation Loss-of-function

Approaches to quantify axonal morphology for the analysis of axonal degeneration

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Neural Regeneration Research 2023年第2期18卷 309-310页

作者： Alex Palumbo Marietta Zille department of Neurobiology Harvard Medical School Department of Cancer Biology Dana-Farber Cancer InstituteBostonMAUSA department of Pharmaceutical Sciences Division of Pharmacology and ToxicologyUniversity of ViennaViennaAustria

Morphological hallmarks of axonal degeneration(AxD):Axons transmit signals from one neuron to another and a re crucial for the proper communication in the nervous system.Therefore,the disintegration of axons,a process... 详细信息

关键词： degeneration axonal Morphological

Metabolic reprogramming in tumors:Contributions of the tumor microenvironment

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Genes & Diseases 2020年第2期7卷 185-198页

作者： Andrew N.Lane Richard M.Higashi Teresa W-M.Fan Center for Environmental and Systems Biochemistry Markey Cancer CenterDepartment of Toxicology and Cancer BiologyUniversity of KentuckyUSA

The genetic alterations associated with cell transformation are in large measure expressed in the metabolic phenotype as cancer cells proliferate and change their local environment,and prepare for metastasis.Qualitatively,the fundamental biochemistry of cancer cells is generally the same as in the untransformed cells,but the cancer cells produce a local environment,the TME,that is hostile to the stromal cells,and compete for nutrients.In order to proliferate,cells need sufficient nutrients,either those that cannot be made by the cells themselves,or must be made from simpler precursors.However,in solid tumors,the nutrient supply is often limiting given the potential for rapid proliferation,and the poor quality of the vasculature.Thus,cancer cells may employ a variety of strategies to obtain nutrients for survival,growth and metastasis.Although much has been learned using established cell lines in standard culture conditions,it is becoming clear from in vivo metabolic studies that this can also be misleading,and which nutrients are used for energy production versus building blocks for synthesis of macromolecules can vary greatly from tumor to tumor,and even within the same tumor.Here we review the operation of metabolic networks,and how recent understanding of nutrient supply in the TME and utilization are being revealed using stable isotope tracers in vivo as well as in vitro.

关键词： cancer metabolism Nutrient supply Stable isotope resolved metabolomics Tumor microenvironment Metabolic flux

cancer-associated fibroblasts express CD1d and activate invariant natural killer T cells under cellular stress

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Cellular & Molecular Immunology 2024年第1期21卷 91-94页

作者： Shengduo Pei Jonas Sjölund Yueyun Pan Kristian Pietras Mikael C.I.Karlsson department of Microbiology Tumor and Cell BiologyKarolinska InstitutetStockholmSweden Division of Translational cancer Research Department of Laboratory MedicineLund University Cancer CentreLund UniversityLundSweden

Invariant natural killer T(iNKT)cells are part of the family of unconventional T cells,and they recognize glycolipid antigens presented on the MHC class I like molecule CD1^([1]).In humans there are five CD1 molecules named CD1a to CD1e,whereas mice use only CD1d for lipid presentation.Functionally,iNKT cells can elicit both cytotoxicity similarly to conventional CD8 T cells and secrete cytokines that influence the adaptive immune response including providing direct T cell help to B cells^([2]).In the context of tumors,they can use both release of granzyme B and use Fas-mediated mechanisms for killing of tumor cells.As iNKT cells use a restricted TCR repertoire and CD1 molecules are non-heterogenous the risk of graft vs host disease is limited and thus these T cells have been an attractive option for off the shelf immunotherapy to treat cancer^([3]).

关键词： killer CD1d cancer