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| 1 | Glioblastoma stem cells(GSCs)epigenetic plasticity and interconversion between differentiated non-GSCs and GSCs显示文摘Cancer stem cells(CSCs)or cancer initiating cells(CICs)maintain self-renewal and multilineage differentiation properties of various tumors,as well as the cellular heterogeneity consisting of several subpopulations within tumors.CSCs display the malignant phenotype,self-renewal ability,altered genomic stability,specific epigenetic signature,and most of the time can be phenotyped by cell surface markers(e.g.,CD133,CD24,and CD44).Numerous studies support the concept that non-stem cancer cells(non-CSCs)are sensitive to cancer therapy while CSCs are relatively resistant to treatment.In glioblastoma stem cells(GSCs),there is clonal heterogeneity at the genetic level with distinct tumorigenic potential,and defined GSC marker expression resulting from clonal evolution which is likely to influence disease progression and response to treatment.Another level of complexity in glioblastoma multiforme(GBM)tumors is the dynamic equilibrium between GSCs and differentiated non-GSCs,and the potential for non-GSCs to revert(dedifferentiate)to GSCs due to epigenetic alteration which confers phenotypic plasticity to the tumor cell population.Moreover,exposure of the differentiated GBM cells to therapeutic doses of temozolomide(TMZ)or ionizing radiation(IR)increases the GSC pool both in vitro and in vivo.This review describes various subtypes of GBM,discusses the evolution of CSC models and epigenetic plasticity,as well as interconversion between GSCs and differentiated non-GSCs,and offers strategies to potentially eliminate GSCs. | Ahmad R.Safa Mohammad Reza Saadatzadeh Aaron A.Cohen-Gadol Karen E.Pollok Khadijeh Bijangi-Vishehsaraei | 2015 | Genes & Diseases2015，2，2： | 5 |
| 2 | Overcoming therapeutic obstacles in inflammatory bowel diseases: A comprehensive review on novel drug delivery strategies显示文摘 | F. Talaei F. Atyabi M. Azhdarzadeh R. Dinarvand A. Saadatzadeh | 2013 | European Journal of Pharmaceutical Sciences2013，，4： | 1 |
| 3 | PTEN and p53 are required for hypoxia induced expression of maspin in glioblastoma cells显示文摘 | Eitel JA Bijangi-Vishehsaraei K Saadatzadeh MR | 2009 | Cell Cycle2009，8，6： | 1 |
| 4 | Production of the mycelial phase of Malassezia in vitro显示文摘 | Saadatzadeh MR Ashbee HR Holland KT | 2001 | Medical Mycology2001，39，： | 1 |
| 5 | Robust Functional Vascular Network Formation In Vivo by Cooperation of Adipose Progenitor and Endothelial Cells显示文摘 | Dmitry O. Traktuev Daniel N. Prater Stephanie Merfeld-Clauss Aravind Raj Sanjeevaiah M Reza Saadatzadeh Michael Murphy Brian H. Johnstone David A. Ingram Keith L. March | 2009 | Circulation Research2009，，12： | 1 |
| 6 | Enhanced TNF-alpha-induced apoptosis in fanconi anemia type C-deficient cells is dependent on apoptosis signal-regulating kinase 1 显示文摘 | Bijangi-Vishehsaraei K Saadatzadeh M Weme A | 2005 | Blood2005，106，： | 1 |
| 7 | Differ- ences in laryngeal neurotrophicfactor gene expression after recurrent laryngeal nerve and vagus nerve injuries 显示文摘 | HalumSL Bijangi-Vishehsaraei K Saadatzadeh MR | 2013 | TheAnnalsofotology rhinology and laryngology2013，122，10： | 1 |
| 8 | Quantitative analysis of wear and wear debris from metal-on-metal hip prostheses tested in a physioIogical hip joint simuIator显示文摘 | Firkins PJ Tipper JL Saadatzadeh MR | 2001 | Biomed Mater Eng2001，11，2： | 1 |
| 9 | PTEN and p53 are required for hypoxia induced expression of maspin in glioblastoma cells显示文摘 | Eitel JA Bijangi-Vishehsaraei K Saadatzadeh MR | 2009 | Cell Cycle2009，8，6： | 1 |
| 10 | 4-(4- Chloro-2-methyphenoxy) -N-hydroxybutanamide(CMH) targets mR- NA of the c-FLIP variants and induces apoptosis in MCF-7 human breast cancer ceils 显示文摘 | Bijangi-Vishehsaraei K Saadatzadeh M R Huang S | 2010 | Mol Cell Biochem2010，342，12： | 1 |
| 11 | Suppression of osteosarcoma progression by engineered lymphocyte-derived proteomes显示文摘Cancer cells tend to develop resistance to chemotherapy and enhance aggressive-ness.A counterintuitive approach is to tame aggressiveness by an agent that acts opposite to chemotherapeutic agents.Based on this strategy,induced tumor-suppressing cells(iTSCs)have been generated from tumor cells and mesenchymal stem cells.Here,we examined the possi-bility of generating iTSCs from lymphocytes by activating PKA signaling for suppressing the pro-gression of osteosarcoma(OS).While lymphocyte-derived CM did not present anti-tumor capabilities,the activation of PKA converted them into iTSCs.Inhibiting PKA conversely gener-ated tumor-promotive secretomes.In a mouse model,PKA-activated CM suppressed tumorinduced bone destruction.Proteomics analysis revealed that moesin(MSN)and calreticulin(Calr),which are highly expressed intracellular proteins in many cancers,were enriched in PKA-activated CM,and they acted as extracellular tumor suppressors through CD44,CD47,and CD91.The study presented a unique option for cancer treatment by generating iTSCs that secret tumor-suppressive proteins such as MSN and Calr.We envision that identifying these tu-mor suppressors and predicting their binding partners such as CD44,which is an FDA-approved oncogenic target to be inhibited,may contribute to developing targeted protein therapy. | Kexin Li Xun Sun Hudie Li Hailan Ma Meng Zhou Kazumasa Minami Keisuke Tamari Kazuhiko Ogawa Pankita HPandya MReza Saadatzadeh Melissa AKacena Karen EPollok Bai-Yan Li Hiroki Yokota | 2023 | Genes & Diseases2023，10，4： | 0 |
| 12 | Emerging targets for glioblastoma stem cell therapy显示文摘Glioblastoma multiforme(GBM),designated as World Health Organization(WHO)grade IV astrocytoma,is a lethal and therapy-resistant brain cancer comprised of several tumor cell subpopulations,including GBM stem cells(GSCs)which are believed to contribute to tumor recurrence following initial response to therapies.Emerging evidence demonstrates that GBM tumors are initiated from GSCs.The development and use of novel therapies including small molecule inhibitors of specific proteins in signaling pathways that regulate sternness,proliferation and migration of GSCs,immunotherapy,and non-coding microRNAs may provide better means of treating GBM.Identification and characterization of GSC-specific signaling pathways would be necessary to identify specific therapeutic targets which may lead to the development of more efficient therapies selectively targeting GSCs.Several signaling pathways including mTOR,AKT,maternal embryonic leucine zipper kinase(MELK),NOTCH1 and Wnt/β-catenin as well as expression of cancer stem cell markers CD133,CD44,Oct4,Sox2,Nanog,and ALDHlA1 maintain GSC properties.Moreover,the data published in the Cancer Genome Atlas(TCGA)specifically demonstrated the activated PI3K/AKT/mTOR pathway in GBM tumorigenesis.Studying such pathways may help to understand GSC biology and lead to the development of potential therapeutic interventions to render them more sensitive to chemotherapy and radiation therapy.Furthemore,recent demonstration of dedifferentiation of GBM cell lines into CSC-like cells prove that any successful therapeutic agent or combination of drugs for GBM therapy must eliminate not only GSCs,but the differentiated GBM cells and the entire bulk of tumor cells. | Ahmad R.Safa Mohammad Reza Saadatzadeh Aaron A.Cohen-Gadol Karen E.Pollok Khadijeh Bijangi-Vishehsaraei | 2016 | The Journal of Biomedical Research2016，30，1： | 0 |
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