Dr. Monther AlAlwan is a scientist at the Stem Cell and Tissue Re-engineering Program (SCTRP), King Faisal Specialist Hospital and Research Centre, as well as an Associate professor at Alfaisal University, Riyadh Saudi Arabia. He holds M.Sc. and Ph.D. in Immunology from Dalhousie University (Halifax, Canada). Dr. AlAlwan conducted a 3-years postdoctoral fellowship studying signaling in immune cells at the University of Manitoba, Canada. During his graduate studies and postdoctoral fellowship, Dr. AlAlwan made substantial contribution in the immunology field, particularly his groundbreaking discovery that highlighted the significance of the dendritic cells in the immunological synapse. After joining the SCTRP in 2007, he shifted gear to study cancer, where he identified novel mechanisms that regulate cancer metastasis and chemoresistance. Currently, he is actively involved in dissecting the molecular pathways that regulate the function of cancer stem cells and how this related to chemoresistance and metastasis. Dr. AlAlwan is an author in 20 peer-reviewed publications, has delivered several invited lectures and is a regular reviewer for various international journals.   

Research Interest: Cell Reprogramming and Induced Pluripotent Stem Cells, Stem Cells and Neural Tissue Engineering, Mammalian Inner Ear Development and Hair Cell Regeneration.

Research Interest: Leptin Receptors (Lepr) are Expressed by Various Types of Stem Cells Including Mesenchymal Stem Cells, Hematopoietic Stem Cells, Embryonic Stem Cells and Induced Pluripotent Stem Cells. Leptin/Lepr Signaling is also a Central Regulator of Metabolism.

Research Interest: Stem Cell Biology; Breast Cancer Dormancy; Neural Regulation of Hematopoiesis, the Immunology and Clinical Application of Adult Human Mesenchymal Stem Cells. 

Research Interest: Cancer Stem Cell, Anticancer Agent, Metastasis, Cell Survival, Cell Migration, Apoptosis, Molecular and Cell Signaling, Transcription Factors, Xenograft Model, Stem Cell Based Therapy.

Dr. Edgar Grinstein is a Principal Investigator at the Heinrich Heine University in Düsseldorf (Germany). He researches hematopoietic stem cells and progenitor cells, signal transduction, gene transcription regulation. He has more than 11 years of experience as Editor-In-Chief at SAGE Publications Inc. (USA) and Libertas Academica (New Zealand), and also serves as Deputy Editor-In-Chief for Baishideng Publishing Group (USA).

Raised in a family of researchers – both parents are PhD scientists - he received his PhD summa cum laude in Molecular Biology from the Humboldt University and the Max-Delbrück Center for Molecular Medicine in Berlin. He has published a number of papers in high-ranking journals and received a highly regarded Research Award from Dr.-Günther- and Imme-Wille-Foundation. Dr. Grinstein qualified as Professor in Molecular Medicine at the University of Düsseldorf in 2008 and is a Visiting Professor at the University of Latvia (Latvia, European Union) since 2010.  

Dr. Grinstein`s research in the field of hematopoietic stem and progenitor cells, funded by research grants from German Research Foundation (DFG) and José Carreras Leukämie-Stiftung (José Carreras Foundation), has focused on markers, signal transduction and transcriptional control. Among other important findings made, his research group provided new insights into the role of the prominent surface marker AC133/CD133 (Leukemia 2015; 29: 2208-2220), that is expressed on stem/progenitor cells in normal hematopoiesis as well as on tumor-initiating cells in certain hematological malignancies. The study analyzed the control of AC133/CD133 expression in hematopoietic stem/progenitor cells, and revealed the impact thereof on molecular network relevant to these cells.

Research Interest: hematopoietic stem cells and progenitor cells, cancer stem cells, stem cell markers, signal transduction, cell cycle control, regulation of apoptosis, gene transcription regulation

Grants: Principal Investigator of stem cell-related projects funded by German Research Foundation (DFG) and by José Carreras Leukämie-Stiftung (José Carreras Foundation)

URL: https://www.wjgnet.com/2218-6204/MemberDetail/42530

publications:

Grinstein, E., and H.-D. Royer. 1995. Multiple octamer-binding proteins are targets for the cell cycle regulated nuclear inhibitor I-92. DNA Cell Biol. 14: 493-500.

Grinstein, E., I. Weinert, B. Droese, M. Pagano, and H.-D. Royer. 1996. Cell cycle regulation of nuclear factor p92 DNA-binding activity by novel phase-specific inhibitors. J. Biol. Chem. 271: 9215-9222.

Bargou, R.C., C. Wagener, K. Bommert, W. Arnold, P.T. Daniel, M.Y. Mapara, E. Grinstein, H.-D. Royer, and B. Dörken. 1996. Blocking of transcription factor E2F/DP by dominant-negative mutants in a normal breast epithelial cell line efficiently inhibits apoptosis and induces tumor growth in SCID mice. J. Exp. Med. 183: 1205-1213.

Bargou, R.C., F. Emmerich, D. Krappmann, K. Bommert, M.Y. Mapara, W. Arnold, H.-D. Royer, E. Grinstein, A. Greiner, C. Scheidereit, and B. Dörken. 1997. Constitutive nuclear factor kappaB-RelA activation is required for proliferation and survival of Hodkin’s desease tumor cells. J. Clin. Invest. 12: 2961-2969.

Janke, J., K. Schlüter, B. Jandrig, M. Theile, K. Kölble, W. Arnold, E. Grinstein, A.  Schwartz, L.E. Schwarz, P.M. Schlag, B.M. Jockusch, and S. Scherneck. 2000. Suppression of tumoriginecity in breast cancer cells by the microfilament protein profilin1. J. Exp. Med. 191: 1675-1685.

Grinstein, E.,* F. Jundt, I. Weinert, P. Wernet, and H.-D. Royer. 2002. Sp1 as G1 cell cycle phase specific transcription factor in epithelial cells. Oncogene. 21: 1485-1492.

Grinstein, E., P. Wernet, P.J. Snijders, F. Rösl, I. Weinert, W. Jia, R. Kraft, Ch. Schewe, M. Schwabe, S. Hauptmann, M. Dietel, Ch. Meijer, and H.-D. Royer. 2002. Nucleolin as activator of human papillomavirus type 18 oncogene transcription in cervical cancer. J. Exp. Med. 196: 1067-1078.

Grinstein, E.,* Y. Shan, L. Karawajew, P.J. Snijders, C.J. Meijer, H.-D. Royer, and P. Wernet. 2006. Cell cycle controlled interaction of nucleolin with the retinoblastoma protein and cancerous cell transformation.  J. Biol. Chem. 281: 22223-22235.

Grinstein, E.,* Y. Du, S. Santourlidis, J. Christ, M. Uhrberg, and P. Wernet. 2007. Nucleolin regulates gene expression in CD34 positive hematopoietic cells. J. Biol. Chem. 282: 12439-12449.

Grinstein, E.,* and P. Wernet. 2007. Cellular signaling in normal and cancerous stem cells. Cell. Signal. 19: 2428-2433.
This was the most read article of the Journal Cell. Signal. from July 2007 till March 2008. Source: SCIENCEDIRECT TOP 25 HOTTEST ARTICLES

Wethkamp, N., H. Hanenberg, C. Suschek, W. Wetzel, S. Heikaus, E. Grinstein, U. Ramp, R. Engers, H. Gabbert, and C. Mahotka. 2011. DAXX-beta and DAXX-gamma: two novel splice variants of the transcriptional co-repressor DAXX. J. Biol. Chem. 19576-19588.

Grinstein, E.,* C. Mahotka, and A. Borkhardt. 2011. Rb and nucleolin antagonize in controlling human CD34 gene expression. Cell. Signal. 23: 1358-1365.

Bhatia, S., S. Reister, C. Mahotka, R. Meisel, A. Borkhardt, and E. Grinstein.* 2015. Control of AC133 / CD133 and impact on human hematopoietic progenitor cells through nucleolin. Leukemia. 29: 2208-2220.

Mahotka, C., S. Bhatia, J. Kollet, and E. Grinstein.* 2018. Nucleolin promotes execution of the hematopoietic stem cell gene expression program. Leukemia. 32: 1865–1868.

Reister, S., C. Mahotka, N. van den Höfel, and  E. Grinstein.* 2019. Nucleolin promotes Wnt signaling in human hematopoietic stem/progenitor cells. Leukemia. 33: 1052-1054.

Research Interest: Tumor Immunology and Immunotherapy, Cancer Stem Cell Biology and Immunology, Obstetrics and Gynecology.

Research Interest: Focuses on Aging-Related Diseases and Stem Cell Transplantation. 

Research Interest: Clinical Pharmacology, Gastroenterology, Pharmaceutical Development, Drug Development, Colorectal Cancer, Inflammatory Bowel Disease, Ulcerative Colitis, Crohn's Disease

Research Interest: Cardiac Therapy, Cardiovascular Disease, Autologous, Tissue-Engineering, Multipotent Stem Cells, Cardiovascular Structures, Regenerative Medicine.

Research Interest: Embryonic Stem Cells, Pluripotency, Induced Pluripotent Cells, Differentiation, Endoderm, Beta Cell, Diabetes, Obesity, Adipose Tissue, Brown Fat, Endothelium, Oxidative Stress, Nitric Oxide, Peroxynitrite, Superoxide, Nanosensors.

Research Interest: Hematopoietic Stem Cell Transplanting, Cell Therapy and Everything in the Field of Publication and Education.

Research Interest: Genes Involved in Cell Cycle Regulation, Differentiation, Apoptosis and Senescence Such as the Retinoblastoma (RB) Family. He has Evaluated the Role of Retinoblastoma Genes in the Regulation of Cell Proliferation, Differentiation and Apoptosis in
Cancer and Normal Stem Cells. In Detail, his Group has Analyzed the Biology of Neural Stem Cells and Mesenchymal Stem Cells. These Studies Prompted the Attention Also on Chromatin
Remodeling Factors that Interact with RB Family Members and Play a Key Role in the Life of StemCells.

Research Interest: Resident Cardiac Stem Cells, Myocardial Regeneration in Basic and Clinical/Translational Studies.

Research Interest:

Two Major Projects are Currently Underway in the Laboratory.
A Cell Reprogramming Technique Has Been Used to Convert Heterogeneous Malignant Breast Cancer Cells into Induced Pluripotent Stem Cells Using Sox2/Oct4/Nanog Proteins. Dr. Wu’s Laboratory is Clarifying these Induced Pluripotent Stem Cells for their Differentiation Potential and Oncogenic Properties, and Try to Develop a Novel Cell Converting Therapy for Malignant Breast Cancer Treatment.
Metastasis, the Spread of Cancer Cells from the Primary Tumor To Distant Organs, Is The Most Dreadful Development Of Breast Cancer, As Well As Other Neoplastic Diseases. Although Metastasis Contributes To Over 90% Of Human Cancer Mortality, The Molecular Mechanism Of This Process Remains Largely Unknown. Dr. Wu’s Laboratory Is In The Process Of Identifying Molecular Signatures Involved In Breast Cancer Metastasis Using Integrative Genetic, Epigenetic And Proteomic Approach, As Well As Animal Models And Clinical Specimens.