- ASSISTANT PROFESSOR Neurosurgery
- ASSISTANT PROFESSOR Developmental and Regenerative Biology
- ASSISTANT PROFESSOR Neuroscience
Dipl. Biol., University of Munich
Ph. D., Max Planck Institute of Neurobiology
Postdoctoral, Stanford University
- Roland Friedel, Ph.D., joined Mount Sinai School of Medicine in 2009, coming from the Helmholtz Research Center for Environmental Health in Munich, Germany. He is an expert in the fields of developmental neurobiology and brain tumor research.
Dr. Friedel's research focuses on the question of how axon guidance molecules control the migration of neural precursors and of brain tumor cells. He is also investigating in collaboration with Prof. Soriano (Department of Developmental & Regenerative Biology) genes that synergize in brain tumor formation with the PDGF growth factor pathway. The identification of genetic factors that contribute to brain tumor growth and spreading will facilitate the development of novel targeted therapeutic strategies.
2001 - 2003
Research Fellowship of Deutsche Forschungsgemeinschaft
ResearchTumors of the brain are amongst the most lethal types of cancer. They account for over 175,000 cases per year worldwide, claiming the lives of thousands of patients (WHO World Cancer Report, 2003). Despite of significant progress in the identification of genes involved in tumorigenesis, the etiology of brain tumors is still largely unknown, and incidence and mortality rates of these cancers have changed little over the past decade. The goal of our research is to identify the genetic factors that contribute to the formation and spreading of brain tumors. The identification of novel diagnostic markers and therapeutic targets will lead to better treatment strategies for this devastating disease.
To identify novel molecules that regulate the invasive spreading behavior of brain tumor cells, we are performing functional genetic analyses with human glioma cell lines in vitro and in transplantation assays. We are focusing our studies on candidate genes of the axon guidance families and their downstream signaling components.
To uncover novel genetic players that control brain tumor growth, we are performing a genetic screen in mice by applying a transposon-based mutagenesis strategy ("PiggyBac") to efficiently mutate genes in a brain-specific manner. In particular, we focus on genes that synergize with PDGF, a growth factor that is well known to cause glioma when overactivated.
Friedel RH, Friedel CC, Bonfert T, Shi R, Rad R, Soriano P. Clonal Expansion Analysis of Transposon Insertions by High-Throughput Sequencing Identifies Candidate Cancer Genes in a PiggyBac Mutagenesis Screen. PLOS ONE 2013; 8(8).
Kuzirian MS, Moore AR, Staudenmaier EK, Friedel RH, Paradis S. The class 4 semaphorin Sema4D promotes the rapid assembly of GABAergic synapses in rodent hippocampus. The Journal of Neuroscience 2013 May; 33(21).
Bradley A, Anastassiadis K, Ayadi A, Battey JF, Bell C, Birling MC, Bottomley J, Brown SD, Bürger A, Bult CJ, Bushell W, Collins FS, Desaintes C, Doe B, Economides A, Eppig JT, Finnell RH, Fletcher C, Fray M, Frendewey D, Friedel RH, Grosveld FG, Hansen J, Hérault Y, Hicks G, Hörlein A, Houghton R, Hrabé de Angelis M, Huylebroeck D, Iyer V, de Jong PJ, Kadin JA, Kaloff C, Kennedy K, Koutsourakis M, Lloyd KC, Marschall S, Mason J, McKerlie C, McLeod MP, von Melchner H, Moore M, Mujica AO, Nagy A, Nefedov M, Nutter LM, Pavlovic G, Peterson JL, Pollock J, Ramirez-Solis R, Rancourt DE, Raspa M, Remacle JE, Ringwald M, Rosen B, Rosenthal N, Rossant J, Ruiz Noppinger P, Ryder E, Schick JZ, Schnütgen F, Schofield P, Seisenberger C, Selloum M, Simpson EM, Skarnes WC, Smedley D, Stanford WL, Stewart AF, Stone K, Swan K, Tadepally H, Teboul L, Tocchini-Valentini GP, Valenzuela D, West AP, Yamamura K, Yoshinaga Y, Wurst W. The mammalian gene function resource: the International Knockout Mouse Consortium. Mammalian Genome 2012 Oct; 23(9-10).
Maier V, Jolicoeur C, Rayburn H, Takegahara N, Kumanogoh A, Kikutani H, Tessier-Lavigne M, Wurst W, Friedel RH. Semaphorin 4C and 4G are ligands of Plexin-B2 required in cerebellar development. Mol Cell Neurosci 2011;.
Negishi-Koga T, Shinohara M, Komatsu N, Bito H, Kodama T, Friedel RH, Takayanagi H. Suppression of bone formation by osteoclastic expression of semaphorin 4D. Nature Medicine 2011;.
Friedel RH, Wurst W, Wefers B, Kühn R. Generating conditional knockout mice. Methods Mol Biol 2011;.
Leslie JR, Imai F, Fukuhara K, Takegahara N, Rizvi TA, Friedel RH, Wang F, Kumanogoh A, Yoshida Y. Ectopic myelinating oligodendrocytes in the dorsal spinal cord as a consequence of altered semaphorin 6D signaling inhibit synapse formation. Development 2011;.
Friedel RH, Soriano P. Gene trap mutagenesis in the mouse. Methods Enzymol 2010;.
Takamatsu H, Takegahara N, Nakagawa Y, Tomura M, Taniguchi M, Friedel RH, Rayburn H, Tessier-Lavigne M, Yoshida Y, Okuno T, Mizui M, Kang S, Nojima S, Tsujimura T, Nakatsuji Y, Katayama I, Toyofuku T, Kikutani H, Kumanogoh A. Semaphorins guide the entry of dendritic cells into the lymphatics by activating myosin II. Nat Immunol 2010;.
Okuno T, Nakatsuji Y, Moriya M, Takamatsu H, Nojima S, Takegahara N, Toyofuku T, Nakagawa Y, Kang S, Friedel RH, Sakoda S, Kikutani H, Kumanogoh A. Roles of Sema4D-plexin-B1 interactions in the central nervous system for pathogenesis of experimental autoimmune encephalomyelitis. Journal of Immunology 2010;.
Zielonka M, Xia J, Friedel RH, Offermanns S, Worzfeld T. A systematic expression analysis implicates Plexin-B2 and its ligand Sema4C in the regulation of the vascular and endocrine system. Experimental cell research 2010;.
Friedel RH. Targeting embryonic stem cells. Methods Mol Biol 2009;.
Korostylev A, Worzfeld T, Deng S, Friedel RH, Swiercz JM, Vodrazka P, Maier V, Hirschberg A, Ohoka Y, Inagaki S, Offermanns S, Kuner R. A functional role for Semaphorin 4D/Plexin B1 interactions in epithelial branching morphogenesis during organogenesis. Development 2008;.
Friedel RH, Kerjan G, Rayburn H, Schuller U, Sotelo C, Tessier-Lavigne M, Chedotal A. Plexin-B2 controls the development of cerebellar granule cells. J Neurosci 2007;.
Friedel RH, Seisenberger C, Kaloff C, Wurst W. EUCOMM--the European conditional mouse mutagenesis program. Brief Funct Genomic Proteomic 2007;.
Miller SF, Summerhurst K, Runker AE, Kerjan G, Friedel RH, Chedotal A, Murphy P, Mitchell KJ. Expression of Plxdc2/TEM7R in the developing nervous system of the mouse. Gene Expr Patterns 2007;.
Osada M, Ito E, Fermin HA, Vazquez-Cintron E, Venkatesh T, Friedel RH, Pezzano M. The Wnt signaling antagonist Kremen1 is required for development of thymic architecture. Clin Dev Immunol 2006;.
Friedel RH, Plump A, Lu X, Spilker K, Jolicoeur C, Wong K, Venkatesh TR, Yaron A, Hynes M, Chen B, Okada A, McConnell SK, Rayburn H, Tessier-Lavigne M. Gene targeting using a promoterless gene trap vector (. Proc Natl Acad Sci U S A 2005;.
Friedel RH, Stubbusch J, Barde YA, Schnurch H. A novel 7-transmembrane receptor expressed in nerve growth factor-dependent sensory neurons. Mol Cel Neurosci 2001;.
Friedel RH, Schnurch H, Stubbusch J, Barde YA. Identification of genes differentially expressed by nerve growth factor- and neurotrophin-3-dependent sensory neurons. Proc Natl Acad Sci U S A 1997;.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Friedel did not report having any of the following types of financial relationships with industry during 2012 and/or 2013: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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