Scientific Symposium Oral Presentations
October 2004, Cambridge, Massachusetts
Session I: Apoptosis
Session II: FANCD2
Session III: Model Organisms and Systems and Miscellaneous
Session IV: DNA Damage Responses and Repair
Session V: Complementation Group
Session VI: Bone Marrow Transplantation
Session VII: Experimental Therapeutics

Session I: Apoptosis

Suk-Hee Lee, PhD Indiana University Cancer Research Institute, Indianapolis, Indiana Regulation of Fanconi Anemia Protein Complex upon Oxidative Stress/Damage.
Laura Haneline, MD Indiana University Cancer Research Institute, Indianapolis, Indiana TNF-α Induces Hyperactivation of Apoptosis Signal-Regulating Kinase 1 in FA Type C Cells.
Sudit Mukhopadhyay, PhD Baylor College of Medicine, Houston, Texas FA Protein Complex Regulates the Activity and Calpain-like Cleavage of the Major Mitochondrial Peroxidase, Peroxiredoxin 3.
Thomas Rünger, MD Boston FA-A and -C Proteins Act Upstream of p53 in the Cellular Response to Ultraviolet Light (UVA and UVB).
Takayuki Yamashita, MD, PhD Institute of Medical Science, The University of Tokyo, Tokyo, Japan Hsc70/Hsp90 Chaperone Machinery Regulates Stability and Nuclear Localization of FANCA.
Grover C. Bagby, Jr., MD Oregon Cancer Institute, Portland, Oregon Clonal Evolution of FA Stem Cells Results from Clonal Adaptation and Clonal Selection. A Report from the FA Transcriptome Consortium.

Session II: FANCD2

Akiko Shimamura, MD, PhD Department of Pediatric Oncolology, Dana Farber Cancer Institute, Boston, Massachusetts Ubiquitinated FANCD2 is Both Necessary and Sufficient to Confer Mitomycin C Resistance in the Absence of a Functional FA Core Complex.
Nigel Jones, PhD School of Biological Sciences, University of Liverpool, Liverpool, UK The Interaction of BRCA2 with both the Monoubiquitinated and Non-monoubiquitinated Forms of FANCD2 is Dependent on FANCG.
Sebastian Nijman, MSc, Graduate Student Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands A Genetic Screen Identifies a De-ubiquitinating Enzyme as a Regulator of FANCD2 Monoubiquitination.
Miriam Ferrer, MSc Department of Medical Oncology/Gene Therapy, Vrije Universiteit Medical Center, Amsterdam, The Netherlands Nuclear-cystoplasmic Shuttling of FANCA is Regulated by CRM-1-dependent Nuclear Export Signals.
Jeff Parvin, MD, PhD Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts The FA Protein, FANCD2, Binds to Holliday Junction DNA.
Paul Andreassen, PhD Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts ATR is Required for the DNA Damage-Activated Monoubiquitination of FANCD2.
Jordi Surrallés, PhD Group of Mutagenesis, Department of Genetics and Microbiology, Universitat Autonoma de Barcelona, Barcelona, Spain Study on the Role of FANCD2 in Base Excision Repair.
Stephen Meyn, MD, PhD, FRCP(C) Genetics and Genomic Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada Nuclear Dynamics of FANCD2, BLM, and TRF2 following DNA Damage.

Session III: Model Organisms and Systems and Miscellaneous

Toshiyasu Taniguchi, MD, PhD Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts Screening of Small Molecule Inhibitors/Agonists of the FA Pathway.
Henri van de Vrugt, PhD Functional Genomics, Department of Clinical and Human Genetics, Vrije Universiteit, Amsterdam, The Netherlands Characterization of Mice with a Disruption of the Fancl/Pog Gene.
Tom Titus, PhD Institute of Neuroscience, University of Oregon, Eugene, Oregon The Fanconi Anemia Gene Complex is Conserved in the Zebrafish.

Session IV: DNA Damage Responses and Repair

Maria Jasin, PhD Department of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York, New York Dougle-strand Breaks and Genomic Integrity - Interplay of Multiple Repair Pathways and Role of the FANC Genes.
Larry Thompson, PhD Biology and Biotechnology Research Program, Lawrence Livermore National Laboratory, Livermore, California A Mechanistic Model for Fanconi Proteins: Preventing Replication Fork Collapse.
Ashok Venkitaraman, PhD MRC Cancer Cell Unit, University of Cambridge, Cambridge, UK Stabilization of Stalled DNA Replication Forks by the Breast Cancer Susceptibility Protein, BRCA2.
Kevin Hiom, PhD MRC Laboratory of Molecular Biology, Cambridge, UK Defining the Relationship between BRCA1/BARD1 and FA.
Alan Ashworth, PhD The Breakthrough Breast Cancer Research Centre Institute of Cancer Research, London, UK Synergy between DNA Repair Pathways Revealed by the Sensitivity of BRCA1 and BRCA2 Mutant Cells to PARP Inhibition.
Alexandra T. Sobeck, PhD Division of Molecular Medicine and Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon FA Proteins and Caretaker Networks: The Chain of Command.
Minoru Takata, MD, PhD Department of Immunology and Molecular Genetics, Kawasawki Medical School, Okayama, Japan Epistasis between FA Protein FANCC and BLM Helicase in Suppressing Spontaneous Sister Chromatid Exchanges.
Robb Moses, MD Deparment of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon The Bloom Syndrome Helicase Acts in the FA Pathway for Interstrand Crosslink Repair.
Muriel Lambert, PhD New Jersey Medical School Effects of siRNA-Mediated Silencing of alphaII Spectrin Gene Expression in Cells Containing DNA Interstrand Cross-links and Their Relationship to FA.
K.J. Patel, PhD, MRCP MRC Laboratory of Molecular Biology, Cambridge, UK The FA Gene FANCC Promotes Homologous Recombination and Error Prone DNA Repair.
Christopher Matthew, PhD Department of Medical and Molecular Genetics and Development, Guy's, King's and St. Thomas' School of Medicine, London, UK Interaction of the FANCG Protein with Multiple Elements of the Homologous Recombination Repair Pathway.
Randy Legerski, PhD Department of Molecular Genetics, MD Anderson Cancer Center, Houston, Texas Factors Involved in the Removal of DNA Interstrand Cross-links.
Azah Tabah, MS Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota A Rad50 Pathway of End-Joining is Defective in Fibroblasts from FA Patients.
Dora Papadopoulo, PhD Insitut Curie-Recherche, Paris, France BRCA/FANC Connection to DNA End-Joining

Session V: Complementation Group

Marieke Levitus, MSc Department of Clinical Genetics and Human Genetics, Vrije Universiteit, Amsterdam, The Netherlands Identification of the FA Group B Gene.
Amom Ruhikanta Meetei, PhD National Institute on Aging, The National Institutes of Health, Baltimore, Maryland Three New Components of the FA Multiprotein Core Complex are Required for FANCD2 Monoubiquitination.
Barbara Godthelp, PhD Department of Toxicogenetics, Leiden University, Leiden, The Netherlands BRCA2 Reverse Mosaicism in FA-B Patient, HSC230: Additional Evidence for Distinct Disease Genes in Complementation Groups B and D1.
Reinhard Kalb, MS Department of Human Genetics, University of Würzburg, Germany Examination of Candidate Genes in Unclassified FA Cell Lines.

Session VI: Bone Marrow Transplantation

Phillip Rosenberg, PhD Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland How Many FA Patients Must Be Transplanted to Prove That a New Conditioning Regimen is Superior to the Standards?
Margaret MacMillan, MD Pediatric Blood and Marrow Program, University of Minnesota, Minneapolis, Minnesota Hematopoietic Cell Transplantation in FA Patients with Biallelic BRCA2 Mutations.
Richard Harris, MD Blood and Marrow Transplant Program, Children's Hospital Medical Center, Cincinnati, Ohio Matched Sibling Donor Bone Marrow Transplantation in FA: An Update of the Cincinnati Children's Experience.
Hiromasa Yabe, MD Specialized Clinical Science Pediatrics, Tokai University, Isehara, Japan Allogeneic Stem Cell Transplantation for Japanese FA Patients by Fludarabine-based Regimen.
Wolfram Ebell, MD Charité Hospital, Humboldt University, Berlin, Germany Update of Unrelated Transplants in FA Using a Fludarabine, Low-Dose Busulfan, Non-Irradiation Protocol (GEFA-Protocol).
Farid Boulad, MD Bone Marrow Transplantation Service, Memorial Sloan-Kettering Cancer Center, New York, New York Fludarabine Based Cytoreductive Regimen and T-cell Depleted Grafts from Unrelated or Mismatched Related Donors.
Sadie Hutson, PhD, RN, CRNP Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland Containment and Invisibility: The Experiences of Siblings of Patients with FA

Session VII: Experimental Therapeutics

Meenakshi Noll, PhD Department of Molecular and Medical Genetics, Oregon Health and Science University, Portland, Oregon Transposon Mediated Hematopoietic Stem Cell Gene Therapy for FA: A Realistic Hope?
D. Wade Clapp, MD Herman B. Wells Center for Pediatric Research, Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana Genetic Correction of FANCC-/- Stem/Progenitor Cells with Helper Free Foamy Virus Corrects Mitomycin C Hypersensitivity in Vitro and Stem Cell Repopulating Ability in Vivo.
David Williams, MD Experimental Hematology, Cincinnati Children's Medical Center, Cincinnati, Ohio Translational and Pre-clinical Studies Trageting Hematopoietic Stem Cell Therapy in Fanconi Anemia.
Uma Lakshmipathy, PhD Stem Cell Institute, Department of Medicine, University of Minnesota, Minneapolis, Minnesota Transplantation of MAPs Isolated from Normal Mice in Fancc-/- Mice.
Fanconi Anemia Research Fund, Inc. Fanconi Anemia Research Fund, Inc.