Biochemistry and Structural Biology  http://www.gbs.uab.edu  http://www.uab.edu/graduate  Back to Main

Faculty Detail    
Name FREDERICK D. GOLDMAN
 
Campus Address ACC 512 Zip 0011
Phone  (205) 638-5855
E-mail  fgoldman@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Ped - Hematology/Oncology  Ped - Hematology/Oncology Professor Emeritus

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 

Biographical Sketch 
1975-1979 B.S., Biology Tulane University, New Orleans, LA 1979-1981 M.S., Immunology University of New Orleans, New Orleans, LA 1981-1985 M.D.Louisiana State University, New Orleans, LA 1985-1988 Pediatric Residency Tulane University School of Medicine New Orleans, LA 1988-1991 Clinical Fellow in Pediatric Hematology/Oncology University of Colorado Health Sciences Center Children’s Hospital, Denver, CO 1989-1992 Postdoctoral Research Fellowship Immunology National Jewish Center for and Respiratory Medicine, Denver, CO 1993-1999 Assistant Professor University of Iowa College of Medicine Department of Pediatrics 1999-2009 Associate Professor University of Iowa College of Medicine Department of Pediatrics 2001-2009 Director, Pediatric Immune Disorders Clinic, University of Iowa College of Medicine 2001-2006 Director, Pediatric Bone Marrow Transplant Program, University of Iowa College of Medicine 2003-2009 Director, University of Iowa Hematopoietic Stem Cell Bank 2009-Present Professor of Pediatrics University of Alabama at Birmingham Division of Pediatric Hematology & Oncology Birmingham, AL 2009-Present Medical Director University of Alabama at Birmingham Lowder Bone Marrow Transplant Program

Society Memberships
Organization Name Position Held Org Link
American Society for Blood and Marrow Transplantation  Member   
American Society of Hematology  Member   
American Society of Pediatric Hematology/Oncology  Member   
International Bone Marrow Transplant `Registry  MemberNon-Malignant Marrow Disorders Working Committee   
Pediatric Bone Marrow Transplant Consortium  Member   



Research/Clinical Interest
Title
Creation of patient-specific gene corrected hematopoietic stem cells in inherited bone marrow failure syndromes using inducible pluripotent stem cell technology
Description
The major research interest of Dr. Goldman’s laboratory relates to understanding the molecular and immunologic mechanisms of bone marrow failure syndromes and congenital immune deficiencies, and translating this information to the promotion of novel stem therapies for these disorders. His work previously focused on Dyskeratosis congenita (DC) and he was involved in the discovery of the autosomal dominant form of this disease, AD DC. More recently, he has been involved in studies assessing the defect in hematopoietic stem cells in DC, and in collaboration with the Daley Lab at Dana Farber, applied iPS cell technology to correct the underlying deficiency in telomerase in reprogrammed DC cells. Studies are currently being performed that are assessing the role of telomerase in defects in oxidative stress and DNA repair. Dr. Goldman has also participated in pre-clinical gene therapy studies for a number of other bone marrow failure disorders and immune deficiencies, and has created an extensive tissue repository with patient samples from many different conditions, including Diamond Blackfan Anemia (DBA), Shwachman Diamond Syndrome, and Fanconi’s anemia. More recently his research interests have shifted to DBA, and in concert with the Townes laboratory, is actively working on gene correction strategies for this condition using iPS cell technology and homologous recombineering. Through our collaboration with Dr. Lamb, the Director of the Stem Cell Processing laboratory and GMP facility at UAB, it is our collective hope that corrected patient iPS cells can be differentiated into hematopoietic stem cells for future transplantation into patients with DBA or other disorders of hematopoiesis.

Selected Publications 
Publication PUBMEDID
3.Ross S, Goldman F, Crabtree J, Schraven B, Koretzky G. The association between CD45 and lck does not require CD4 and is independent of TCR stimulation. Biochemical and Biophysical Research Communications, 198:88-94, 1994.  8292053 
2.Horvis R, Donovan J, Musci M, Motto D, Goldman F, Ross S, Koretzky G. Rescue of signaling by a chimeric protein containing the cytoplasmic domain of CD45. Science, 260:544-546, 1993  8475387 
6.Kook H, Goldman F, Trigg ME, Giller R, Rumelhart S, Holida M, Lee N, Peters C, Comito M, Padley D, Huling D. Reconstruction of the immune system after unrelated or partially matched T-cell depleted bone marrow transplantation in children: Immunophenotypic analysis and factors affecting the speed of recovery. Blood, 88:1089-1097, 1996.  8704219  
8.Kook H, Goldman F, Giller R, Goeken N, Peters C, Comito M, Rumelhart S, Holida M, Lee N, Trigg, ME. Reconstruction of the immune system after unrelated or partially matched T-cell depleted bone marrow transplantation in children: Functional analyses of lymphocytes and correlation with immunophenotypic recovery following transplant. Clinical and Diagnostic Laboratory Immunology, 4(1):93-103, 1997.  9008290 
7.Goldman F, Crabtree J, Hohl R, Lewis K, Koretzky G. Lovastatin inhibits T cell antigen receptor signaling by disruption of the ras-independent pathway. Blood, 88:4611-4619, 1996.  9036944 
9 Goldman F, Crabtree J, Hollenback, C, Koretzky G. Sequestration of p56lck by gp120, a model for TCR desensitization. Journal of Immunology, 158(5):2017-2024, 1997.  9036944 
11.Gilman, AL, Kooy, NW, Atkins, DL, Ballas, Z, Rumelhart, S, Holida, M, Lee, N, Goldman, F. Complete heart block in association with graft-versus-host disease. Bone Marrow Transplantation, 21:85-88, 1998.  9486500 
12.Goldman F, Ballas Z, Shutte B, Kemp J, Hollenback C, Noraz N, Taylor N. Defective expression of p56lck in an infant with severe combined immunodeficiency. Journal of Clinical Investigation, 102(2):421-29, 1998.  9664084  

Keywords
gene therapy, telomerase, hematopoiesis, inducible pluripotent stem cells, oxidative stress, DNA damage response pathways