Hematology & Oncology
Secondary: Biochemistry & Molecular Genetics
Campus Address: SHEL 413, Zip 2182
1720 2nd Avenue South, SHEL 413
Birmingham, AL 35294-2182
Clinic Phone: (205) 801-8415
Office Phone: (205) 934-2992
For an appointment, call (205) 934-9999 or toll free 1 (800) UAB-8816.
A graduate of Boston University in Boston, Massachusetts, Dr. Davis completed medical school at the University of Alabama School of Medicine (UASOM), where he also served his internship, residency, and the ABIM academic subspecialty research fellowship clinical investigator pathway in Hematology/Oncology. He is Professor of Medicine, Microbiology, and Biochemistry and Molecular Genetics in the division of Hematology/Oncology. He is board certified in Hematology.
Dr. Davis' clinical expertise is in Hematology/Oncology with a specific focus on B cell chronic lymphocytic leukemia (CLL) and lymphoproliferatve disorders.
Hematology, American Board of Internal Medicine
Education & Training:
1987 - 1992 B.A., Biology, Boston University
1992 - 1997 M.D., Medicine, University of Alabama at Birmingham
1997 - 1998 Intern, Internal Medicine, University of Alabama at Birmingham
1999 - 2003 Postdoctoral Fellow, Hematology/Oncology and Immunology, University of Alabama at Birmingham
Attending Physician, Active Staff, Medicine Service: Hematology/Oncology
Director, Multidisciplinary Molecular Interaction Core (MMIC)
Senior Scientist, UAB Comprehensive Cancer Center
Scientist, UAB Comprehensive Arthritis, Musculoskeletal, and Autoimmunity Center
Member, UAB Center for AIDS Research
Member, UAB Comprehensive Diabetes Center
Member, UAB Diabetes Research Center
Faculty, Graduate Biomedical Sciences - Themes: Cancer Biology, Immunology, and Pathobiology & Molecular Medicine
Faculty, Medical Scientist Training Program (MSTP) - Research Areas: Cancer Biology, Immunology and Inflammation, and Molecular Genetics & Disease
UAB Department of Medicine Walter B. Frommeyer, Jr., Fellowship in Investigative Medicine Physician Scientist Award (2000-2001); UAB Department of Medicine J. Claude Bennett Award for Excellence in Research by an Associate Fellow (2001, 2002); Leukemia and Lymphoma Society Special Fellow Career Development Award (2003); NIH-NIAID K08 Mentored Clinical Scientist Development Award (2003); Dana Foundation Human Immunology Program Award (2005); V Foundation for Cancer Research Scholar Award (2005); Member, Henry Kunkel Society (2006); Cancer Research Institute Investigator Award (2006); American Cancer Society Research Scholar Award (2008); CLL Global Research Foundation Award (2008); Member, Southern Society for Clinical Investigation (2012); Lupus Research Institute Novel Research Grant Award (2013).
American Association of Immunologists (AAI)
American Society of Hematology (ASH)
Henry Kunkel Society
Southern Society for Clinical Investigation (SSCI)
Dr. Davis' laboratory is focused on the cellular and molecular immunobiology of lymphocytes in normal and diseased conditions. He has been broadly trained as a physician-scientist with a background in basic lymphocyte development and receptor biology. As a postdoctoral fellow he co-discovered a multigene family that encodes Fc receptor-like (FCRL) molecules with tyrosine-based regulatory potential that are expressed by subpopulations of lymphocytes in normal and diseased states. Current work involves investigating FCRL members in humans and mice to define their functional roles in normal and aberrant immune conditions. Work by his group and through productive collaborations has provided a better understanding of these receptors in basic immunology as well as in clinically important autoimmune and malignant conditions. Beyond his role as a physician-scientist, he also serves as Director of the UAB Multidisciplinary Molecular Interaction (MMIC) Core Facility which supports the operation of a Biacore T200 instrument. This technology allows for the determination of very sensitive kinetic interactions between macromolecules and/or small drugs using surface plasmon resonance (SPR).
- Davis, R.S., Wang, Y., Kubagawa, H., and M.D. Cooper: Identification of a Family of Fc Receptor Homologs with Preferential B Cell Expression. (2001) Proc. Natl Acad. Sci., 98: 9772-9777. PMCID: PMC55528
- Ehrhardt, G. R. A., Davis, R.S., Hsu, J.T., Leu, C-M., Ehrhardt, A., and Cooper, M.D. The inhibitory potential of FcRH4 on memory B cells. (2003) Proc. Natl. Acad. Sci. USA 100:13489-13494. PMCID: PMC263841.
- Davis, R.S., Stephan, R.P., Chen, C.-C., Dennis, G. Jr. and Cooper, M. D. Differential B Cell Expression of Mouse Fc Receptor Homologs. (2004) Int. Immunol. 16:1343-1353. PMID: 15302849.
- Leu, C-M., Davis, R.S., Gartland, L.A., Fine, D.F., and Cooper, M.D. FcRH1: an activation co-receptor on human B cells. (2005) Blood 105:1121-1126. PMID: 15479727.
- Ehrhardt, G. R. A., Hsu, J.T., Gartland, L, Leu, C-M, Zhang, S., Davis, R.S. and Cooper, M.D. Expression of the immunoregulatory molecule FcRH4 defines a distinctive tissue-based population of memory B cells. (2005) J Exp Med 202: 783-791. PMCID: PMC2212938.
- Won, W-J.,Foote, J.B., Odom, M., Pan, J., Kearney, J.F., and Davis, R.S. FcRH3 Is a Novel Immunoregulatory Marker of Marginal Zone and B1 B cells. (2006) J. Immunol. 177:6815-23. PMID: 17082595
- Davis, R.S. Fc Receptor Homologs. (2007) Ann. Rev. Immunol. 25:525-60. PMID: 17201682
- Hirano, M., Davis, R.S., Fine, W.D., Nakamura, S., Shimizu, K., Yagi, H., Kato, K., Stephan, R.P., Cooper M.D. IgEb immune complexes activate macrophages through FcgammaRIV binding. (2007) Nat Immunol. Jul;8(7):762-71. Epub 2007 Jun 10. PubMed PMID: 17558411.
- Li, F.J., Ding, S., Pan, J., Shakhmatov, M.A., Kashentseva, E., Wu, J., Li, Y.F., Soong, S.J., Chiorazzi, N., and Davis, R.S. FCRL2 expression predicts IgVH mutation status and clinical progression in chronic lymphocytic leukemia. (2008) Blood 112:179-87.PMCID: PMC2435687.
- Gibson, A.W., Li, F.J., Wu, J., Edberg, J.C., Su, K., Cafardi, J., Wiener, H., Tiwari, H., Kimberly, R.P., and Davis, R.S. The FCRL3-169CT promoter single-nucleotide polymorphism, which is associated with systemic lupus erythematosus in a Japanese population, predicts expression of receptor protein on CD19+ B cells. (2009) Arthritis Rheum 60:3510-2. PMCID: PMC2784265
- Schreeder, D. M., Cannon, J. P., Wu, J., Li, R., Shakhmatov, M. A., and Davis, R. S. Cutting Edge:FCRL6 is an MHC class II receptor. (2010) J. Immunol, 185:23-7. PMID: 20519654
- Campbell, J.A., Davis, R.S., Lilly, L.M., Fremont, D.H., French, A.R., and Carayannopoulos, L.N. Cutting Edge: FCRL5 on Innate B Cells is Targeted by a Poxvirus MHC Class I-like Immunoevasin. (2010) J. Immunol, 185:28-32. PMCID: PMC3321838
- Sohn, H. W., Krueger, P. D., Davis, R.S., and S. K. Pierce. The Potential of FCRL4 to Function as an Adaptive to Innate Molecular Switch in Exhausted Memory B Cells. (2011) Blood. 118:6332-41. PMCID: PMC3236118
- Zhu, Z., Li, R., Li, H., Zhou, T., and Davis, R.S. FCRL5 exerts binary and compartment-specific influence on innate-like B-cell receptor signaling. (2013) Proc. Natl. Acad. Sci. USA. 110:E1282-90. PMCID: PMC3619311
- Li FJ, Schreeder DM, Li R, Wu J, Davis RS. FCRL3 promotes TLR9-induced B-cell activation and suppresses plasma cell differentiation. (2013) Eur J Immunol. Nov;43(11):2980-92. 10.1002/eji:201243068. Epub 2013 Aug 12. PubMed PMID: 23857366; PubMed Central PMCID: PMC3838486.
Additional Publications:See a complete listing of publications on PubMed, a service of the National Library of Medicine.
Postdoc Positions Available
A postdoctoral position is available in the laboratory of Dr. Randall Davis to investigate pathways of lymphocyte development and function of a novel family of Fc receptor-like molecules (FCRL). Studies involve establishing human and mouse disease models, exploring signaling potential and gene regulation. M.D. and/or Ph.D. is required. Please send curriculum vitae and names of three references to: Randall S. Davis, M.D. 1720 2nd Avenue South, SHEL 402, Birmingham, AL 35294-2182 or via email to email@example.com.
We have a very interactive group comprised of graduate students, medical residents, postdoctoral fellows, and research associates.
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