Pradip Akolkar, Ph.D. 

Division of Emerging and Transfusion Transmitted Diseases
Officer of Blood Research and Review
Center for Biologics Research and Evaluation
Rockville, MD

Background:

B.Sc., M.S. University of Baroda, Baroda, India
M.Sc., M.S. University of Baroda, Baroda, India
Ph.D., M.S. University of Baroda, Baroda, India

Research Interests:

The preceptor is senior regulatory scientist in the CBER division responsible for the review of tests used to screen blood donors for transfusion-transmissible agents including emerging infectious diseases (EIDs) and for the review of HIV diagnostics.

Proposed Research Project for FDA Fellow:

The FDA fellow participating in this program will be intimately involved in the process of evaluation and approval of blood donor screening tests and HIV diagnostics. This includes donor tests for HIV-1, hepatitis B, hepatitis C, and West Nile virus. In addition, the fellow will evaluate tests that are used as an aid in the diagnosis of HIV infection (including rapid HIV tests, potential over-the-counter HIV tests, and tests designed to close the window period of HIV infection) and monitor HIV viral load and genotype as an adjunct to anti-retroviral therapy. The fellow will be involved in the development of policy that affects the approval and use of these tests and will have the opportunity to work with other Centers at FDA and with other agencies within HHS with which we collaborate to assure that the tests we regulate are safe and effective.

Selected Recent Publications:

1. Srinivasan K, Akolkar PN, Taffs RE and Hewlett IK. Absence of detectable viremia in plasma and peripheral blood mononuclear cells from smallpox vaccinees: implication for blood safety. Transfusion. 2006; 46:1589-1592.
2. Srinivasan K, Lee S, Sylvester D, Wood O, Akolkar PN, and Hewlett IK. Performance of serologic assays used in donor testing with plasma from smallpox vaccinnees. Transfusion. 2006; 46:1847-1848
3. Akolkar PN, Gulwani-Akolkar B, Lin X-Y , Zhou Z, Simins I, Daly M, Katz S, Levine J, Present D, Gelb B, Desnick R, Mayer L, and Silver J. The IBD1 locus for susceptibility to Crohn’s disease has a greater impact in Ashkenazi Jews with early onset disease. Am. J. Gastroentrol.2001; 96:1127-1132
4. Kim SR, Sitz KV, Schere AM, Loomis-Price LD, Kim JH, Anderson DW, Nau M, Michael NL, Chang G, Akolkar PN, Gulwani-Akolkar B, Silver J, Birx DL. Comparison of HIV-1 envelope-specific CD4+ T cell lines simultaneously established from peripheral blood mononuclear cells and lymph node biopsy in 2 HIV-1 infected individuals. 1997 J.Immunol. 1997;159:5162-5167.
5. Akolkar PN, Gulwani-Akolkar B, and Silver J. T cell receptor repertoire in health and disease. CRC Handbook of Human Immunology Eds.Leffell MS, Donnenberg AD and Rose NR, pp:567-698. CRC Press, New York. 1997.
6. Akolkar PN, Gulwani-Akolkar B and Silver J. Differential patterns of T-cell receptor BV-specific activation of T cells by gp120 from different HIV strains. Scand J Immunol.1995; 42:598-606.
7. Akolkar PN, Gulwani-Akolkar B, Chirmule N, Kalyanaraman VS, Pergolizzi R, Pahwa S, Macphail S, and Silver J. The HIV glycoprotein gp160 has superantigen-like activity. Clin. Immunol. Immunopath.1995; 76:255-265.
8. Akolkar PN, Gulwani-Akolkar B, Robinson MA and Silver J. The influence of non-HLA genes on the human T-cell receptor repertoire. Scand. J. Immunol. 1995; 42:248-256.
9. Silver J, Gulwani-Akolkar B and Akolkar PN. The influence of genetics, environment and disease state on the human T cell receptor repertoire. Annals NY Acad Sci, 1995; 756:28-53.

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Abdu I. Alayash, Ph.D. 

Principle Investigator and
Chief of Laboratory of Biochemistry and Vascular Biology (LBVB),
Division of Hematology, Office of Blood Research and Review,
Center for Biologics Evaluation and Research
Bethesda, MD

Background:

B.S., Baghdad University, Iraq
Ph.D., Essex University, Essex, England

Research Interests: 

Hemoglobin-based oxygen carriers (HBOCs), also referred to as “blood substitutes,” have the potential to reduce need for blood transfusion and to deliver oxygen; however, they have shown evidence of toxicity. Improved in vitro and in vivo biomarkers to better predict and monitor toxicity is the focus of our ongoing research. Such biomarkers could enhance the potential for safe use of these investigational products in clinical trials.

Proposed Research Project for FDA Fellow:

The FDA Fellow participating in this research program will aid in determining the extent and nature of HBOCs' oxidation under hypoxic conditions in vascular endothelial cell culture followed by a systemic analysis of hypoxia-inducible factor (HIF-1a)-mediated gene expressions under these conditions. The extent of tissue oxygenation and biochemical oxidation of HBOCs in rat (high antioxidant levels) and guinea pig (low antioxidant levels) models of blood for HBOC exchange transfusion are also being evaluated. Key metabolic pathways that are associated with HIF1α gene expression in various organs are measured. Mass-spectrometry-based proteomics technologies in the characterization of oxidatively modified HBOCs under in vitro cell-culture and in vivo animal models will also be employed.

Selected Recent Publications:

1. Buehler, P.W., Vallelian, F., Mikolajczyk, M.G., Schoedon, G., Schweizer, G., Alayash, A.I., and Schaer, D.G. Structural stabilization in tetrameric or polymeric hemoglobin determines its affinity towards endogenous antioxidant scavenger pathways. Antioxid. Redox. Signal 10:1449-1462, 2008.
2. Bonilla, W.D., Jia, J., Alayash, A.I. and Lopez-Garriga, J. Heme pocket geometry of Lucina pectinata hemoglobin II restricts nitric oxide and peroxide entry: A model of ligand control for the design of a stable oxygen carrier. Biochemistry 46:10451-10460, 2007.
3. Buehler, P.W., D'Agnillo, F., and Alayash, A.I. Effects of endogenous ascorbate on oxidation, oxygenation and toxicokinetics of cell-free modified hemoglobin after exchange transfusion in rat and guinea pig. J. Pharm. Exp. Ther. 323:49-60, 2007.
4. Jia, Y., Buehler, P.W., Boykins, R.A., Venable, R.M., and Alayash, A.I. Structural basis of peroxide mediated changes in human hemoglobin: A novel oxidative pathway. J. Biol. Chem. 282:4894-4907, 2007.
5. Buehler, P.W., Boykins, R.A., Norris, S., and Alayash, A.I. Chemical characterization of diaspirin cross-linked hemoglobin polymerized with polyethylene glycol. Anal. Chem. 78:4634-4641, 2006.
6. Dunne, J.M., Caron, A., Menu, P., Buehler, P.W., Alayash, A.I., Wilson, M.T., Faivre, B., and Cooper, C.E. Ascorbate removes key precursors to oxidative damage by cell free hemoglobin in vitro and in vivo. Biochem. J. 399:513-542, 2006.
7. Schaer, D.J., Schaer, C.A., Buehler, P.W., Schoedon, G., Alayash, A.I., and Schaffner, A. CD163 is the macrophage scavenger receptor for native and chemically modified hemoglobins in the absence of haptoglobin. Blood 107:373-380, 2006.
8. Buehler, R.W., Boykins, R.A., Jia, Y., Norris, S., Freedberg, D.I., and Alayash, A.I. Structural and functional characterization of glutaraldehyde polymerized bovine hemoglobin and its isolated fractions. Anal. Chem. 77:3466-3478, 2005.
9. Boykins, R.A., Jia, Y., Buehler, P.W., Venable, R., and Alayash, A.I. O-Raffinose cross-linked hemoglobin lacks site-specific chemistry in the central cavity: structural and functional consequences of b93Cys modification. Proteins 59:840-855, 2005.
10. Rochon, G., Caron, A., Toussaint-Hacquard, M., Alayash, A. I., Gentils, M., Labrude, P., Stoltz, J.F., Menu, P. Infusion of stroma-free hemoglobin at physiologically maintained viscosity delays the onset of vasoconstriction in acute normovolemic hemodilution. Hypertension 43:1-6, 2004.

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Andrew P. Byrnes, Ph.D. 

Division of Cellular and Gene Therapies
Office of Cellular, Tissue and Gene Therapies
Center for Biologics Evaluation and Research
Bethesda, MD

Background:

B.S., M.S., Yale University
Ph.D., University of Oxford, England

Research Interests:

Safety of gene therapy vectors: Adenoviruses are common DNA viruses that can be engineered to create non-replicating gene therapy vectors. There are close to 100 clinical trials in the US that use adenovirus vectors for gene delivery or anti-tumor therapy. Administering these vectors through the vascular system would be an ideal route in many situations, potentially allowing adenovirus vectors to target a variety of tissues or widely-disseminated metastatic tumors. One significant barrier is that adenovirus vectors are quickly cleared from the circulation by macrophages in the liver, which limits the amount of vector that can reach the intended target. We have recently identified the cellular receptors and processes that are responsible for this vector clearance, and further work is centered on how to design vectors that evade these receptors. Another difficult barrier to gene therapy with adenovirus vectors is the body's ability to detect virus-based vectors through the innate immune system, which can trigger a variety of potentially dangerous responses. We are studying macrophages, cytokines, complement and other types of mediators to learn why they have an innate ability to recognize and respond to adenovirus vectors. Our long term goal is to develop vectors that are safer and more effective.

Proposed Research Project for FDA Fellow:

The FDA fellow participating in this program will study how the innate immune system recognizes adenovirus vectors and help to evaluate methods for decreasing these responses, with the aim of developing safer methods of gene therapy. Research will include in vivo work with rodent models, including knockout mice. Training will include intimate involvement in regulatory review of gene therapy clinical products as well as course work and regulatory staff meetings.

Selected Recent Publications:

1. Xu, Z., J. Tian, J.S. Smith and A.P. Byrnes (2008). Clearance of adenovirus by Kupffer cells is mediated by scavenger receptors, natural antibodies and complement. Journal of Virology 82: 11705-11713.
2. Smith, J.S., Z. Xu, J. Tian, S.C. Stevenson and A.P. Byrnes (2008). Interaction of systemically-delivered adenoviral vectors with Kupffer cells in mouse liver. Human Gene Therapy 19: 547-554.
3. Smith, J.S., Z. Xu and A.P. Byrnes (2008). A quantitative assay for measuring clearance of adenovirus vectors by Kupffer cells. Journal of Virological Methods 147: 54-60.
4. Lee, M.B., M.M. McMenamin, A.P. Byrnes, H.M. Charlton and M.J. Wood (2008). Th1 cytokines are upregulated by adenoviral vectors in the brains of primed mice. NeuroReport 19: 1187-1192.
5. Manickan, E., J.S. Smith, J. Tian, J.N. Lozier, T.L. Eggerman, J. Muller and A.P. Byrnes (2006). Rapid Kupffer cell death after intravenous injection of adenovirus vectors. Molecular Therapy 13: 108-117.
6. Han, J., R.L. Farnsworth, J.L. Tiwari, J. Tian, H. Lee, P. Ikonomi, A.P. Byrnes, J.L. Goodman and R.K. Puri (2006). Quality prediction of cell substrates using gene expression profiles. Genomics 87: 552-559.
7. Byrnes, A.P. (2005). Challenges and future prospects in gene therapy. IDrugs 8: 993-996.
8. Smith, J.S., J. Tian, J.N. Lozier and A.P. Byrnes (2004). Severe pulmonary pathology after intravenous administration of adenovirus vectors in cirrhotic rats. Molecular Therapy 9: 932-941.
9. Smith, J.S., J. Tian, J. Muller and A.P. Byrnes (2004). Unexpected pulmonary uptake of adenovirus vectors in animals with chronic liver disease. Gene Therapy 11: 431-438.
10. Simek, S., A. Byrnes and S. Bauer (2002). FDA perspectives on the use of the adenovirus reference material. BioProcessing 1: 40-42.

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Deborah Hursh, Ph.D. 

Division of Cellular and Gene Therapies
Office of Cellular, Tissue and Gene Thereapies
Bethesda, MD

Background:

B.A., New College, Sarasota, Fla.
M.S., University of Denver
Ph.D., Indiana University, Bloomington
Previous Employment: American University, Asst. Prof (1996-2000)

Research Interests:

Cell therapy and the use of engineered tissues are critical emerging areas of medical intervention for repair and regeneration of diseased, damaged or aging tissues. For these therapies to be both safe and effective, it will be necessary to be able to reliably predict the final fate of transplanted immature cells and engineered tissues. Immature cells or tissues that mature along an unpredicted path will not provide effective treatment, and can cause serious adverse consequences, such as tumors.

What kind of cell a precursor cell becomes (i.e., cell fate) after administration as a cell therapy product is largely directed by cellular communication networks. This communication is carried out by proteins called growth factors that are secreted from cells. Many such growth factor networks regulate the maturation of cells, and can work in collaboration or opposition to each other, depending of the cellular context. Thus, to ensure that cell and tissue therapy products manufactured outside an organism can be used effectively, we seek to capture the communication code used by particular cell types and translate this knowledge to predict how transplanted cell and tissue products will respond to the environment into which they are transplanted.

Proposed Research Project for FDA Fellow:

FDA Fellows participating in this program will aid the staff in promoting the development of the projects. This research program uses a simple organism as a model to study cell-cell communication during maturation. We are focusing on several vital cell factors, including Bone Morphogenesis Protein, Wnt and Hedgehog signaling pathways, all of which are critical for cell maturation. We carry out genetic screening to identify molecules involved in cell-cell communication networks. By this method, we identify genes that can serve as predictive indicators of cell fate. Such markers will be critical for the characterization of cell therapies, particularly those derived from stem cells. We are also studying how adverse consequences, such as the death of the cells, occur when cell communication is disrupted or mis-regulated.

Selected Recent Publications:

1. Lee, H., Stultz, B.G., and Hursh, D.A. (2007) The Zic family member, odd-paired, regulates the Drosophila Bone Morphogenetic Protein, decapentaplegic, during adult head development. Development 134:1301-1310.
2. Stultz, B.G., Lee, H., Ramon, K., and Hursh, D.A. (2006) Decapentaplegic head capsule mutations disrupt novel peripodial expression controlling the morphogenesis of the Drosophila ventral head. Dev. Biol. 296: 329-339.
3. 3.Stultz, B.G., Jackson, D., Mortin, M.A., Xiang Yang, Beachy, P.A., and Hursh D.A. (2006)Transcriptional activation by extradenticle in the Drosophila visceral mesoderm. Dev. Biol. 290: 482-494.
4. Bi, X., Jones, T., Abbasi, F., Lee, H., Stultz, B., Hursh, D.A., and Mortin, M.A. (2005) Drosophila caliban, a nuclear export mediator, can function as a tumor suppressor in human lung cancer cells. Oncogene 24: 8229-8239.
5. Stultz, B.G., Ray, R.P., and Hursh, D.A. (2005) Analysis of the Shortvein Cis-Regulatory Region of the decapentaplegic Gene of Drosophila melanogaster Genesis 42:181-192.
6. Yang, Y., van Beest, M., Clevers, H., Jones, T., Hursh,D.A., and M.A Mortin. (2000) decapentaplegic is a direct target of dTCF repression in the Drosophila visceral mesoderm. Development 127: 3695-3702
7. van de Wetering, M., Cavallo R., Dooijes D., van Beest, M., van Es, J., Loureiro J., Ypma A., Hursh D., Jones T., Bejsovec A., Peifer M., Mortin, M. and H. Clevers. (1997) Armadillo co-activates transcription driven by the product of the Drosophila segment polarity gene dTCF. Cell 88: 789-799.
8. Sun, B., Hursh D.A., Jackson, D., and P.A. Beachy. (1995) Ultrabithorax protein is necessary but not sufficient for full activation of decapentaplegic expression in visceral mesoderm. EMBO Journal 14: 520-535.
9. Hursh, D. A., Padgett, R.W., and W.M. Gelbart. (1993) Cross regulation of decapentaplegic and Ultrabithorax transcription in the embryonic visceral mesoderm of Drosophila. Development 117: 1211-1222.

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Malcolm Moos, M.D., Ph.D. 

Division of Cellular and Gene Therapies
Office of Cellular, Tissue and Gene Therapy
Center for Biologics Evaluation and Research
Bethesda, MD

Background:

B.S., Stanford University
Ph.D., Pharmacology, University of Minnesota Medical School
M.D., University of Minnesota Medical School

Research Interests:

Tissues and organs can be damaged by accident, battle trauma, or disease. Improved methods of repair, replacement, or regeneration of damaged tissues and organs are an important public health goal. Novel biological products containing living cells show great promise for use as therapies in these settings, but design, manufacture, and testing of these products has proven very challenging. A major obstacle to successful development has been great uncertainty regarding how best to evaluate experimental cell-based products analytically in order to develop process controls and release specifications that predict product performance reliably.

To meet this challenge, we identify the biological processes that cells can use to repair damage within the body, and the components that control these processes. This information will help guide sponsors in the development and regulatory approval of novel therapeutic product approaches, lead to improved manufacturing methods, and guide development of laboratory tests that will help ensure consistent, safe, and effective cellular products. The research program uses a vertebrate embryology model (the South African clawed frog Xenopus) that is particularly useful for identifying the key biological mechanisms that control repair and regeneration and the interactions between these components. We focus on the medically critical, but complicated process of joint development and perform detailed functional analyses of the proteins involved. We have identified several molecules that help control processes such as joint morphogenesis, blood development, and formation of the nervous system. The work has also uncovered ways in which different proteins cooperate to achieve precisely localized control during the formation of complex structures like joints.

Proposed Research Project for FDA Fellow:

The FDA fellow participating in this program would conduct research to evaluate molecules we have discovered for their therapeutic potential and inclusion in tests for product quality, safety and efficacy evaluations of cellular products before release for clinical use. Others are being evaluated for their ability to repair or regenerate specific structures, such as joint surfaces, tendons, and ligaments. Currently, we are attempting to clarify various interactions between the key signaling pathways with the eventual goal of defining the signaling network components essential to creating and maintaining cell and tissue constructs that are effective clinically. Two active areas of current effort are improved methods for characterizing cell based products and application of network theory/systems biology to design of next-generation products.

Selected Recent Publications:

1. Thomas, JT and Moos, M Jr. (2007).Vg1 has specific processing requirements that restrict its action to body axis patterning centers.
   Dev. Biol. 310, 129-139.
2. Thomas, JT, Prakash, D, Weih, K and Moos, M Jr. (2006). CDMP1/GDF5 has specific processing requirements that restrict its action to joint surfaces. J. Biol. Chem. 281, 26725-26733.
3. Moos, M. Jr. (2002). Regulatory philosophy for comparability protocols. Dev Biol (Basel) 109,53-56.
4. Wang S, Krinks M, Kleinwaks L, Moos M Jr. (1997).A novel Xenopus homologue of bone morphogenetic protein-7 (BMP-7). Genes Funct.1, 259-71.
5. Lin K, Wang S, Julius MA, Kitajewski J, Moos M Jr, Luyten FP. (1997) The cysteine-rich frizzled domain of Frzb-1 is required and sufficient for modulation of Wnt signaling. Proc Natl Acad Sci U S A. 94, 11196-200.
6. Wang S, Krinks M, Moos M Jr. (1997) Frzb-1, an antagonist of Wnt-1 and Wnt-8, does not block signaling by Wnts -3A, -5A, or -11. Biochem Biophys Res Commun. 236, 502-4
7. Wang S, Krinks M, Lin K, Luyten FP, Moos M Jr. (1997). Frzb, a secreted protein expressed in the Spemann organizer, binds and inhibits Wnt-8. Cell, 88, 757-66.
8. Wang S, Krinks M, Lin K, Luyten FP, Moos M Jr. (1997). Frzb, a secreted protein expressed in the Spemann organizer, binds and inhibits Wnt-8. Cell, 88, 757-66.
9. Hoang B, Moos M Jr, Vukicevic S, Luyten FP.(1996). Primary structure and tissue distribution of FRZB, a novel protein related to Drosophila frizzled, suggest a role in skeletal morphogenesis. J Biol Chem. 271, 26131-7.
10. Moos M Jr, Wang S, Krinks M. (1995). Anti-dorsalizing morphogenetic protein is a novel TGF-beta homolog expressed in the Spemann organizer. Development 1214, 293-301.

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Donna Przepiorka, M.D., Ph.D. 

Medical Officer, Clinical Evaluation Branch (CEB)
Division of Clinical Evaluation and Pharmacology/Toxicology (DCEPT)
Center for Biologics Evaluation Research (CBER)
Rockville, MD

Background:

B.S. (Biochemistry) Illinois Benedictine College, Lisle, IL
M.D. University of Illinois, Chicago, IL
Ph.D. (Microbiology and Immunology) University of Illinois, Chicago, IL

Research Interests:

The products that the Office of Cellular, Tissue, and Gene Therapies (OCTGT) regulates include gene therapies (ex vivo transduction of cells and direct injection of product), tumor vaccines, xenotransplantation, stem cells (embryonic and adult), tissue preparations (fetal and adult), combination products (biologic plus drug or device), and bioengineered tissues. Dr. Przepiorka has a special interest in design and monitoring of early phase clinical trials for novel therapies. She is a member of the RAC Clinical Trial Design Working Group.

Proposed Research Project for FDA Fellow:

The FDA fellow participating in this program would develop proficiency in the evaluation of clinical trials for products regulated by OCTGT. An understanding of the strategies for design of early phase clinical trials and the importance of these trials in the overall product development pathway will be acquired. There is also opportunity for the assessment of new clinical trial endpoints for novel therapeutics.

Selected Recent Publications:

1. Kao G, Kim H, Gatzo L, Madison H, Daley H, Ritz J, Przepiorka D, Burger S, Kelley L, Vierra-Green C, Flesch S, Spellman S, Miller J, Confer D. Impact of storage conditions on marrow and peripheral blood stem cell products stored over 72 hours. Biol Blood Marrow Transplant 14(S2):93, 2008.
2. Honea S, Crenshaw C, Brenner S, McClune B, Bradley R, Przepiorka D. In vivo validation of single platform measurement of CD34 in peripheral blood stem cells. Cytotherapy 8(S1):54, 2006.
3. Martin PJ, Weisdorf D, Przepiorka D, Hirschfeld S, Farrell A, Rizzo JD, Foley R, Socie G, Carter S, Couriel D, Schultz KR, Flowers MED, Filipovich AH, Saliba R, Vogelsang GB, Pavletic SZ, Lee SJ. National Institutes of Health Consensus Development Project on Criteria for Clinical Trials in Chronic Graft-Versus-Host Disease: VI. Design of Clinical Trials Working Group Report. Biol Blood Marrow Transplant 12:491, 2006.
4. Bollard CM, Gottschalk S, Huls MH, Molldrem J, Przepiorka D, Rooney CM, Heslop HE. In vivo expansion of LMP 1 and 2-specific T cells in a patient who received donor-derived EBV-specific T cells after allogeneic stem cell transplantation. Leuk Lymphoma 47:837, 2006.
5. Murray JL, Gillogly ME, Przepiorka D, Brewer H, Ibrahim NK, Booser DJ, Hortobagyi GN, Kudelka AP, Grabstein KH, Cheever MA, Ioannides CG. Toxicity, immunogenicity, and induction of E75-specific tumor-lytic CTLs by HER-2 peptide E75 (369-377) combined with granulocyte macrophage colony-stimulating factor in HLA-A2+ patients with metastatic breast and ovarian cancer. Clin Cancer Res 8:3407, 2002.
6. Savary CA, Grazziutti ML, Przepiorka D, Tomasovic SP, McIntyre BW, Woodside DG, Pellis NR, Peirson DL, Rex JH. Effects of simulated microgravity on human dendritic cells. In Vitro Cell Dev Biol 37:216, 2001.
7. Kornblau SM, Marini FC, Snell V, Stiouf I, Przepiorka D, Stephens C, Champlin R. Generation of retrovirally transduced murine suicidal lymphocytes and pre-emptive control of graft-vs-host disease in a murine allogeneic transplant model. Cancer Res 61:3355, 2001.
8. Grazziutti M, Przepiorka D, Rex JH, Braunschweig I, Vadhan-Raj S, Savary CA. Dendritic cell-mediated stimulation of the in vitro lymphocyte response to Aspergillus. Bone Marrow Transplant 27:647, 2001.
9. Przepiorka D, Kernan N, Ippoliti C, Papadopoulos E, Giralt S, Khouri I, Lu J-G, Gajewski J, Durett A, Cleary K, Champlin R, Andersson B, Light S. Daclizumab, a humanized anti-IL-2 receptor alpha chain antibody for treatment of acute graft-versus-host disease. Blood 95:83, 2000.
10. Przepiorka D, Lu J-G, Anderlini P, Korbling M, Donato M, Champlin R, Gee A, van Vlasselaer P. Debulking blood stem cell collections by density gradient centrifugation in a closed vessel system. Cytother 1:111, 1999

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