Aug 22, 2002 · Serial transplants demonstrated protection in secondary recipients and confirmed the transduction of transplantable stem cells. Thus, these data. The ability of the MDR1 gene to protect hematopoietic cells from the myelotoxicity of anticancer drugs was determined by reconstituting patients with gene-modified CD34cells, one half of which were transduced with a retroviral vector containing the MDR1 multidrug resistance gene G1MD, while the other half were transduced with a retroviral vector containing the neomycin resistance NeoR gene. Bone Marrow Cell Dihydrofolate Reductase Autologous Bone Marrow Transplantation Drug Resistance Genes Murine Bone Marrow Cell These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This study was undertaken to analyze the hematotoxicity of paclitaxel Taxol® and to test whether transduction of repopulating hematopoietic cells with a retroviral vector SF1m expressing the human multidrug resistance 1 gene MDR1 would permit dose intensification following bone marrow transplantation BMT.While the regimen chosen 8×20 mg/kg i.p. within 12 days produced a non. The generation of high titer retroviral vectors permits transduction of stem cells with a variety of genes and leads to long-term marking in the blood of recipient mice. Optimized promoter/enhancers facilitate high-level transgene expression in mice transplanted with transduced bone marrow BM cells.
Tulin Budak-Alpdogan, Debabrata Banerjee and Joseph R Bertino, Hematopoietic stem cell gene therapy with drug resistance genes: an update, Cancer Gene Therapy, 10.1038/sj.cgt.7700866, 12, 11, 849-863, 2005. Drug Resistance of Normal Hematopoietic Stem Cells Jan Moreb, M.D., and James R. Zucali, Ph.D. We have previously shown that preincubation with interleukin-1 IL-1 and tumor necrosis factor alpha TNFa can protect normal hematopoietic progenitors but not leukemic cells from the toxicity of 4-hydroperoxy-cyclophosphamide 4-HC, an active derivative of cyclophosphamide.
Get this from a library! Marrow protection: transduction of hematopoietic cells with drug resistance genes. augmentation of methotrexate resistance with co-expression of metabolically related genes; protection of bone marrow cells from toxicity of chemotherapeutic agents targeted toward thymidylate synthase by transfer of mutant forms of. ISBN: 3805568282 9783805568289: OCLC Number: 41137560: Description: vii, 184 pages: illustrations; 25 cm. Contents: Basic Principles of Gene Transfer in Hematopoietic Stem Cells / M. Sadelain, C. May and S. Rivella / [and others] --Optimizing Conditions for Gene Transfer into Human Hematopoietic Cells / M.A.S. Moore and K.L. MacKenzie --Transfer of the MDR-1 Gene into Hematopoietic Cells / A. bone marrow would be the combination of one or more drug resistance genes with MDRl for the protection of hematopoietic precursors against the toxic effects of several families of anticancer drugs. One such class of drug resistance genes is the glutathione transferase family 16. Members of this family of cnzmcs including the TT.Â«,and. Marg Pena,1 Erin Morrey,2 H. Trent Spencer.2. Transduced hematopoietic stem cells have stably engrafted and differentiated into myeloid cells containing ADA mean range at 1 year in bone marrow lineages, 3.5 to 8.9% and lymphoid cells.
This study reports efficient transduction of human CD34cells with a drug resistance gene allowing post-transduction selection using lentivirus under low-MOI conditions that did not require cytokine stimulation or viral concen- tration. Marrow protection - transduction of hematopoietic cells with drug resistance genes. Cytotherapy. 2001;32:67–84. Article CAS PubMed Google Scholar. Request PDF On Nov 1, 2008, Joseph R Bertino published Transfer of Drug Resistance Genes into Hematopoietic Stem Cells for Marrow Protection Find, read and cite all the research you need on. Resistance is not mediated through increased drug efflux or metabolism, but is shown to emerge from leukaemia stem cells both ex vivo and in vivo. Chromatin-bound BRD4 is globally reduced in resistant cells, whereas the expression of key target genes such as Myc remains unaltered, highlighting the existence of alternative mechanisms to regulate. Transgenic overexpression of chemotherapy resistance CTX-R genes in hematopoietic stem- and progenitor cells, also referred to as chemo- or myeloprotective gene therapy, represents a potential strategy to overcome this problem [1, 2].
Utilization of chemotherapy for treatment of tumors is mainly limited by its hematological toxicity. Because of the low level expression of drug resistance genes, transduction of hematopoietic progenitors with multidrug resistance 1 MDR1 or multidrug resistance-associated protein 1 MRP1 genes should provide protection from chemotherapy toxicity. Because of the low level expression of drug resistance genes, transduction of hematopoietic progenitors with multidrug resistance 1 MDR1 or multidrug resistance-associated protein 1 MRP1 genes should provide protection from chemotherapy toxicity. that overexpression of the multidrug resistance gene MDR1 in murine bone marrow cells results in protection from hemato-poietic toxicity from chemotherapy drugs that are substrates for the MDR1 drug efflux pump 7–9. Subsequent studies in mice reconstituted with hematopoietic cells. Successful transfer of drug resistance genes into hematopoietic cells may allow the administration of higher doses of chemotherapy and, thus, increase regression of chemosensitive tumors. The interest in the use of MRP as an alternative to MDR1 for bone marrow protection lies. Drug-resistant variants of DHFR have been expressed in human umbilical cord blood CD34cells after gammaretroviral vector transduction. 39,40 However, in clinical trials to treat X-linked severe combined immunodeficiency by transduction of hematopoietic cells with gammaretroviral vectors, genotoxicity was observed. 41 Although deep sequencing.
To protect bone marrow cells from the toxicity of chemotherapy, a multidrug resistant gene or a dihydrofolate reductase gene has been introduced into stem cells. These genes, however, are not capable of conferring refractoriness to alkylating agents AA, which are some of the most commonly used agents in chemotherapy regimens. INTRODUCTION. Hematopoietic stem cell transplantation HSCT is a mainstay of treatment for hereditary disorders and lymphohematopoietic malignancies, and is the most commonly employed modality for ex vivo gene therapy. However, this procedure often entails myeloablative conditioning by irradiation and/or cytotoxic drugs which incur significant morbidity [1, 2], and low engraftment rates. MGMT with O6-benzylguanine 6-BG and protection of sensitive tissues, such as hematopoietic stem and progenitor cells, using genetic modifica-tion with 6-BG-resistant MGMT mutants. We have used retroviral-medi-ated gene transfer to transduce murine hematopoietic bone marrow cells with MGMT point mutants showing resistance to 6-BG depletionin. Finally, because of the rapid advancements in gene-editing techniques, correction of CD34cells isolated from patients with FA is now feasible, using gene-targeting strategies. Taken together, these advances indicate that gene therapy can soon be used as an efficient and safe alternative for the hematopoietic treatment of patients with FA.
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