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10.1016/j.jaci.2015.04.027 http://scihub22266oqcxt.onion/10.1016/j.jaci.2015.04.027 C4641002!4641002 !26055221     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26055221 &cmd=llinks): Failed to open stream: HTTP request failed! 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Radiation-sensitive severe combined immunodeficiency: The arguments for and against conditioning before hematopoietic cell transplantation--what to do? |pdf=|usr=}}{{26055221 }} gab.com Text Radiation-sensitive severe combined immunodeficiency: The arguments for and against conditioning before hematopoietic cell transplantation--what to do JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26055221 #FOAvip Defects in DNA cross-link repair 1C (DCLRE1C), protein kinase DNA activated catalytic polypeptide (PRKDC), ligase 4 (LIG4), NHEJ1, and NBS1 involving the nonhomologous end-joining (NHEJ) DNA repair pathway result in radiation-sensitive severe combined immunodeficiency (SCID). Results of hematopoietic cell transplantation for radiation-sensitive SCID suggest that minimizing exposure to alkylating agents and ionizing radiation is important for optimizing survival and minimizing late effects. However, use of preconditioning with alkylating agents is associated with a greater likelihood of full T- and B-cell reconstitution compared with no conditioning or immunosuppression alone. A reduced-intensity regimen using fludarabine and low-dose cyclophosphamide might be effective for patients with LIG4, NHEJ1, and NBS1 defects, although more data are needed to confirm these findings and characterize late effects. For patients with mutations in DCLRE1C (Artemis-deficient SCID), there is no optimal approach that uses standard dose-alkylating agents without significant late effects. Until nonchemotherapy agents, such as anti-CD45 or anti-CD117, become available, options include minimizing exposure to alkylators, such as single-agent low-dose targeted busulfan, or achieving T-cell reconstitution, followed several years later with a conditioning regimen to restore B-cell immunity. Gene therapy for these disorders will eventually remove the issues of rejection and graft-versus-host disease. Prospective multicenter studies are needed to evaluate these approaches in this rare but highly vulnerable patient population. Twit Text FOAVip Radiation-sensitive severe combined immunodeficiency: The arguments for and against conditioning before hematopoietic cell transplantation--what to do ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26055221 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26055221 #FOAvip English Wikipedia <ref>{{Cite pmid|26055221 }}</ref> Radiation-sensitive severe combined immunodeficiency: The arguments for and against conditioning before hematopoietic cell transplantation--what to do? #MMPMID26055221 Cowan MJ ; Gennery AR J Allergy Clin Immunol 2015[Nov]; 136 (5 ): 1178-85 PMID26055221 show ga Defects in DNA cross-link repair 1C (DCLRE1C), protein kinase DNA activated catalytic polypeptide (PRKDC), ligase 4 (LIG4), NHEJ1, and NBS1 involving the nonhomologous end-joining (NHEJ) DNA repair pathway result in radiation-sensitive severe combined immunodeficiency (SCID). Results of hematopoietic cell transplantation for radiation-sensitive SCID suggest that minimizing exposure to alkylating agents and ionizing radiation is important for optimizing survival and minimizing late effects. However, use of preconditioning with alkylating agents is associated with a greater likelihood of full T- and B-cell reconstitution compared with no conditioning or immunosuppression alone. A reduced-intensity regimen using fludarabine and low-dose cyclophosphamide might be effective for patients with LIG4, NHEJ1, and NBS1 defects, although more data are needed to confirm these findings and characterize late effects. For patients with mutations in DCLRE1C (Artemis-deficient SCID), there is no optimal approach that uses standard dose-alkylating agents without significant late effects. Until nonchemotherapy agents, such as anti-CD45 or anti-CD117, become available, options include minimizing exposure to alkylators, such as single-agent low-dose targeted busulfan, or achieving T-cell reconstitution, followed several years later with a conditioning regimen to restore B-cell immunity. Gene therapy for these disorders will eventually remove the issues of rejection and graft-versus-host disease. Prospective multicenter studies are needed to evaluate these approaches in this rare but highly vulnerable patient population. |*Hematopoietic Stem Cell Transplantation [MESH] |Animals [MESH] |Cell Cycle Proteins/genetics [MESH] |DNA Ligase ATP [MESH] |DNA Ligases/genetics [MESH] |DNA Repair Enzymes/genetics [MESH] |DNA Repair/genetics [MESH] |DNA-Activated Protein Kinase/genetics [MESH] |DNA-Binding Proteins/genetics [MESH] |Endonucleases [MESH] |Genetic Therapy [MESH] |Humans [MESH] |Immunotherapy [MESH] |Nuclear Proteins/genetics [MESH] |Radiation [MESH] |Radiation Tolerance/immunology [MESH] |Severe Combined Immunodeficiency/*immunology/therapy [MESH]Radiation-sensitive severe combined immunodeficiency: The arguments fo(epmc).pdf DeepDyve Pubget Overpricing