Loss of Mismatched HLA in Leukemia after Stem-Cell Transplantation
Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the donor. All five patients had a relapse, and at the time of relapse, genomic HLA typing of leukemic blasts could not detect the recipient's...
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| Vydané v: | The New England journal of medicine Ročník 361; číslo 5; s. 478 - 488 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Waltham, MA
Massachusetts Medical Society
30.07.2009
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| ISSN: | 0028-4793, 1533-4406, 1533-4406 |
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| Abstract | Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the donor. All five patients had a relapse, and at the time of relapse, genomic HLA typing of leukemic blasts could not detect the recipient's HLA haplotype that differed from the donor's. The loss of the haplotype was due to uniparental disomy. In vitro, the donor's T cells reacted against leukemic blasts obtained at the time of diagnosis, not against blasts obtained at relapse. The results indicate the presence of a mutation that allowed the leukemic cells to escape the immunosurveillance of the donor's T cells.
Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the donor. All five patients had a relapse, and at the time of relapse, genomic HLA typing of leukemic blasts could not detect the recipient's HLA haplotype that differed from the donor's.
Transplantation of hematopoietic stem cells from a haploidentical family donor who shares only one HLA haplotype with the recipient is a potentially curative option for patients with high-risk hematologic cancers who lack an HLA-matched donor.
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The major limitation of this strategy is the risk of severe graft-versus-host disease (GVHD), which can result from alloreactions mediated by donor T cells against the recipient's unshared HLA haplotype. Since the publication of studies on extensively T-cell–depleted grafts,
1
,
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a variety of strategies have been developed to prevent or control GVHD after transfer of haploidentical T cells.
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,
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The feasibility and efficacy of . . . |
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| AbstractList | Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the donor. All five patients had a relapse, and at the time of relapse, genomic HLA typing of leukemic blasts could not detect the recipient's HLA haplotype that differed from the donor's. The loss of the haplotype was due to uniparental disomy. In vitro, the donor's T cells reacted against leukemic blasts obtained at the time of diagnosis, not against blasts obtained at relapse. The results indicate the presence of a mutation that allowed the leukemic cells to escape the immunosurveillance of the donor's T cells.
Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the donor. All five patients had a relapse, and at the time of relapse, genomic HLA typing of leukemic blasts could not detect the recipient's HLA haplotype that differed from the donor's.
Transplantation of hematopoietic stem cells from a haploidentical family donor who shares only one HLA haplotype with the recipient is a potentially curative option for patients with high-risk hematologic cancers who lack an HLA-matched donor.
1
–
3
The major limitation of this strategy is the risk of severe graft-versus-host disease (GVHD), which can result from alloreactions mediated by donor T cells against the recipient's unshared HLA haplotype. Since the publication of studies on extensively T-cell–depleted grafts,
1
,
2
a variety of strategies have been developed to prevent or control GVHD after transfer of haploidentical T cells.
4
,
5
The feasibility and efficacy of . . . Transplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer and are at high risk for relapse. The donor T-cell infusions associated with such transplantation can promote post-transplantation immune reconstitution and control residual disease.BACKGROUNDTransplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer and are at high risk for relapse. The donor T-cell infusions associated with such transplantation can promote post-transplantation immune reconstitution and control residual disease.We identified 43 patients who underwent haploidentical transplantation and infusion of donor T cells for acute myeloid leukemia or myelodysplastic syndrome and conducted post-transplantation studies that included morphologic examination of bone marrow, assessment of hematopoietic chimerism with the use of short-tandem-repeat amplification, and HLA typing. The genomic rearrangements in mutant variants of leukemia were studied with the use of genomic HLA typing, microsatellite mapping, and single-nucleotide-polymorphism arrays. The post-transplantation immune responses against the original cells and the mutated leukemic cells were analyzed with the use of mixed lymphocyte cultures.METHODSWe identified 43 patients who underwent haploidentical transplantation and infusion of donor T cells for acute myeloid leukemia or myelodysplastic syndrome and conducted post-transplantation studies that included morphologic examination of bone marrow, assessment of hematopoietic chimerism with the use of short-tandem-repeat amplification, and HLA typing. The genomic rearrangements in mutant variants of leukemia were studied with the use of genomic HLA typing, microsatellite mapping, and single-nucleotide-polymorphism arrays. The post-transplantation immune responses against the original cells and the mutated leukemic cells were analyzed with the use of mixed lymphocyte cultures.In 5 of 17 patients with leukemia relapse after haploidentical transplantation and infusion of donor T cells, we identified mutant variants of the original leukemic cells. In the mutant leukemic cells, the HLA haplotype that differed from the donor's haplotype had been lost because of acquired uniparental disomy of chromosome 6p. T cells from the donor and the patient after transplantation did not recognize the mutant leukemic cells, whereas the original leukemic cells taken at the time of diagnosis were efficiently recognized and killed.RESULTSIn 5 of 17 patients with leukemia relapse after haploidentical transplantation and infusion of donor T cells, we identified mutant variants of the original leukemic cells. In the mutant leukemic cells, the HLA haplotype that differed from the donor's haplotype had been lost because of acquired uniparental disomy of chromosome 6p. T cells from the donor and the patient after transplantation did not recognize the mutant leukemic cells, whereas the original leukemic cells taken at the time of diagnosis were efficiently recognized and killed.After transplantation of haploidentical hematopoietic stem cells and infusion of donor T cells, leukemic cells can escape from the donor's antileukemic T cells through the loss of the mismatched HLA haplotype. This event leads to relapse.CONCLUSIONSAfter transplantation of haploidentical hematopoietic stem cells and infusion of donor T cells, leukemic cells can escape from the donor's antileukemic T cells through the loss of the mismatched HLA haplotype. This event leads to relapse. Background Transplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer and are at high risk for relapse. The donor T-cell infusions associated with such transplantation can promote post-transplantation immune reconstitution and control residual disease. Methods We identified 43 patients who underwent haploidentical transplantation and infusion of donor T cells for acute myeloid leukemia or myelodysplastic syndrome and conducted post-transplantation studies that included morphologic examination of bone marrow, assessment of hematopoietic chimerism with the use of short-tandem-repeat amplification, and HLA typing. The genomic rearrangements in mutant variants of leukemia were studied with the use of genomic HLA typing, microsatellite mapping, and single-nucleotide-polymorphism arrays. The post-transplantation immune responses against the original cells and the mutated leukemic cells were analyzed with the use of mixed lymphocyte cultures. Results In 5 of 17 patients with leukemia relapse after haploidentical transplantation and infusion of donor T cells, we identified mutant variants of the original leukemic cells. In the mutant leukemic cells, the HLA haplotype that differed from the donor's haplotype had been lost because of acquired uniparental disomy of chromosome 6p. T cells from the donor and the patient after transplantation did not recognize the mutant leukemic cells, whereas the original leukemic cells taken at the time of diagnosis were efficiently recognized and killed. Conclusions After transplantation of haploidentical hematopoietic stem cells and infusion of donor T cells, leukemic cells can escape from the donor's antileukemic T cells through the loss of the mismatched HLA haplotype. This event leads to relapse. Transplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer and are at high risk for relapse. The donor T-cell infusions associated with such transplantation can promote post-transplantation immune reconstitution and control residual disease. We identified 43 patients who underwent haploidentical transplantation and infusion of donor T cells for acute myeloid leukemia or myelodysplastic syndrome and conducted post-transplantation studies that included morphologic examination of bone marrow, assessment of hematopoietic chimerism with the use of short-tandem-repeat amplification, and HLA typing. The genomic rearrangements in mutant variants of leukemia were studied with the use of genomic HLA typing, microsatellite mapping, and single-nucleotide-polymorphism arrays. The post-transplantation immune responses against the original cells and the mutated leukemic cells were analyzed with the use of mixed lymphocyte cultures. In 5 of 17 patients with leukemia relapse after haploidentical transplantation and infusion of donor T cells, we identified mutant variants of the original leukemic cells. In the mutant leukemic cells, the HLA haplotype that differed from the donor's haplotype had been lost because of acquired uniparental disomy of chromosome 6p. T cells from the donor and the patient after transplantation did not recognize the mutant leukemic cells, whereas the original leukemic cells taken at the time of diagnosis were efficiently recognized and killed. After transplantation of haploidentical hematopoietic stem cells and infusion of donor T cells, leukemic cells can escape from the donor's antileukemic T cells through the loss of the mismatched HLA haplotype. This event leads to relapse. |
| Author | Cosentino, Cristian Casucci, Monica Bordignon, Claudio Ciceri, Fabio Perrelli, Nicola Flavio Bernardi, Massimo Forno, Barbara Peccatori, Jacopo Stanghellini, Maria Teresa Lupo Vago, Luca Angius, Andrea Zanussi, Monica Mazzi, Benedetta Roncarolo, Maria Grazia Rossini, Silvano Bonini, Chiara Perna, Serena Kimi Bondanza, Attilio Barlassina, Cristina Torri, Federica Corti, Consuelo Ferrari, Maurizio Fleischhauer, Katharina |
| Author_xml | – sequence: 1 givenname: Luca surname: Vago fullname: Vago, Luca – sequence: 2 givenname: Serena Kimi surname: Perna fullname: Perna, Serena Kimi – sequence: 3 givenname: Monica surname: Zanussi fullname: Zanussi, Monica – sequence: 4 givenname: Benedetta surname: Mazzi fullname: Mazzi, Benedetta – sequence: 5 givenname: Cristina surname: Barlassina fullname: Barlassina, Cristina – sequence: 6 givenname: Maria Teresa Lupo surname: Stanghellini fullname: Stanghellini, Maria Teresa Lupo – sequence: 7 givenname: Nicola Flavio surname: Perrelli fullname: Perrelli, Nicola Flavio – sequence: 8 givenname: Cristian surname: Cosentino fullname: Cosentino, Cristian – sequence: 9 givenname: Federica surname: Torri fullname: Torri, Federica – sequence: 10 givenname: Andrea surname: Angius fullname: Angius, Andrea – sequence: 11 givenname: Barbara surname: Forno fullname: Forno, Barbara – sequence: 12 givenname: Monica surname: Casucci fullname: Casucci, Monica – sequence: 13 givenname: Massimo surname: Bernardi fullname: Bernardi, Massimo – sequence: 14 givenname: Jacopo surname: Peccatori fullname: Peccatori, Jacopo – sequence: 15 givenname: Consuelo surname: Corti fullname: Corti, Consuelo – sequence: 16 givenname: Attilio surname: Bondanza fullname: Bondanza, Attilio – sequence: 17 givenname: Maurizio surname: Ferrari fullname: Ferrari, Maurizio – sequence: 18 givenname: Silvano surname: Rossini fullname: Rossini, Silvano – sequence: 19 givenname: Maria Grazia surname: Roncarolo fullname: Roncarolo, Maria Grazia – sequence: 20 givenname: Claudio surname: Bordignon fullname: Bordignon, Claudio – sequence: 21 givenname: Chiara surname: Bonini fullname: Bonini, Chiara – sequence: 22 givenname: Fabio surname: Ciceri fullname: Ciceri, Fabio – sequence: 23 givenname: Katharina surname: Fleischhauer fullname: Fleischhauer, Katharina |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21804290$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19641204$$D View this record in MEDLINE/PubMed |
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| Keywords | Incompatibility Medicine HLA-System Stem cell Major histocompatibility system Loss Hematopoietic cell Stem cell transplantation Class I histocompatibility antigen Tumor cell |
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| Snippet | Five patients with acute myelogenous leukemia received hematopoietic stem-cell transplants from a haploidentical donor. They also received T cells from the... Transplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer and are at... Background Transplantation of hematopoietic stem cells from partially matched family donors is a promising therapy for patients who have a hematologic cancer... |
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| SubjectTerms | Adult Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Bone marrow Bone marrow, stem cells transplantation. Graft versus host reaction Cells, Cultured Chromosomes, Human, Pair 6 General aspects Graft vs Leukemia Effect - genetics Graft vs Leukemia Effect - immunology Haplotypes Hematopoietic Stem Cell Transplantation Histocompatibility Testing HLA Antigens - genetics Humans Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - immunology Leukemia, Myeloid, Acute - therapy Lymphocytes Major Histocompatibility Complex Medical sciences Mutation Myelodysplastic Syndromes Recurrence Retrospective Studies Stem cells T-Lymphocytes - immunology Transfusions. Complications. Transfusion reactions. Cell and gene therapy Transplantation Chimera Transplants & implants |
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| Title | Loss of Mismatched HLA in Leukemia after Stem-Cell Transplantation |
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