Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy
Abstract Acute myeloid leukemia (AML) is a heterogeneous disease characterized by the expansion of immature myeloid cells in the bone marrow (BM) and peripheral blood (PB) resulting in failure of normal hematopoiesis and life-threating cytopenia. Allogeneic hematopoietic stem cell transplantation (a...
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Format: | Article |
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BMC
2023-11-01
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Series: | Molecular Cancer |
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Online Access: | https://doi.org/10.1186/s12943-023-01889-6 |
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author | Tatjana Sauerer Giuliano Filippini Velázquez Christoph Schmid |
author_facet | Tatjana Sauerer Giuliano Filippini Velázquez Christoph Schmid |
author_sort | Tatjana Sauerer |
collection | DOAJ |
description | Abstract Acute myeloid leukemia (AML) is a heterogeneous disease characterized by the expansion of immature myeloid cells in the bone marrow (BM) and peripheral blood (PB) resulting in failure of normal hematopoiesis and life-threating cytopenia. Allogeneic hematopoietic stem cell transplantation (allo-HCT) is an established therapy with curative potential. Nevertheless, post-transplant relapse is common and associated with poor prognosis, representing the major cause of death after allo-HCT. The occurrence of relapse after initially successful allo-HCT indicates that the donor immune system is first able to control the leukemia, which at a later stage develops evasion strategies to escape from immune surveillance. In this review we first provide a comprehensive overview of current knowledge regarding immune escape in AML after allo-HCT, including dysregulated HLA, alterations in immune checkpoints and changes leading to an immunosuppressive tumor microenvironment. In the second part, we draw the line from bench to bedside and elucidate to what extend immune escape mechanisms of relapsed AML are yet exploited in treatment strategies. Finally, we give an outlook how new emerging technologies could help to improve the therapy for these patients, and elucidate potential new treatment options. |
first_indexed | 2024-03-11T11:07:42Z |
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id | doaj.art-a5ef648ec10743a7a70ccb15d4c61d8a |
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issn | 1476-4598 |
language | English |
last_indexed | 2024-03-11T11:07:42Z |
publishDate | 2023-11-01 |
publisher | BMC |
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series | Molecular Cancer |
spelling | doaj.art-a5ef648ec10743a7a70ccb15d4c61d8a2023-11-12T12:08:30ZengBMCMolecular Cancer1476-45982023-11-0122112210.1186/s12943-023-01889-6Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapyTatjana Sauerer0Giuliano Filippini Velázquez1Christoph Schmid2Department of Hematology and Oncology, Augsburg University Hospital and Medical Faculty, Bavarian Cancer Research Center (BZKF) and Comprehensive Cancer Center AugsburgDepartment of Hematology and Oncology, Augsburg University Hospital and Medical Faculty, Bavarian Cancer Research Center (BZKF) and Comprehensive Cancer Center AugsburgDepartment of Hematology and Oncology, Augsburg University Hospital and Medical Faculty, Bavarian Cancer Research Center (BZKF) and Comprehensive Cancer Center AugsburgAbstract Acute myeloid leukemia (AML) is a heterogeneous disease characterized by the expansion of immature myeloid cells in the bone marrow (BM) and peripheral blood (PB) resulting in failure of normal hematopoiesis and life-threating cytopenia. Allogeneic hematopoietic stem cell transplantation (allo-HCT) is an established therapy with curative potential. Nevertheless, post-transplant relapse is common and associated with poor prognosis, representing the major cause of death after allo-HCT. The occurrence of relapse after initially successful allo-HCT indicates that the donor immune system is first able to control the leukemia, which at a later stage develops evasion strategies to escape from immune surveillance. In this review we first provide a comprehensive overview of current knowledge regarding immune escape in AML after allo-HCT, including dysregulated HLA, alterations in immune checkpoints and changes leading to an immunosuppressive tumor microenvironment. In the second part, we draw the line from bench to bedside and elucidate to what extend immune escape mechanisms of relapsed AML are yet exploited in treatment strategies. Finally, we give an outlook how new emerging technologies could help to improve the therapy for these patients, and elucidate potential new treatment options.https://doi.org/10.1186/s12943-023-01889-6Acute myeloid leukemiaImmune escapeAllogeneic stem cell transplantationRelapseHuman leukocyte antigenImmune checkpoints |
spellingShingle | Tatjana Sauerer Giuliano Filippini Velázquez Christoph Schmid Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy Molecular Cancer Acute myeloid leukemia Immune escape Allogeneic stem cell transplantation Relapse Human leukocyte antigen Immune checkpoints |
title | Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy |
title_full | Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy |
title_fullStr | Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy |
title_full_unstemmed | Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy |
title_short | Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy |
title_sort | relapse of acute myeloid leukemia after allogeneic stem cell transplantation immune escape mechanisms and current implications for therapy |
topic | Acute myeloid leukemia Immune escape Allogeneic stem cell transplantation Relapse Human leukocyte antigen Immune checkpoints |
url | https://doi.org/10.1186/s12943-023-01889-6 |
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