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Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies
Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years...
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Published in: | Cancers 2019-12, Vol.12 (1), p.69 |
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description | Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years (especially in younger patients) that allogenic hematopoietic stem cell transplantation (allo-HSCT) remains the only curative treatment in AML and the first therapeutic option for high-risk patients. After allo-HSCT, relapse is still a major complication, and is observed in about 50% of patients. Current evidence suggests that relapse is not due to clonal evolution, but instead to the ability of the AML cell population to escape immune control by a variety of mechanisms including the altered expression of HLA-molecules, production of anti-inflammatory cytokines, relevant metabolic changes and expression of immune checkpoint (ICP) inhibitors capable of "switching-off" the immune response against leukemic cells. Here, we review the main mechanisms of immune escape and identify potential strategies to overcome these mechanisms. |
doi_str_mv | 10.3390/cancers12010069 |
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Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years (especially in younger patients) that allogenic hematopoietic stem cell transplantation (allo-HSCT) remains the only curative treatment in AML and the first therapeutic option for high-risk patients. After allo-HSCT, relapse is still a major complication, and is observed in about 50% of patients. Current evidence suggests that relapse is not due to clonal evolution, but instead to the ability of the AML cell population to escape immune control by a variety of mechanisms including the altered expression of HLA-molecules, production of anti-inflammatory cytokines, relevant metabolic changes and expression of immune checkpoint (ICP) inhibitors capable of "switching-off" the immune response against leukemic cells. Here, we review the main mechanisms of immune escape and identify potential strategies to overcome these mechanisms.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers12010069</identifier><identifier>PMID: 31881776</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acute myeloid leukemia ; Antigens ; Chemotherapy ; Cytokines ; Genes ; Hematopoietic stem cells ; Histocompatibility antigen HLA ; Immune checkpoint ; Immune evasion ; Immune response ; Immunology ; Immunotherapy ; Inflammation ; Leukemia ; Lymphocytes ; Myeloid leukemia ; Review ; Risk groups ; Stem cell transplantation ; Stem cells ; Transplants & implants</subject><ispartof>Cancers, 2019-12, Vol.12 (1), p.69</ispartof><rights>2019 by the authors. Licensee MDPI, Basel, Switzerland. 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Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years (especially in younger patients) that allogenic hematopoietic stem cell transplantation (allo-HSCT) remains the only curative treatment in AML and the first therapeutic option for high-risk patients. After allo-HSCT, relapse is still a major complication, and is observed in about 50% of patients. Current evidence suggests that relapse is not due to clonal evolution, but instead to the ability of the AML cell population to escape immune control by a variety of mechanisms including the altered expression of HLA-molecules, production of anti-inflammatory cytokines, relevant metabolic changes and expression of immune checkpoint (ICP) inhibitors capable of "switching-off" the immune response against leukemic cells. Here, we review the main mechanisms of immune escape and identify potential strategies to overcome these mechanisms.</description><subject>Acute myeloid leukemia</subject><subject>Antigens</subject><subject>Chemotherapy</subject><subject>Cytokines</subject><subject>Genes</subject><subject>Hematopoietic stem cells</subject><subject>Histocompatibility antigen HLA</subject><subject>Immune checkpoint</subject><subject>Immune evasion</subject><subject>Immune response</subject><subject>Immunology</subject><subject>Immunotherapy</subject><subject>Inflammation</subject><subject>Leukemia</subject><subject>Lymphocytes</subject><subject>Myeloid leukemia</subject><subject>Review</subject><subject>Risk groups</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transplants & implants</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkc1LXTEQxUNpUbGu3ZVAN7p4NR_3JTddFOShPsG2C1_XYYxz-yI3yW2SK_jfN8UPrNlMyPzmMCeHkEPOvkhp2ImD6DAXLhhnTJl3ZE8wLRZKme79q_suOSjljrUjJddK75Bdyfuea632yHAZwhyRnhUHE1IYKma6xgA1Tclj9Y5eVwx0heNINxlimUaIFapPkR6tr1eb46_0PKdAv6PbQvQlFFoT_ZHusQ1sMcPksXwkHwYYCx481X3y6_xss1ovrn5eXK5Orxau63VdiK4flDBcMhiUkZxplFJzXHaam1sub5xDZfitQ8EGLlGDgE63R1B64KyX--Tbo-403wRsXKwZRjtlHyA_2ATe_t-Jfmt_p3urGVdLYZrA0ZNATn9mLNUGX1wzDxHTXKxofyiWuu9FQz-_Qe_SnGOzZ0VbWDHTNBt18ki5nErJOLwsw5n9F6N9E2Ob-PTawwv_HJr8C12mmaA</recordid><startdate>20191225</startdate><enddate>20191225</enddate><creator>Bernasconi, Paolo</creator><creator>Borsani, Oscar</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6043-3367</orcidid><orcidid>https://orcid.org/0000-0001-7805-7806</orcidid></search><sort><creationdate>20191225</creationdate><title>Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies</title><author>Bernasconi, Paolo ; Borsani, Oscar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-248f629130af693107e3371e54719d13bcce691dce20f13e7a2a47ccea67f1083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acute myeloid leukemia</topic><topic>Antigens</topic><topic>Chemotherapy</topic><topic>Cytokines</topic><topic>Genes</topic><topic>Hematopoietic stem cells</topic><topic>Histocompatibility antigen HLA</topic><topic>Immune checkpoint</topic><topic>Immune evasion</topic><topic>Immune response</topic><topic>Immunology</topic><topic>Immunotherapy</topic><topic>Inflammation</topic><topic>Leukemia</topic><topic>Lymphocytes</topic><topic>Myeloid leukemia</topic><topic>Review</topic><topic>Risk groups</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Transplants & implants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bernasconi, Paolo</creatorcontrib><creatorcontrib>Borsani, Oscar</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bernasconi, Paolo</au><au>Borsani, Oscar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2019-12-25</date><risdate>2019</risdate><volume>12</volume><issue>1</issue><spage>69</spage><pages>69-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. 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subjects | Acute myeloid leukemia Antigens Chemotherapy Cytokines Genes Hematopoietic stem cells Histocompatibility antigen HLA Immune checkpoint Immune evasion Immune response Immunology Immunotherapy Inflammation Leukemia Lymphocytes Myeloid leukemia Review Risk groups Stem cell transplantation Stem cells Transplants & implants |
title | Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies |
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