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The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia

In general, acute myeloid leukemia (AML) is an aggressive and heterogeneous disease that is characterized by rapid cellular proliferation and high mortality. One of the mutations related to AML is the Flt3-ITD mutation, which is found in approximately 25% of patients. In this mini-review, we investi...

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Autores principales: Shapoorian, Hooriyeh, Zalpoor, Hamidreza, Ganjalikhani-Hakemi, Mazdak
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8975045/
https://www.ncbi.nlm.nih.gov/pubmed/35402842
http://dx.doi.org/10.1097/BS9.0000000000000092
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author Shapoorian, Hooriyeh
Zalpoor, Hamidreza
Ganjalikhani-Hakemi, Mazdak
author_facet Shapoorian, Hooriyeh
Zalpoor, Hamidreza
Ganjalikhani-Hakemi, Mazdak
author_sort Shapoorian, Hooriyeh
collection PubMed
description In general, acute myeloid leukemia (AML) is an aggressive and heterogeneous disease that is characterized by rapid cellular proliferation and high mortality. One of the mutations related to AML is the Flt3-ITD mutation, which is found in approximately 25% of patients. In this mini-review, we investigate the function of dendritic cells and T cells based on Flt3-ITD mutation and immune evasion as a result of this abnormality. Finally, we discuss some AML therapeutic strategies, including targeting Flt3 on DCs and TIM-3 on T cells as immune receptors to treat this hematopoietic malignancy.
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spelling pubmed-89750452022-04-07 The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia Shapoorian, Hooriyeh Zalpoor, Hamidreza Ganjalikhani-Hakemi, Mazdak Blood Sci Review Article In general, acute myeloid leukemia (AML) is an aggressive and heterogeneous disease that is characterized by rapid cellular proliferation and high mortality. One of the mutations related to AML is the Flt3-ITD mutation, which is found in approximately 25% of patients. In this mini-review, we investigate the function of dendritic cells and T cells based on Flt3-ITD mutation and immune evasion as a result of this abnormality. Finally, we discuss some AML therapeutic strategies, including targeting Flt3 on DCs and TIM-3 on T cells as immune receptors to treat this hematopoietic malignancy. Lippincott Williams & Wilkins 2021-10-18 /pmc/articles/PMC8975045/ /pubmed/35402842 http://dx.doi.org/10.1097/BS9.0000000000000092 Text en Copyright © 2021 The Authors. Published by Wolters Kluwer Health Inc., on behalf of the Chinese Association for Blood Sciences. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/)
spellingShingle Review Article
Shapoorian, Hooriyeh
Zalpoor, Hamidreza
Ganjalikhani-Hakemi, Mazdak
The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title_full The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title_fullStr The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title_full_unstemmed The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title_short The correlation between Flt3-ITD mutation in dendritic cells with TIM-3 expression in acute myeloid leukemia
title_sort correlation between flt3-itd mutation in dendritic cells with tim-3 expression in acute myeloid leukemia
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8975045/
https://www.ncbi.nlm.nih.gov/pubmed/35402842
http://dx.doi.org/10.1097/BS9.0000000000000092
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