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Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples

Cellular metabolic changes reflect the characteristics of patients with acute myeloid leukemia (AML) caused by genetic variations, which are important in establishing AML treatment. However, little is known about the metabolic profile of patients with genetic variation-induced AML. Furthermore, the...

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Autores principales: Kim, Hyun Kyu, Son, Su Young, Oh, Jae Sang, Song, Ye Na, Byun, Ja Min, Koh, Youngil, Hong, Junshik, Yoon, Sung-Soo, Lee, Choong Hwan, Shin, Dong-Yeop, Lee, Man Ryul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471543/
https://www.ncbi.nlm.nih.gov/pubmed/34564403
http://dx.doi.org/10.3390/metabo11090586
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author Kim, Hyun Kyu
Son, Su Young
Oh, Jae Sang
Song, Ye Na
Byun, Ja Min
Koh, Youngil
Hong, Junshik
Yoon, Sung-Soo
Lee, Choong Hwan
Shin, Dong-Yeop
Lee, Man Ryul
author_facet Kim, Hyun Kyu
Son, Su Young
Oh, Jae Sang
Song, Ye Na
Byun, Ja Min
Koh, Youngil
Hong, Junshik
Yoon, Sung-Soo
Lee, Choong Hwan
Shin, Dong-Yeop
Lee, Man Ryul
author_sort Kim, Hyun Kyu
collection PubMed
description Cellular metabolic changes reflect the characteristics of patients with acute myeloid leukemia (AML) caused by genetic variations, which are important in establishing AML treatment. However, little is known about the metabolic profile of patients with genetic variation-induced AML. Furthermore, the metabolites differ with disease progression. Here, metabolites in the bone marrow serum of ten patients with AML and healthy individuals were analyzed using gas chromatography–mass spectrometry. Compared with that in healthy individuals, expression of most metabolites decreased in patients with AML; hydroxylamine, 2-hydroxybutyric acid, monomethylphosphate, and ethylphosphate expression was unusually increased in the patients. We further examined serial metabolite changes across the initial diagnosis, postremission, and relapse phases. Patients with relapse showed increased metabolite expression compared with those in the diagnostic phase, confirming that patients with AML had aggressively modified leukemic cells. However, a clear difference in metabolite distribution was not observed between the diagnosis and complete remission phases, suggesting that the metabolic microenvironment did not change significantly despite complete remission. Interestingly, metabolite profiles differed with genetic variations in leukemic cells. Our results, which were obtained using paired samples collected during AML progression, provide valuable insights for identifying vulnerable targets in the AML metabolome and developing new treatment strategies.
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spelling pubmed-84715432021-09-28 Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples Kim, Hyun Kyu Son, Su Young Oh, Jae Sang Song, Ye Na Byun, Ja Min Koh, Youngil Hong, Junshik Yoon, Sung-Soo Lee, Choong Hwan Shin, Dong-Yeop Lee, Man Ryul Metabolites Article Cellular metabolic changes reflect the characteristics of patients with acute myeloid leukemia (AML) caused by genetic variations, which are important in establishing AML treatment. However, little is known about the metabolic profile of patients with genetic variation-induced AML. Furthermore, the metabolites differ with disease progression. Here, metabolites in the bone marrow serum of ten patients with AML and healthy individuals were analyzed using gas chromatography–mass spectrometry. Compared with that in healthy individuals, expression of most metabolites decreased in patients with AML; hydroxylamine, 2-hydroxybutyric acid, monomethylphosphate, and ethylphosphate expression was unusually increased in the patients. We further examined serial metabolite changes across the initial diagnosis, postremission, and relapse phases. Patients with relapse showed increased metabolite expression compared with those in the diagnostic phase, confirming that patients with AML had aggressively modified leukemic cells. However, a clear difference in metabolite distribution was not observed between the diagnosis and complete remission phases, suggesting that the metabolic microenvironment did not change significantly despite complete remission. Interestingly, metabolite profiles differed with genetic variations in leukemic cells. Our results, which were obtained using paired samples collected during AML progression, provide valuable insights for identifying vulnerable targets in the AML metabolome and developing new treatment strategies. MDPI 2021-08-31 /pmc/articles/PMC8471543/ /pubmed/34564403 http://dx.doi.org/10.3390/metabo11090586 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Hyun Kyu
Son, Su Young
Oh, Jae Sang
Song, Ye Na
Byun, Ja Min
Koh, Youngil
Hong, Junshik
Yoon, Sung-Soo
Lee, Choong Hwan
Shin, Dong-Yeop
Lee, Man Ryul
Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title_full Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title_fullStr Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title_full_unstemmed Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title_short Metabolic Profiling during Acute Myeloid Leukemia Progression Using Paired Clinical Bone Marrow Serum Samples
title_sort metabolic profiling during acute myeloid leukemia progression using paired clinical bone marrow serum samples
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471543/
https://www.ncbi.nlm.nih.gov/pubmed/34564403
http://dx.doi.org/10.3390/metabo11090586
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