Aberrant Lipid Metabolic Signatures in Acute Myeloid Leukemia
© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissionsoup.com..
Leukemogenesis is a complex process that involves multiple stages of mutation in either hematopoietic stem or progenitor cells, leading to cancer development over time. Acute myeloid leukemia (AML) is an aggressive malignancy that affects myeloid cells. The major disease burden is caused by immature blast cells, which are eliminated using conventional chemotherapies. Unfortunately, relapse is a leading cause of death in AML patients, with 30%-80% experiencing it within 2 years of initial treatment. The dominant cause of relapse in leukemia is the presence of therapy-resistant leukemic stem cells (LSCs). These cells express genes related to stemness that are frequently difficult to eradicate and tend to survive standard treatments. Studies have demonstrated that by targeting the metabolic pathways of LSCs, it is possible to improve outcomes and extend the survival of those afflicted by leukemia. The overwhelming evidence suggests that lipid metabolism is reprogrammed in LSCs, leading to an increase in fatty acid uptake and de novo lipogenesis. Genes regulating this process also play a crucial role in therapy evasion. In this concise review, we summarize the lipid metabolism in normal hematopoietic cells, AML blast cells, and AML LSCs. We also compare the lipid metabolic signatures in de novo versus therapy-resistant AML blast and LSCs. We further discuss the metabolic switches, cellular crosstalk, potential targets, and inhibitors of lipid metabolism that could alleviate treatment resistance and relapse.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:42 |
|---|---|
| Enthalten in: |
Stem cells (Dayton, Ohio) - 42(2024), 3 vom: 14. März, Seite 200-215 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Singh, Pooja [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Acute myeloid leukemia |
|---|
| Anmerkungen: |
Date Completed 15.03.2024 Date Revised 15.03.2024 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1093/stmcls/sxad095 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM366585878 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM366585878 | ||
| 003 | DE-627 | ||
| 005 | 20240315233027.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240108s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1093/stmcls/sxad095 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1330.xml |
| 035 | |a (DE-627)NLM366585878 | ||
| 035 | |a (NLM)38167958 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Singh, Pooja |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Aberrant Lipid Metabolic Signatures in Acute Myeloid Leukemia |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 15.03.2024 | ||
| 500 | |a Date Revised 15.03.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © The Author(s) 2024. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissionsoup.com. | ||
| 520 | |a Leukemogenesis is a complex process that involves multiple stages of mutation in either hematopoietic stem or progenitor cells, leading to cancer development over time. Acute myeloid leukemia (AML) is an aggressive malignancy that affects myeloid cells. The major disease burden is caused by immature blast cells, which are eliminated using conventional chemotherapies. Unfortunately, relapse is a leading cause of death in AML patients, with 30%-80% experiencing it within 2 years of initial treatment. The dominant cause of relapse in leukemia is the presence of therapy-resistant leukemic stem cells (LSCs). These cells express genes related to stemness that are frequently difficult to eradicate and tend to survive standard treatments. Studies have demonstrated that by targeting the metabolic pathways of LSCs, it is possible to improve outcomes and extend the survival of those afflicted by leukemia. The overwhelming evidence suggests that lipid metabolism is reprogrammed in LSCs, leading to an increase in fatty acid uptake and de novo lipogenesis. Genes regulating this process also play a crucial role in therapy evasion. In this concise review, we summarize the lipid metabolism in normal hematopoietic cells, AML blast cells, and AML LSCs. We also compare the lipid metabolic signatures in de novo versus therapy-resistant AML blast and LSCs. We further discuss the metabolic switches, cellular crosstalk, potential targets, and inhibitors of lipid metabolism that could alleviate treatment resistance and relapse | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a acute myeloid leukemia | |
| 650 | 4 | |a hematopoietic stem cells | |
| 650 | 4 | |a leukemic blast cells | |
| 650 | 4 | |a leukemic stem cells | |
| 650 | 4 | |a lipid metabolism | |
| 650 | 4 | |a relapse | |
| 650 | 7 | |a Lipids |2 NLM | |
| 700 | 1 | |a Murali, Roopak |e verfasserin |4 aut | |
| 700 | 1 | |a Shanmugam, Sri Gayathri |e verfasserin |4 aut | |
| 700 | 1 | |a Thomas, Steve |e verfasserin |4 aut | |
| 700 | 1 | |a Scott, Julius |e verfasserin |4 aut | |
| 700 | 1 | |a Warrier, Sudha |e verfasserin |4 aut | |
| 700 | 1 | |a Arfuso, Frank |e verfasserin |4 aut | |
| 700 | 1 | |a Dharmarajan, Arun |e verfasserin |4 aut | |
| 700 | 1 | |a Gandhirajan, Rajesh Kumar |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Stem cells (Dayton, Ohio) |d 1994 |g 42(2024), 3 vom: 14. März, Seite 200-215 |w (DE-627)NLM074655477 |x 1549-4918 |7 nnns |
| 773 | 1 | 8 | |g volume:42 |g year:2024 |g number:3 |g day:14 |g month:03 |g pages:200-215 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1093/stmcls/sxad095 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 42 |j 2024 |e 3 |b 14 |c 03 |h 200-215 | ||