Feasible diet and circadian interventions reduce in vivo progression of FLT3-ITD-positive acute myeloid leukemia.

acute myeloid leukemia circadian rhythm diet time-restricted feeding

Journal

Cancer medicine
ISSN: 2045-7634
Titre abrégé: Cancer Med
Pays: United States
ID NLM: 101595310

Informations de publication

Date de publication:
Jan 2024
Historique:
revised: 29 11 2023
received: 02 05 2023
accepted: 09 01 2024
medline: 9 2 2024
pubmed: 9 2 2024
entrez: 9 2 2024
Statut: ppublish

Résumé

Acute myeloid leukemia (AML) with an internal tandem duplication in the fms-like tyrosine kinase receptor 3 gene (FLT3-ITD) is associated with poor survival, and few studies have examined the impact of modifiable behaviors, such as nutrient quality and timing, in this subset of acute leukemia. The influence of diet composition (low-sucrose and/or low-fat diets) and timing of diet were tested in tandem with anthracycline treatment in orthotopic xenograft mouse models. A pilot clinical study to test receptivity of pediatric leukemia patients to macronutrient matched foods was conducted. A role for the circadian protein, BMAL1 (brain and muscle ARNT-like 1), in effects of diet timing was studied by overexpression in FLT3-ITD-bearing AML cells. Reduced tumor burden in FLT3-ITD AML-bearing mice was observed with interventions utilizing low-sucrose and/or low-fat diets, or time-restricted feeding (TRF) compared to mice fed normal chow ad libitum. In a tasting study, macronutrient matched low-sucrose and low-fat meals were offered to pediatric acute leukemia patients who largely reported liking the meals. Expression of the circadian protein, BMAL1, was heightened with TRF and the low-sucrose diet. BMAL1 overexpression and treatment with a pharmacological inducer of BMAL1 was cytotoxic to FLT3-ITD AML cells. Mouse models for FLT3-ITD AML show that diet composition and timing slows progression of FLT3-ITD AML growth in vivo, potentially mediated by BMAL1. These interventions to enhance therapy efficacy show preliminary feasibility, as pediatric leukemia patients responded favorable to preparation of macronutrient matched meals.

Sections du résumé

BACKGROUND BACKGROUND
Acute myeloid leukemia (AML) with an internal tandem duplication in the fms-like tyrosine kinase receptor 3 gene (FLT3-ITD) is associated with poor survival, and few studies have examined the impact of modifiable behaviors, such as nutrient quality and timing, in this subset of acute leukemia.
METHODS METHODS
The influence of diet composition (low-sucrose and/or low-fat diets) and timing of diet were tested in tandem with anthracycline treatment in orthotopic xenograft mouse models. A pilot clinical study to test receptivity of pediatric leukemia patients to macronutrient matched foods was conducted. A role for the circadian protein, BMAL1 (brain and muscle ARNT-like 1), in effects of diet timing was studied by overexpression in FLT3-ITD-bearing AML cells.
RESULTS RESULTS
Reduced tumor burden in FLT3-ITD AML-bearing mice was observed with interventions utilizing low-sucrose and/or low-fat diets, or time-restricted feeding (TRF) compared to mice fed normal chow ad libitum. In a tasting study, macronutrient matched low-sucrose and low-fat meals were offered to pediatric acute leukemia patients who largely reported liking the meals. Expression of the circadian protein, BMAL1, was heightened with TRF and the low-sucrose diet. BMAL1 overexpression and treatment with a pharmacological inducer of BMAL1 was cytotoxic to FLT3-ITD AML cells.
CONCLUSIONS CONCLUSIONS
Mouse models for FLT3-ITD AML show that diet composition and timing slows progression of FLT3-ITD AML growth in vivo, potentially mediated by BMAL1. These interventions to enhance therapy efficacy show preliminary feasibility, as pediatric leukemia patients responded favorable to preparation of macronutrient matched meals.

Identifiants

pubmed: 38334474
doi: 10.1002/cam4.6949
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e6949

Subventions

Organisme : NIH HHS
ID : R21NR019532
Pays : United States
Organisme : NIH HHS
ID : P30 CA016672
Pays : United States

Informations de copyright

© 2024 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

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Auteurs

Megan Rodriguez (M)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Baharan Fekry (B)

Institute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center (UT Health), Houston, Texas, USA.

Brianna Murphy (B)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Mary Figueroa (M)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
University of Texas MD Anderson Cancer Center UT Health Houston Graduate School of Biomedical Sciences, Houston, Texas, USA.

Tiewei Cheng (T)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Margaret Raber (M)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
School of Public Health, Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas, Houston, Texas, USA.

Lisa Wartenberg (L)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Donna Bell (D)

Department of Pediatrics Patient Care, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Lisa Triche (L)

Department of Pediatrics Patient Care, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Karla Crawford (K)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Huaxian Ma (H)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Kendra Allton (K)

Bionutrition Research Core, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Ruwaida Ahmed (R)

Institute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center (UT Health), Houston, Texas, USA.

Jaime Tran (J)

Institute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center (UT Health), Houston, Texas, USA.

Christine Ranieri (C)

Bionutrition Research Core, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Marina Konopleva (M)

Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Michelle Barton (M)

Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Cesar Nunez (C)

Department of Pediatrics Patient Care, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Kristin Eckel-Mahan (K)

Institute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center (UT Health), Houston, Texas, USA.

Joya Chandra (J)

Department of Pediatrics-Research, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.

Classifications MeSH