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Somatic mtDNA mutation burden shapes metabolic plasticity in leukemogenesis.
Sci Adv
January 2025
Department of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Article Synopsis
- The study investigates how somatic mitochondrial DNA mutations influence the development of leukemia, specifically through experiments with hematopoietic progenitor cells (HPCs) from genetically modified mice.
- Researchers found that recipients of heterozygous mtDNA mutator HPCs had a higher spontaneous leukemia incidence, while homozygous mtDNA mutator HPCs had a lower incidence when combined with NMyc overexpression.
- Both types of HPCs exhibited mitochondrial function impairments, but only heterozygous HPCs adapted to the metabolic demands of NMyc overexpression, as demonstrated by altered glucose utilization linked to metabolic changes in homozygous HPCs.
CORRECTION CRITERIA FOR THE BONE TISSUE STRUCTURE DISORDERS IN CHILDREN LIVING IN RADIOLOGICALLY CONTAMINATED TERRITORIES AFTER THE CHORNOBYL NPP ACCIDENT.
Probl Radiac Med Radiobiol
December 2024
State Institution «National Research Center of Radiation Medicine, Hematology and Oncology of the National Academy of Medical Sciences of Ukraine», 53 Yuriia Illienka Str., Kyiv, 04050, Ukraine.
Objective: To determine the structure of abnormalities of bone tissue and substantiate the management tactics inacute lymphoblastic leukemia (ALL) pediatric patients and in children with no oncohematological disorders, livingin radiologically contaminated territories (RCT).
Materials And Methods: Children (n = 220) living in RCT were the study participants i.e.
Emerging functions of FMNL1 in myeloid neoplasms: insights from bioinformatics to biological and pharmacological landscapes.
Transl Cancer Res
November 2024
Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo, Brazil.
Background: Myeloid neoplasms encompass disorders characterized by abnormal myeloid cell proliferation and differentiation, including myelodysplastic syndromes (MDS), myeloproliferative neoplasms, acute myeloid leukemia (AML), and chronic myeloid leukemia (CML). Formin-like protein 1 (FMNL1) is involved in the regulation of the actin cytoskeleton and is predominantly expressed in hematopoietic cells. Given its role in leukemia cell proliferation, survival, migration, and invasion, this study investigates FMNL1 expression in normal hematopoiesis and myeloid neoplasms and explores associations with clinical-laboratory characteristics, mutational status, and survival outcomes in AML.
View Article and Find Full Text PDFPRMT1 Promotes the Self-renewal of Leukemia Stem Cells by Regulating Protein Synthesis.
Adv Sci (Weinh)
December 2024
State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou, 510632, China.
The application of tyrosine kinase inhibitors (TKIs) has revolutionized the management of chronic myeloid leukemia (CML). However, disease relapse and progression particularly due to persistent leukemia stem cells (LSCs) remain a big challenge in the clinic. Therefore, validation of the therapeutic vulnerability in LSCs is urgently needed.
View Article and Find Full Text PDFIron regulates MT1-MMP-mediated proMMP-2 activation and cancer cell invasion.
Biochem Biophys Res Commun
January 2025
Division of Education for Global Standard, Institute of Liberal Arts and Science, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan. Electronic address:
Cellular iron plays a crucial role in many crucial physiological processes. Excessive iron retention due to iron influx and efflux imbalance contributes to cancer development and proliferation, as well as malignant conversion. Membrane-type 1 matrix metalloproteinase (MT1-MMP) plays a crucial role in tumor invasion and metastasis, because this enzyme can degrade various extracellular matrix components and cleave membrane tethered proteins on the cell surface.
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