Parasitic Behavior of Leukemic Cells in Systemic Host Metabolism.

Cell Metab

The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network, Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, ON, Canada; The University of Hong Kong, Hong Kong. Electronic address:

Published: December 2018

Metabolic reprogramming is a hallmark of cancer cell metabolism. Recently, in Cancer Cell, Ye and colleagues (2018) reported that leukemic cells have the capacity to modulate glucose metabolism in multiple organs of their host, thereby increasing the glucose resources available for malignant cell growth.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cmet.2018.11.011DOI Listing

Publication Analysis

Top Keywords

leukemic cells
8
cancer cell
8
parasitic behavior
4
behavior leukemic
4
cells systemic
4
systemic host
4
host metabolism
4
metabolism metabolic
4
metabolic reprogramming
4
reprogramming hallmark
4

Similar Publications

CD56 CD16 cells represent a distinct mature NK cell subset with altered phenotype and are associated with adverse clinical outcome upon expansion in AML.

Front Immunol

January 2025

Team Immunity and Cancer, Cancer Research Center of Marseille (CRCM), Inserm U1068, CNRS UMR7258, Paoli-Calmettes Institute, University of Aix-Marseille UM105, Marseille, France.

Introduction: Acute myeloid leukemia (AML) is a rare haematological cancer with poor 5-years overall survival (OS) and high relapse rate. Leukemic cells are sensitive to Natural Killer (NK) cell mediated killing. However, NK cells are highly impaired in AML, which promote AML immune escape from NK cell immune surveillance.

View Article and Find Full Text PDF

Non-myeloablative hematopoietic cell transplantation (HCT) is a curative option for individuals with sickle cell disease (SCD). Our traditional goal with this approach has been to achieve a state of mixed donor/recipient chimerism. Recently, we reported an increased risk of hematologic malignancies (HMs) in adults with SCD following graft failure or mixed chimerism.

View Article and Find Full Text PDF

Deciphering cell states and the cellular ecosystem to improve risk stratification in acute myeloid leukemia.

Brief Bioinform

November 2024

State Key Laboratory of Cellular Stress Biology, Xiang'an Hospital, School of Life Sciences, Faculty of Medicine and Life Sciences, Xiamen University, No. 4221, Xiang'an South Road, Xiamen, Fujian 361102, China.

Acute myeloid leukemia (AML) demonstrates significant cellular heterogeneity in both leukemic and immune cells, providing valuable insights into clinical outcomes. Here, we constructed an AML single-cell transcriptome atlas and proposed sciNMF workflow to systematically dissect underlying cellular heterogeneity. Notably, sciNMF identified 26 leukemic and immune cell states that linked to clinical variables, mutations, and prognosis.

View Article and Find Full Text PDF

Atovaquone and Selinexor as a Novel Combination Treatment Option in Acute Myeloid Leukemia.

Cancer Lett

January 2025

Division Pharmacology, Department of Pharmacology, Physiology and Microbiology, Karl Landsteiner University of Health Sciences, Krems, Austria. Electronic address:

Acute myeloid leukemia (AML) is the most common acute leukemia and is predominantly affecting older patients. It is a heterogenous disease, showing a broad spectrum of genomic alterations and mutations that influence the clinical outcome and treatment options. The expression of the signal transducer and activator of transcription 3 (STAT3) is often dysregulated in AML and its constitutive activation is associated with poor outcome.

View Article and Find Full Text PDF

One hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!