Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Metabolic characterization of imatinib-resistant BCR-ABL T315I chronic myeloid leukemia cells indicates down-regulation of glycolytic pathway and low ROS production.

Leukemia & lymphoma - 1 Sept 2016

Ko Byung Woong, Han Jeongsu, Heo Jun Young, Jang Yunseon, Kim Soo Jeong, Kim Jungim, Lee Min Joung, Ryu Min Jeong, Song Ik Chan, Jo Young Suk, Kweon Gi Ryang

Abstract excerpt

Long-term imatinib treatment induces drug-resistant chronic myeloid leukemia (CML) cells harboring T315I gate keeper mutation of breakpoint cluster region (BCR)-ABL oncogenic kinase. However, although cell proliferation is coupled with cellular energy status in CML carcinogenesis, the metabolic characteristics of T315I-mutant CML cells have never been investigated. Here, we analyzed cell proliferation activities...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antioxidants
Share to Energy Metabolism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Glycolysis

Share to Imatinib Mesylate

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Metabolic Networks and Pathways

Share to Reactive Oxygen Species

Source

Identifiers

PMID: 26854822
DOI: 10.3109/10428194.2016.1142086

Genes

BCR
SOD2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Metabolic characterization of imatinib-resistant BCR-ABL T315I chronic myeloid leukemia cells indicates down-regulation of glycolytic pathway and low ROS production.PMID 26854822Read ↗

Modulation of energy metabolism to overcome drug resistance in chronic myeloid leukemia cells through induction of autophagySemantic proximity Read ↗

Chronic myeloid leukemia stem cells display alterations in expression of genes involved in oxidative phosphorylation.Semantic proximity Read ↗

Exploiting metabolic vulnerabilities for personalized therapy in acute myeloid leukemiaSemantic proximity Read ↗

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in CancerSemantic proximity Read ↗

Mitochondrial metabolism as a potential therapeutic target in myeloid leukaemiaSemantic proximity Read ↗

Cell Cycle Regulation by Oncogenic Tyrosine Kinases in Myeloid Neoplasias: From Molecular Redox Mechanisms to Health ImplicationsSemantic proximity Read ↗

Energy metabolism is co-determined by genetic variants in chronic lymphocytic leukemia and influences drug sensitivitySemantic proximity Read ↗

The Glycolytic Gatekeeper PDK1 defines different metabolic states between genetically distinct subtypes of human acute myeloid leukemia.Semantic proximity Read ↗

Reactive oxygen species (ROS) are a key determinant of cancer's metabolic phenotype.Semantic proximity Read ↗

The differential activation of metabolic pathways in leukemic cells depending on their genotype and micro-environmental stress.Semantic proximity Read ↗

Oxidative stress and hypoxia in normal and leukemic stem cells.Semantic proximity Read ↗

GFI1B acts as a metabolic regulator in hematopoiesis and acute myeloid leukemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.