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

Chemotherapeutic drugs elicit stemness and metabolic alteration to mediate acquired drug-resistant phenotype in acute myeloid leukemia cell lines.

Leukemia research - 1 May 2023

Illangeswaran Raveen Stephen Stallon, Jebanesan Daniel Zechariah Paul, Sivakumar Kezia Kanimozhi, Vidhyadharan Rakhi Thalayattu, Rajamani Bharathi M, Janet Nancy Beryl, David Ernest, Velayudhan Shaji Ramachandran, Mathews Vikram, Balasubramanian Poonkuzhali

Abstract excerpt

Chemotherapy resistance leading to disease relapse is a significant barrier in treating acute myeloid leukemia (AML). Metabolic adaptations have been shown to contribute to therapy resistance. However, little is known about whether specific therapies cause specific metabolic changes. We established cytarabine-resistant (AraC-R) and Arsenic trioxide-resistant (ATO-R) AML cell lines, displaying distinct cell...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Agents
Share to Arsenic Trioxide

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to Cytarabine

Share to Leukemia, Myeloid, Acute

Share to Phenotype

Source

Identifiers

PMID: 36906941
DOI: 10.1016/j.leukres.2023.107054

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Chemotherapeutic drugs elicit stemness and metabolic alteration to mediate acquired drug-resistant phenotype in acute myeloid leukemia cell lines.PMID 36906941Read ↗

Metabolic adaptation drives arsenic trioxide resistance in acute promyelocytic leukemiaSemantic proximity Read ↗

Mechanisms of chemotherapy failure in refractory/relapsed acute myeloid leukemia: the role of cytarabine resistance and mitochondrial metabolismSemantic proximity Read ↗

Arsenic trioxide resistance in acute promyelocytic leukemia: More to it than PML mutationsSemantic proximity Read ↗

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

Advances in pathogenesis research and challenges in treatment development for acute myeloid leukemia.Semantic proximity Read ↗

Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative MetabolismSemantic proximity Read ↗

Activation of RAS/MAPK pathway confers MCL-1 mediated acquired resistance to BCL-2 inhibitor venetoclax in acute myeloid leukemiaSemantic proximity Read ↗

Mitochondrial metabolism as a target for acute myeloid leukemia treatmentSemantic proximity Read ↗

ASAH1-mediated sphingolipid metabolic reprogramming in venetoclax resistance of AML: beyond the monocytic phenotypes.Semantic proximity Read ↗

Targeting Cellular Metabolism in Acute Myeloid Leukemia and The Role of Patient Heterogeneity.Semantic proximity Read ↗

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

Targeting Acute Myeloid Leukemia Stem Cells Through Perturbation of Mitochondrial CalciumSemantic proximity Read ↗

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