c-Myc-Induced Therapy Resistance in Leukemia: Mechanisms and Emerging Therapeutic Opportunities

Dysregulation of the c-Myc oncogene is a pivotal event in leukemia pathogenesis and therapy resistance. This review synthesizes current evidence, illustrating that c-Myc drives leukemogenesis by enhancing proliferation, inhibiting apoptosis, and upregulating immune checkpoints like PD-L1. Its overexpression is linked to poor treatment outcomes across various leukemia subtypes. Directly targeting c-Myc remains challenging; however, indirect epigenetic modifiers (BET inhibitors), transcriptional disruption (CDK9 inhibitors), and combination therapies emerge as promising strategies to suppress its oncogenic activity and overcome resistance, paving the way for improved clinical management.

Authors

Institutions

Publication Details

Journal
Medical Sciences
Published
2026-06-16
DOI
https://doi.org/10.3390/medsci14020325
Primary Topic
Protein Degradation and Inhibitors
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

c-Myc-Induced Therapy Resistance in Leukemia: Mechanisms and Emerging Therapeutic Opportunities

Hossein Kalarestaghi, Javad Arabpour, Sahar Sadat Moosavi, Ali Rafat et al.
Medical Sciences
Protein Degradation and Inhibitors
article

c-Myc-Induced Therapy Resistance in Leukemia: Mechanisms and Emerging Therapeutic Opportunities

Hossein Kalarestaghi, Javad Arabpour, Sahar Sadat Moosavi, Ali Rafat, Zeinab Mazloumi, Reza Nejati, Khadijeh Dizaji Asl, Haniye Yarahmadi, Hediye Khalkhali
article en

Abstract

Dysregulation of the c-Myc oncogene is a pivotal event in leukemia pathogenesis and therapy resistance. This review synthesizes current evidence, illustrating that c-Myc drives leukemogenesis by enhancing proliferation, inhibiting apoptosis, and upregulating immune checkpoints like PD-L1. Its overexpression is linked to poor treatment outcomes across various leukemia subtypes. Directly targeting c-Myc remains challenging; however, indirect epigenetic modifiers (BET inhibitors), transcriptional disruption (CDK9 inhibitors), and combination therapies emerge as promising strategies to suppress its oncogenic activity and overcome resistance, paving the way for improved clinical management.

Medical SciencesVol. 14(2)
Fox Chase Cancer Center (US), Islamic Azad University of Tabriz (IR), Tarbiat Modares University (IR), Tabriz University of Medical Sciences (IR), Kashan University of Medical Sciences (IR), Ardabil University of Medical Sciences (IR), Temple University Health System (US)
Good health and well-being
Openalex Percentile: Top 12%
Protein Degradation and Inhibitors
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.