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Updated: Sep 15, 2025
07:38
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
276
Potential therapeutic targets in chronic myeloid leukemia
1School of Biotechnology, Banaras Hindu University, Varanasi, U.P., 221005, India.
Medical Oncology (Northwood, London, England)
|July 17, 2025
Summary
New strategies are needed to overcome resistance to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML). Targeting pathways like oxidative stress, apoptosis, and using gene editing offers promising avenues for curative CML treatment.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- Chronic myeloid leukemia (CML) is driven by the BCR::ABL oncoprotein, with tyrosine kinase inhibitors (TKIs) improving survival.
- Resistance to TKIs, leukemia stem cell persistence, and relapse necessitate alternative therapeutic strategies.
- Oxidative stress pathways are implicated in CML development and resistance, presenting a target for intervention.
Purpose of the Study:
- To review promising therapeutic targets beyond TKIs for CML treatment.
- To explore novel approaches including suppressor pathways, autophagy, BCL-2 family proteins, and microRNAs.
- To discuss gene editing and USP inhibition for overcoming resistance and achieving curative outcomes.
Main Methods:
- Literature review of current and emerging therapeutic strategies for CML.
- Analysis of molecular pathways involved in CML pathogenesis and treatment resistance.
- Exploration of novel targets such as tumor suppressors, autophagy, BCL-2 proteins, and microRNAs.
Main Results:
- Restoring tumor suppressor function (PTPRG, p53) can enhance apoptosis and complement TKIs.
- Modulating autophagy and targeting BCL-2 family proteins offer ways to overcome apoptotic resistance.
- MicroRNAs (miRNAs) present opportunities for advanced treatment by modulating oncogenic and apoptotic pathways.
Conclusions:
- Combining novel therapeutic approaches with next-generation TKIs is crucial for deeper remissions in CML.
- Gene editing and USP inhibition are emerging strategies to target oncogenic drivers and overcome resistance.
- Personalized and comprehensive treatment strategies are essential for achieving curative outcomes in CML patients.
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