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Therapy Response and Outcome Explained by Leukemia Cell of Origin
Zhimin Gu1, Kathryn E Dickerson1, Jian Xu2
1Children's Medical Center Research Institute, Department of Pediatrics, Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, Texas.
Cancer Discovery
|October 2, 2020
Summary
Researchers uncovered a new mechanism in acute myeloid leukemia involving cell of origin and the EVI1 transcription factor. This discovery offers a new strategy to overcome drug resistance in chemoresistant leukemias.
Area of Science:
- Oncology
- Molecular Biology
- Hematology
Background:
- Mixed lineage leukemia-rearranged acute myeloid leukemia (MLL-r AML) is a challenging subtype.
- Understanding the molecular drivers of therapeutic resistance is crucial for improving patient outcomes.
Purpose of the Study:
- To delineate a novel mechanism linking cell of origin, EVI1, and therapeutic susceptibility in MLL-r AML.
- To identify potential therapeutic strategies to overcome drug resistance in chemoresistant leukemias.
Main Methods:
- Investigated the role of the transcription factor EVI1.
- Analyzed the relationship between cell of origin and apoptotic priming.
- Assessed therapeutic susceptibility in preclinical models.
Main Results:
- Identified a cell of origin-dependent program involving EVI1.
- Demonstrated that this program influences apoptotic priming and drug resistance.
- Showcased the potential of targeting this mechanism to sensitize leukemic cells to therapy.
Conclusions:
- A novel mechanism involving cell of origin and EVI1 dictates therapeutic susceptibility in MLL-r AML.
- This understanding provides a basis for developing combination therapies to overcome chemoresistance.
- Targeting this pathway may offer a new avenue for treating resistant acute myeloid leukemia.
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