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Multiomic State-Transitions Reveal Post-Treatment Transcriptome Desynchronization in Acute Myeloid Leukemia.

Jennifer Rangel Ambriz¹, Ziang Chen¹, Yu-Hsuan Fu²

¹Department of Computational and Quantitative Medicine, Beckman Research Institute, City of Hope National Medical Center, Duarte, California, 91010.

Biorxiv : the Preprint Server for Biology

|June 4, 2026

Summary

This summary is machine-generated.

Chemotherapy causes a delay in microRNA (miRNA) responses compared to messenger RNA (mRNA) in acute myeloid leukemia (AML) mouse models. The Dlk1-Dio3 locus miRNAs are key drivers of this transcriptomic desynchronization, offering potential therapeutic targets.

Keywords:

AML Dlk1-Dio3 gene expression dynamics mathematical modeling multiomics

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Published on: September 1, 2019

Area of Science:

* Molecular biology
* Systems biology
* Hematologic oncology

Background:

* Peripheral blood transcriptome dynamics are vital for understanding leukemia progression and treatment outcomes.
* Gene expression patterns influence abnormal cell states, disease heterogeneity, and resistance to therapy.
* Studying temporal transcriptomic changes provides insights into leukemia's complex behavior.

Purpose of the Study:

* To investigate the temporal dynamics of messenger RNA (mRNA) and microRNA (miRNA) transcriptomes in a mouse model of acute myeloid leukemia (AML) after chemotherapy.
* To model transcriptomic changes using a mathematical framework representing Brownian motion in a multiomic potential landscape.
* To identify the molecular drivers behind chemotherapy-induced transcriptomic desynchronization.

Main Methods:

* Utilized a mathematical model of state-transitions to analyze peripheral blood mRNA and miRNA transcriptomes.
* Employed Brownian motion simulation within a two-dimensional multiomic potential landscape.
* Performed clustering analysis to identify specific miRNA clusters responsible for temporal delays.

Main Results:

* Observed an asymmetric shift in the multiomic potential landscape post-chemotherapy, causing desynchronization between mRNA and miRNA responses.
* mRNA transcriptomes showed immediate response, while miRNA transcriptomes exhibited a delay of approximately two weeks.
* Identified a prominent cluster of miRNAs from the imprinted Dlk1-Dio3 locus as the primary driver of this temporal delay.

Conclusions:

* The Dlk1-Dio3 locus plays a significant role in AML chemotherapy response and treatment-induced transcriptomic desynchronization.
* This study provides the first evidence linking the Dlk1-Dio3 locus to AML chemotherapy dynamics.
* The developed framework offers a novel, dynamics-based approach for identifying therapeutic targets in hematologic malignancies.