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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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A guide to epigenetics in leukaemia stem cells.

Shuchi Agrawal-Singh1,2, Jaana Bagri1,2, Nathalie Sakakini1,2

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|October 24, 2023
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Summary

Leukaemia stem cells drive cancer growth through epigenetic changes. Understanding these epigenetic alterations and patient heterogeneity is key to developing new therapies for myeloid neoplasms.

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epigenetic plasticityheterogeneityleukaemia stem cellsmyeloid neoplasmssingle cell studies and multiomicstargeting LSC

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Area of Science:

  • Hematology
  • Cancer Biology
  • Epigenetics

Background:

  • Leukaemia stem cells (LSCs) are central to haematological malignancies, causing disease initiation, relapse, and resistance.
  • LSCs exhibit phenotypic and epigenetic plasticity, leading to complex and heterogeneous diseases.
  • Epigenetic deregulation plays a crucial role in the evolution of these malignancies.

Purpose of the Study:

  • To review the principles of epigenetic deregulation in the evolution of haematological malignancies.
  • To discuss methods for quantifying clonal heterogeneity using single-cell resolution data.
  • To explore the integration of genetic and epigenetic information for understanding patient heterogeneity and clinical response.

Main Methods:

  • Review of recent studies on mutational, transcriptional, and epigenetic landscapes at single-cell resolution.
  • Analysis of longitudinal patient samples to identify resistance mechanisms.
  • Integration of genetic and epigenetic data to understand disease progression.

Main Results:

  • Epigenetic plasticity of LSCs contributes to disease heterogeneity and evolution.
  • Single-cell resolution studies reveal complex mutational, transcriptional, and epigenetic landscapes.
  • Integrating genetic and epigenetic data enhances understanding of inter- and intra-patient heterogeneity.
  • Longitudinal analyses identify mechanisms of resistance in myeloid neoplasms.

Conclusions:

  • Targeting aberrant epigenetic processes holds promise for eradicating LSCs and improving therapeutic outcomes.
  • A deeper understanding of epigenetic deregulation and clonal heterogeneity is crucial for effective treatment strategies.
  • Integrating multi-omics data provides critical insights into disease evolution and patient response.