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Enhancer dysfunction in leukemia.

Anand S Bhagwat1, Bin Lu1, Christopher R Vakoc1

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY.

Blood
|February 15, 2018
PubMed
Summary
This summary is machine-generated.

Hematopoietic cancers involve altered gene regulation by transcription factors (TFs) and enhancers. Understanding these changes in leukemia can reveal new therapeutic strategies targeting the enhancer landscape.

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Area of Science:

  • Genomics
  • Molecular Biology
  • Cancer Research

Background:

  • Hematopoietic cancers arise from disrupted transcriptional regulation.
  • Transcription factors (TFs) control gene expression by binding to DNA regulatory elements.
  • Enhancers are critical genomic regions that modulate gene activity.

Purpose of the Study:

  • To review how altered enhancer landscapes contribute to leukemia pathogenesis.
  • To highlight genetic mutations affecting enhancer-binding proteins and DNA in leukemia.
  • To discuss small molecules that reprogram enhancer landscapes for therapeutic benefit.

Main Methods:

  • Review of existing literature on transcriptional regulation in hematopoietic cancers.
  • Analysis of genome-scale measurements of enhancer activity.
  • Examination of genetic alterations in enhancer elements and associated proteins in leukemia.

Main Results:

  • Deregulation of transcriptional machinery, particularly TFs, is a key driver of hematopoietic cancers.
  • Abnormal enhancer configurations are increasingly recognized in cancer cells, including leukemia.
  • Genetic mutations in enhancer-binding proteins and enhancer DNA are implicated in leukemia development.

Conclusions:

  • Alterations in enhancer landscapes are integral to leukemia pathogenesis.
  • Targeting enhancer reprogramming with small molecules shows therapeutic promise for leukemia.