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Aberrant splicing in B-cell acute lymphoblastic leukemia.

Kathryn L Black1, Ammar S Naqvi1,2, Mukta Asnani1

  • 1Department of Pathology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

Nucleic Acids Research
|October 26, 2018
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Summary

Pediatric B-cell acute lymphoblastic leukemia (B-ALL) exhibits widespread aberrant splicing, even without mutations in splicing factors. This deregulation, particularly involving hnRNPA1, drives significant changes in gene expression, contributing to leukemia development.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Aberrant splicing is a known feature in leukemias with mutations in splicing factor (SF)-encoding genes.
  • The prevalence and mechanisms of aberrant splicing in pediatric B-cell acute lymphoblastic leukemia (B-ALL) without SF mutations remain unclear.

Purpose of the Study:

  • To investigate the prevalence of aberrant splicing in pediatric B-ALL where SFs are not mutated.
  • To identify specific splicing alterations and their associated genes and pathways in B-ALL.
  • To explore the role of post-transcriptional deregulation of SFs in B-ALL pathogenesis.

Main Methods:

  • Comparative analysis of RNA sequencing data from pediatric B-ALL samples and normal pro-B cells.
  • Identification and characterization of local splice variations (LSVs).
  • Knockdown experiments of hnRNPA1 in B-lymphoblastoid cells to identify regulated splicing events.
  • Analysis of LSVs in known leukemia and lymphoma driver genes.

Main Results:

  • Thousands of aberrant LSVs were identified per B-ALL sample, with 279 LSVs in 241 genes consistently present.
  • Identified genes were enriched in RNA processing pathways and included approximately 100 SFs, notably hnRNPA1.
  • hnRNPA1 knockdown revealed a distinct splicing signature in B-ALL, with identified LSVs in cancer drivers like DICER1 and NT5C2.
  • Aberrant splicing was more prevalent than somatic mutations in common B-ALL driver genes.

Conclusions:

  • Post-transcriptional deregulation of splicing factors can induce widespread splicing changes in B-ALL.
  • Aberrant splicing, independent of SF mutations, is a significant contributor to pediatric B-ALL pathogenesis.
  • Splicing factor deregulation represents a potential therapeutic target in B-ALL.