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Related Experiment Video

Updated: Feb 7, 2026

Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia
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SH2B3 aberrations enriched in iAMP21 B lymphoblastic leukemia.

L B Baughn1, M M Meredith2, L Oseth2

  • 1Division of Laboratory Genetics and Genomics, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street SW, Rochester, MN, United States.

Cancer Genetics
|July 15, 2018
PubMed
Summary

Genetic analysis of childhood acute lymphoblastic leukemia (ALL) reveals deletions in SH2B3 are common in the high-risk iAMP21 subtype. This finding suggests potential new therapeutic targets for improving patient outcomes.

Keywords:
Acute lymphoblastic leukemiaChromosomal microarraySH2B3iAMP21

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Area of Science:

  • Pediatric Hematology Oncology
  • Cancer Genomics
  • Molecular Biology

Background:

  • Acute lymphoblastic leukemia (ALL) is the most common childhood cancer.
  • While survival rates for pediatric B-cell ALL (B-ALL) are high, outcome variability persists within subgroups.
  • Advanced genomic techniques improve the characterization of leukemic clones.

Purpose of the Study:

  • To investigate novel genetic aberrations in pediatric B-ALL.
  • To understand the biologic mechanisms and heterogeneity of poor-prognosis ALL subtypes.
  • To identify potential therapeutic targets for high-risk ALL.

Main Methods:

  • Utilized chromosomal microarray and fluorescence in situ hybridization (FISH) to analyze genetic aberrations.
  • Screened for genome-wide copy number aberrations and nucleotide variations.
  • Focused on the intrachromosomal amplification of chromosome 21 (iAMP21) subtype.

Main Results:

  • Deletions of the SH2B3 gene were found to be enriched in leukemias with iAMP21.
  • SH2B3 encodes a negative regulator of tyrosine kinase and cytokine signaling pathways.
  • Enrichment of SH2B3 aberrations suggests a role in disease progression for the iAMP21 subtype.

Conclusions:

  • Loss of SH2B3 may contribute to the progression of iAMP21 ALL.
  • These findings raise the possibility of targeting tyrosine kinase pathways in iAMP21 ALL.
  • Further research into SH2B3 aberrations could identify novel therapeutic strategies for high-risk pediatric ALL.