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Inhibition of Bcl-xL expression sensitizes T-cell acute lymphoblastic leukemia cells to chemotherapeutic drugs

  • H. Elizabeth Broome*
  • , Alice L. Yu
  • , Mitch Diccianni
  • , Bruce M. Camitta
  • , Brett P. Monia
  • , Nicholas M. Dean
  • *Corresponding author for this work
  • University of California at San Diego
  • Midwest Children’s Cancer Center
  • Ionis Pharmaceuticals

Research output: Contribution to journalJournal Article peer-review

30 Scopus citations

Abstract

We have examined the effects of antisense oligonucleotides to bcl-x on the survival and chemosensitivity of CEM cells, a T-acute lymphoblastic leukemia (T-ALL) cell line. Also, we have measured the levels of Bcl-2, Bcl-x, and Bax in 20 cases of T-ALL. By 18 h after the bcl-x antisense treatment, CEM cells showed over a 75% reduction in the levels of Bcl-xL protein and over 30% decreased viable cell counts compared with cells treated with the control oligonucleotide. The combination of bcl-x antisense plus either dexamethasone or doxorubicin showed either strong synergistic or additive killing of CEM cells, respectively. These findings indicate that bcl-x antisense has cytotoxic activity and increases chemotherapy-induced cell death in CEM cells, a model for T-ALL.

Original languageEnglish
Pages (from-to)311-316
Number of pages6
JournalLeukemia Research
Volume26
Issue number3
DOIs
StatePublished - 2002
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Antisense
  • Drug sensitivity
  • Glucocorticoid
  • T-ALL
  • bcl-2
  • bcl-x

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