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Related Experiment Video

Updated: Jun 22, 2026

High-throughput Fluorometric Measurement of Potential Soil Extracellular Enzyme Activities
12:33

High-throughput Fluorometric Measurement of Potential Soil Extracellular Enzyme Activities

Published on: November 15, 2013

[Not Available].

Lyse A Norian1, Tamara A Kucaba, James K Earel

  • 1Department of Urology and Interdisciplinary Graduate Program in Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.

Journal of Oncology
|June 24, 2009
PubMed
Summary
This summary is machine-generated.

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Histone deacetylase inhibitors (HDACis) can sensitize resistant B-cell chronic lymphocytic leukemia (B-CLL) cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) therapy. This combination enhances cancer cell death while sparing normal cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows promise for cancer therapy by inducing apoptosis in malignant cells.
  • Resistance to TRAIL-mediated apoptosis is a significant challenge for its standalone therapeutic use, particularly in primary tumor cells.
  • B-cell chronic lymphocytic leukemia (B-CLL) cells often exhibit resistance to TRAIL-induced apoptosis.

Purpose of the Study:

  • To investigate the efficacy of combining histone deacetylase inhibitors (HDACis) with TRAIL therapy.
  • To determine if HDAC inhibition can overcome TRAIL resistance in primary B-CLL cells.
  • To assess the impact of HDACis on TRAIL receptor expression and apoptotic pathways in B-CLL.

Main Methods:

  • Primary B-CLL cells and peripheral blood mononuclear cells were treated with HDAC inhibitors.

Related Experiment Videos

Last Updated: Jun 22, 2026

High-throughput Fluorometric Measurement of Potential Soil Extracellular Enzyme Activities
12:33

High-throughput Fluorometric Measurement of Potential Soil Extracellular Enzyme Activities

Published on: November 15, 2013

  • Cells were subsequently exposed to TRAIL to assess apoptosis induction.
  • Expression levels of TRAIL receptors, caspases, and antiapoptotic proteins (e.g., Bcl-2) were analyzed.

    • Main Results:

    • HDAC inhibition significantly increased TRAIL receptor expression on B-CLL cells.
    • HDACis enhanced caspase activation and decreased Bcl-2 expression in B-CLL cells.
    • Combination therapy resulted in enhanced TRAIL-induced apoptosis in B-CLL cells, with minimal effect on normal cells.

    Conclusions:

    • Pretreatment with HDAC inhibitors can sensitize TRAIL-resistant B-CLL cells to TRAIL-mediated apoptosis.
    • Combination therapy of HDAC inhibitors and TRAIL presents a promising strategy for B-CLL treatment.
    • This approach may offer a targeted therapeutic option with reduced toxicity to normal tissues.