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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
05:18

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HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA Double-Strand Break repair capacity

Jan C Purrucker1, Andreas Fricke, Mei Fang Ong

  • 1Division of Immunotherapy and Gene Therapy, Department of Internal Medicine I, José Carreras Research Center, Saarland University Medical Center, Homburg/Saar, Germany.

Oncology Reports
|December 4, 2009
PubMed

Insights

Histone deacetylase inhibitors (HDACi) increase cancer cell radiosensitivity but impair DNA repair in healthy fibroblasts. This highlights potential genotoxic risks, necessitating careful patient selection and education for HDACi cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Histone deacetylase inhibitors (HDACi) show promise in cancer treatment due to efficacy and low toxicity.
  • Limited research exists on HDACi effects on normal tissue cells.

Purpose of the Study:

  • To investigate the impact of HDAC inhibitors on healthy human fibroblasts.
  • To assess the genotoxic potential of HDAC inhibitors in normal cells.

Main Methods:

  • Treatment of healthy human fibroblasts with suberoylanilide hydroxamic acid (SAHA), MS275, sodium butyrate, and valproic acid.
  • Evaluation of radiosensitivity and DNA double-strand break (DSB) repair capacity.

Main Results:

  • HDAC inhibitor treatment led to increased radiosensitivity in normal fibroblasts.
  • A reduced capacity for DSB repair was observed in HDACi-treated cells.

Conclusions:

  • HDAC inhibitors may possess genotoxic effects on normal tissues.
  • Potential risks necessitate stringent clinical indications and patient/physician education, especially for long-term use or combination therapies.

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