Dynamics of tumor hypoxia in response to patupilone and ionizing radiation

PLoS One. 2012;7(12):e51476. doi: 10.1371/journal.pone.0051476. Epub 2012 Dec 10.

Abstract

Tumor hypoxia is one of the most important parameters that determines treatment sensitivity and is mainly due to insufficient tumor angiogenesis. However, the local oxygen concentration in a tumor can also be shifted in response to different treatment modalities such as cytotoxic agents or ionizing radiation. Thus, combined treatment modalities including microtubule stabilizing agents could create an additional challenge for an effective treatment response due to treatment-induced shifts in tumor oxygenation. Tumor hypoxia was probed over a prolonged observation period in response to treatment with different cytotoxic agents, using a non-invasive bioluminescent ODD-Luc reporter system, in which part of the oxygen-dependent degradation (ODD) domain of HIF-1α is fused to luciferase. As demonstrated in vitro, this system not only detects hypoxia at an ambient oxygen concentration of 1% O(2), but also discriminates low oxygen concentrations in the range from 0.2 to 1% O(2). Treatment of A549 lung adenocarcinoma-derived tumor xenografts with the microtubule stabilizing agent patupilone resulted in a prolonged increase in tumor hypoxia, which could be used as marker for its antitumoral treatment response, while irradiation did not induce detectable changes in tumor hypoxia. Furthermore, despite patupilone-induced hypoxia, the potency of ionizing radiation (IR) was not reduced as part of a concomitant or adjuvant combined treatment modality.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers, Tumor / metabolism
  • Cell Death / drug effects
  • Cell Death / radiation effects
  • Cell Hypoxia / drug effects
  • Cell Hypoxia / radiation effects
  • Cell Line, Tumor
  • Cobalt / pharmacology
  • Combined Modality Therapy
  • Epothilones / pharmacology
  • Epothilones / therapeutic use*
  • Genes, Reporter
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / chemistry
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Luciferases / metabolism
  • Mice
  • Mice, Nude
  • Neoplasms / drug therapy
  • Neoplasms / pathology*
  • Neoplasms / radiotherapy
  • Nitroimidazoles / pharmacology
  • Oxygen / pharmacology
  • Partial Pressure
  • Protein Structure, Tertiary
  • Radiation, Ionizing*
  • Xenograft Model Antitumor Assays

Substances

  • Biomarkers, Tumor
  • Epothilones
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Nitroimidazoles
  • Cobalt
  • pimonidazole
  • Luciferases
  • cobaltous chloride
  • Oxygen
  • epothilone B

Grants and funding

This work was supported by the Swiss Cancer League, the Swiss National Science Foundation, the Vontobel-Stiftung (all to MP) and the KFSP Tumor Oxygenation of the University Zurich. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.