title: Radiosensitization of p53-deficient lung cancer cells by pre-treatment with cytostatic compounds.
abstract: OBJECTIVE
  This study specifies a strategy to improve radiotherapy by partial synchronization of p53-deficient cancer cells (FaDu and H1299) in mitosis using taxol, with protecting p53 wild-type cells (A549) by the prior administration of cytostatic compounds. Cytotoxic and cytostatic effects of ionizing radiation, cisplatin, doxorubicin and taxol, administrated alone or in combination were investigated in vitro by flow cytometry.
  
  
  RESULTS
  A protective effect of doxorubicin but not cisplatin was found after administration of triple sequence with ionizing radiation and taxol. It was found that preliminary administration of doxorubicin induced growth arrest and protected A549 cells from the taxol/radiation treatment, while simultaneously killing FaDu and H1299 cells.
  
  
  CONCLUSIONS
  The proposed therapeutic strategy allows protection of p53 wild-type cells and selectively increases radiosensitivity of p53-deficient cancer cells.
authors.affiliation: Biological and Molecular Imaging, OncoRay -- National Center for Radiation Research in Oncology, Carl Gustav Carus Medical Faculty, Dresden University of Technology, Dresden, Germany. Sergey.Tokalov@googlemail.com
authors.forename: Sergey V
authors.initials: SV
authors.lastname: Tokalov
authors.forename: Nasreddin
authors.initials: N
authors.lastname: Abolmaali
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D045744:Cell Line, Tumor; D002945:Cisplatin / Q000494:pharmacology; D004317:Doxorubicin / Q000494:pharmacology; D005434:Flow Cytometry; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism* / Q000473:pathology; D011836:Radiation Tolerance / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53; D004317:Doxorubicin; D002945:Cisplatin