Document Detail


Different mechanisms of cell death in radiosensitive and radioresistant p53 mutated head and neck squamous cell carcinoma cell lines exposed to carbon ions and x-rays.
MedLine Citation:
PMID:  19362238     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: We initiated studies on the mechanisms of cell death in head and neck squamous cell carcinoma cell lines (HNSCC) since recent clinical trials have shown that local treatment of HNSCC by carbon hadrontherapy is less efficient than it is in other radioresistant cancers.
METHODS AND MATERIALS: Two p53-mutated HNSCC cell lines displaying opposite radiosensitivity were used. Different types of cell death were determined after exposure to carbon ions (33.6 and 184 keV/microm) or X-rays.
RESULTS: Exposure to radiation with high linear energy transfer (LET) induced clonogenic cell death for SCC61 (radiosensitive) and SQ20B (radioresistant) cells, the latter systematically showing less sensitivity. Activation of an early p53-independent apoptotic process occurred in SCC61 cells after both types of irradiation, which increased with time, dose and LET. In contrast, SQ20B cells underwent G2/M arrest associated with Chk1 activation and Cdc2 phosphorylation. This inhibition was transient after X-rays, compared with a more prolonged and LET-dependent accumulation after carbon irradiation. After release, a LET-dependent increase of polyploid and multinucleated cells, both typical signs of mitotic catastrophe, was identified. However, a subpopulation of SQ20B cells was able to escape mitotic catastrophe and continue to proliferate.
CONCLUSIONS: High LET irradiation induced distinct types of cell death in HNSCC cell lines and showed an increased effectiveness compared with X-rays. However, the reproliferation of SQ20B may explain the potential locoregional recurrence observed among some HNSCC patients treated by hadrontherapy. An adjuvant treatment forcing the tumor cells to enter apoptosis may therefore be necessary to improve the outcome of radiotherapy.
Authors:
Mira Maalouf; Gersende Alphonse; Anthony Colliaux; Michaël Beuve; Selena Trajkovic-Bodennec; Priscillia Battiston-Montagne; Isabelle Testard; Olivier Chapet; Marcel Bajard; Gisela Taucher-Scholz; Claudia Fournier; Claire Rodriguez-Lafrasse
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of radiation oncology, biology, physics     Volume:  74     ISSN:  1879-355X     ISO Abbreviation:  Int. J. Radiat. Oncol. Biol. Phys.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-04-13     Completed Date:  2009-04-21     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  7603616     Medline TA:  Int J Radiat Oncol Biol Phys     Country:  United States    
Other Details:
Languages:  eng     Pagination:  200-9     Citation Subset:  IM    
Affiliation:
Université Lyon I, Université de Lyon, France.
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MeSH Terms
Descriptor/Qualifier:
CDC2 Protein Kinase / metabolism
Carbon Radioisotopes / pharmacology
Carcinoma, Squamous Cell / radiotherapy*
Cell Death* / physiology
Cell Line, Tumor
G2 Phase / radiation effects
Genes, p53 / genetics
Head and Neck Neoplasms / radiotherapy*
Humans
Linear Energy Transfer
Mitosis / radiation effects
Protein Kinases / metabolism
Radiation Tolerance* / genetics
beta-Galactosidase / metabolism
Chemical
Reg. No./Substance:
0/Carbon Radioisotopes; EC 2.7.-/Protein Kinases; EC 2.7.11.1/Checkpoint kinase 1; EC 2.7.11.22/CDC2 Protein Kinase; EC 3.2.1.23/beta-Galactosidase

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