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  • 1
    Language: English
    In: International journal of radiation oncology, biology, physics, 2010, Vol.78 (4), p.1177-1183
    Description: Purpose To present the first direct experimental in vitro comparison of the biological effectiveness of range-equivalent protons and carbon ion beams for Chinese hamster ovary cells exposed in a three-dimensional phantom using a pencil beam scanning technique and to compare the experimental data with a novel biophysical model. Methods and Materials Cell survival was measured in the phantom after irradiation with two opposing fields, thus mimicking the typical patient treatment scenario. The novel biophysical model represents a substantial extension of the local effect model, previously used for treatment planning in carbon ion therapy for more than 400 patients, and potentially can be used to predict effectiveness of all ion species relevant for radiotherapy. A key feature of the new approach is the more sophisticated consideration of spatially correlated damage induced by ion irradiation. Results The experimental data obtained for Chinese hamster ovary cells clearly demonstrate that higher cell killing is achieved in the target region with carbon ions as compared with protons when the effects in the entrance channel are comparable. The model predictions demonstrate agreement with these experimental data and with data obtained with helium ions under similar conditions. Good agreement is also achieved with relative biological effectiveness values reported in the literature for other cell lines for monoenergetic proton, helium, and carbon ions. Conclusion Both the experimental data and the new modeling approach are supportive of the advantages of carbon ions as compared with protons for treatment-like field configurations. Because the model predicts the effectiveness for several ion species with similar accuracy, it represents a powerful tool for further optimization and utilization of the potential of ion beams in tumor therapy.
    Subject(s): Radiology ; Hematology, Oncology and Palliative Medicine ; Ion beam therapy ; Relative biological effectiveness (RBE) ; Biophysical model ; Treatment planning ; Biological and medical sciences ; Treatment. General aspects ; Treatment with physical agents ; Medical sciences ; Radiation therapy and radiosensitizing agent ; Tumors ; Carbon - therapeutic use ; Cricetinae ; Cricetulus ; Benchmarking - methods ; Ions - therapeutic use ; Protons - therapeutic use ; Helium ; Cell Survival - radiation effects ; CHO Cells - radiation effects ; Animals ; Radiobiology ; Models, Biological ; Radiotherapy - methods ; Relative Biological Effectiveness ; Phantoms, Imaging ; Radiation Injuries, Experimental ; Cell Survival - physiology ; Comparative analysis ; Radiotherapy ; Scanning devices ; NEOPLASMS ; BEAMS ; ION BEAMS ; FERMIONS ; IONS ; MEDICINE ; PROTONS ; ELEMENTARY PARTICLES ; NUCLEAR MEDICINE ; NUCLEONS ; PLANNING ; DISEASES ; THERAPY ; RBE ; CHARGED PARTICLES ; RADIOLOGY AND NUCLEAR MEDICINE ; CARBON IONS ; RADIOTHERAPY ; BARYONS ; HADRONS ; RADIOLOGY
    ISSN: 0360-3016
    E-ISSN: 1879-355X
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: Alma/SFX Local Collection
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  • 2
    Language: English
    In: International journal of radiation oncology, biology, physics, 2007, Vol.68 (3), p.873-882
    Description: Background: The majority of glioblastoma multiforme (GBM) cells express the epidermal growth factor receptor (EGFR). The present study evaluates the combination of temozolomide (TMZ), EGFR inhibition, and radiotherapy (RT) in GBM cell lines. Methods and Materials: Human GBM cell lines U87, LN229, LN18, NCH 82, and NCH 89 were treated with various combinations of TMZ, RT, and the monoclonal EGFR antibody cetuximab. Responsiveness of glioma cells to the combination treatment was measured by clonogenic survival. Results: Overall, double and triple combinations of RT, TMZ, and cetuximab lead to additive cytotoxic effects (independent toxicity). A notable exception was observed for U87 and LN 18 cell lines, where the combination of TMZ and cetuximab showed substantial antagonism. Interestingly, in these two cell lines, the combination of RT with cetuximab resulted in a substantial increase in cell killing over that expected for independent toxicity. The triple combination with RT, cetuximab, and TMZ was nearly able to overcome the antagonism for the TMZ/cetuximab combination in U87, however only marginally in LN18, GBM cell lines. Conclusion: It appears that EGFR expression is not correlated with cytotoxic effects exerted by cetuximab. Combination treatment with TMZ, cetuximab and radiation resulted in independent toxicity in three out of five cell lines evaluated, the antagonistic effect of the TMZ/cetuximab combination in two cell lines could indicate that TMZ preferentially kills cetuximab-resistant cells, suggesting for some cross-talk between toxicity mechanisms. Expression of EGFR was no surrogate marker for responsiveness to cetuximab, alone or in combination with RT and TMZ.
    Subject(s): Radiology ; Hematology, Oncology and Palliative Medicine ; Human glioma cells ; Temozolomide ; Toxicity ; EGFR ; Radiation ; Cell Survival - drug effects ; Dacarbazine - administration & dosage ; Antineoplastic Combined Chemotherapy Protocols - administration & dosage ; Humans ; Epidermal Growth Factor - metabolism ; Antineoplastic Agents - administration & dosage ; Radiation Dosage ; Cell Survival - radiation effects ; Dose-Response Relationship, Drug ; Antibodies, Monoclonal, Humanized ; Antibodies, Monoclonal - administration & dosage ; Chemotherapy, Adjuvant - methods ; Glioblastoma - pathology ; Dacarbazine - analogs & derivatives ; Cell Line, Tumor ; Epidermal Growth Factor - antagonists & inhibitors ; Glioblastoma - metabolism ; Cetuximab ; Dose-Response Relationship, Radiation ; Epidermal growth factor ; Radiotherapy ; Gliomas ; Nuclear radiation ; Cells ; ANTIBODIES ; GLIOMAS ; GROWTH FACTORS ; INHIBITION ; IN VITRO ; CELL KILLING ; RADIOLOGY AND NUCLEAR MEDICINE ; TOXICITY ; RADIOTHERAPY ; RECEPTORS
    ISSN: 0360-3016
    E-ISSN: 1879-355X
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: Alma/SFX Local Collection
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  • 3
    Language: English
    In: International journal of radiation oncology, biology, physics, 2007, Vol.69 (3), p.887-894
    Description: Purpose Telomerase activity represents a radiation-inducible function, which may be targeted by a double-strand break (DSB)–activated signal transduction pathway. Therefore, the effects of DNA-PK inhibitors (Wortmannin and LY294002) on telomerase upregulation after irradiation were studied. In addition, the role of trans-dominant inhibition of poly(ADP-ribosyl)ation, which strongly reduces DSB rejoining, was assessed in comparison with 3-aminobenzamide. Methods and Materials COM3 rodent cells carry a construct for the dexamethasone-inducible overexpression of the DNA-binding domain of PARP1 and exhibit greatly impaired DSB rejoining after irradiation. Telomerase activity was measured using polymerase chain reaction ELISA 1 h after irradiation with doses up to 10 Gy. Phosphorylation status of PKB/Akt and of PKCα/βII was assessed by western blotting. Results No telomerase upregulation was detectable for irradiated cells with undisturbed DSB rejoining. In contrast, incubation with LY294002 or dexamethasone yielded pronounced radiation induction of telomerase activity that could be suppressed by Wortmannin. 3-Aminobenzamide not only was unable to induce telomerase activity but also suppressed telomerase upregulation upon incubation with LY294002 or dexamethasone. Phospho-PKB was detectable independent of irradiation or dexamethasone pretreatment, but was undetectable upon incubations with LY294002 or Wortmannin, whereas phospho-PKC rested detectable. Conclusions Telomerase activation postirradiation was triggered by different treatments that interfere with DNA DSB processing. This telomerase upregulation, however, was not reflected by the phosporylation status of the putative mediators of TERT activation, PKB and PKC. Although an involvement of PKB in TERT activation is not supported by the present findings, a respective role of PKC isoforms other than α/βII cannot be ruled out.
    Subject(s): Radiology ; Hematology, Oncology and Palliative Medicine ; Irradiation ; Double-strand breaks ; LY294002 ; Telomerase ; Wortmannin ; Cell Line ; Phosphorylation ; DNA Repair - physiology ; Enzyme Inhibitors - pharmacology ; Morpholines - pharmacology ; Enzyme Activation - drug effects ; Enzyme Activation - radiation effects ; Up-Regulation - drug effects ; Poly Adenosine Diphosphate Ribose - metabolism ; Animals ; Dexamethasone - pharmacology ; Proteins - metabolism ; Androstadienes - pharmacology ; DNA Breaks, Double-Stranded - drug effects ; Protein Kinase C - metabolism ; Telomerase - radiation effects ; Proteins - drug effects ; Telomerase - metabolism ; Benzamides - pharmacology ; Chromones - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Index Medicus ; DEXAMETHASONE ; RODENTS ; PHOSPHORYLATION ; RADIATION DOSES ; ADP ; IONIZING RADIATIONS ; STRAND BREAKS ; IRRADIATION ; RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS ; POLYMERASE CHAIN REACTION ; DNA ; BIOLOGICAL REPAIR ; ENZYME IMMUNOASSAY
    ISSN: 0360-3016
    E-ISSN: 1879-355X
    Source: Backfile Package - All of Back Files EBS [ALLOFBCKF]
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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