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5R radioterapii

Kukołowicz P., Dąbrowska E.

Inżynier i Fizyk Medyczny

2014

Vol. 3, nr 4

165--167

Relationships between EGFR-initiated signalling, DNA double-strand break rejoining and survival in X-irradiated human glioma M059 cells

Grądzka I., Buraczewska I., Szumiel I.

Nukleonika

2008

Vol. 53, No. 2

37-44

The aim of this study was to investigate the effect of signalling inhibition on survival and double-strand break (DSB) rejoining in cells differing in sensitivity to inhibitors, X-rays and bleomycin. Human glioma M059 cells, K (relatively radioresistant) and J (radiosensitive, defective in DSB rejoining for lack of DNA-dependent protein kinase catalytic subunit, DNA-PKcs) were pretreated with signalling inhibitors: tyrphostin AG 1478, specific for epidermalgrowth- factor-receptor (EGFR) kinase or PD 98059, specific for kinase MEK 1/2 (mitogen-activated, extracellular signal-activated kinases 1 and 2). Subsequently, the cells were X-irradiated or treated with bleomycin. Cell survival was determined by clonogenicity test. DSB rejoining was monitored with the use of pulsed-field gel electrophoresis (PFGE). We found that in X-irradiated M059 K cells EGFR kinase activity was necessary for efficient DSB rejoining and the kinase inhibitor, tyrphostin AG 1478, acted as radiosensitizer in the dose range that reduced cell survival to 0.7-0.8. Inhibition of EGFR kinase, however, did not decrease survival or affect DSB rejoining in DNA-PKcs-deficient M059 J cells. These results indicated that the decrease in cell survival was due to a disturbed DSB rejoining by the DNA-PK dependent system. In contrast, inhibition of MEK 1/2 kinase on EGFR downstream signalling pathway by PD 98059 did not affect DSB rejoining in either cell line and exerted a radioprotective effect.

The influence of fractionated radiation on proliferation, cell cycle and apoptosis of normal human dermal fibroblasts

Adamczyk A., Gasińska A.

Nukleonika

2005

Vol. 50,suppl.2

9-12

The aim of the study was to investigate the changes in proliferation rate, cell cycle and apoptosis of normal skin fibroblasts during fractionated irradiation with a fraction dose of 2 Gy. Fibroblasts were irradiated 5 days per week for 12 days using gamma irradiation. Twenty four hours after each fraction, and for three days after finishing experiment the cells were harvested, fixed, and BrdUrd labelling index (BrdUrdLI), cell cycle and level of apoptosis and debris were assessed. It was found that fractionated irradiation caused disturbances in the proliferation rate and the cell cycle. Irradiation caused also constant, statistically significant increase in the number of G2M cells and level of apoptosis and debris, which was observed even during 3 days after irradiation. Data indicate non equal biological effect of each fraction dose. Block at G2/M phase suggests accumulation of sublethal damage and increased radiosensitivity, which was manifested by elevated level of cell death (apoptosis and debris).