Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part III. Different Signals Can Lead to Apoptosis and May Influence Sensitivity to Killing by DNA Double-strand Breakage

Radford, Ian R.; Murphy, T K

doi:10.1080/09553009414550261

Cited by 102 publications

(34 citation statements)

References 16 publications

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“…Such an arrest may take place at different points in the cell cycle. Exposure to radiation induced a more pronounced G 2 /M block, and in those cases apoptosis appeared to be manifest at the time of cells release from the G 2 /M block, during the subsequent G 1 phase [38,39].…”

Section: Discussionmentioning

confidence: 99%

Kinetics of apoptotic markers in exogeneously induced apoptosis of EL4 cells

Jessel

Haertel

Socaciu

et al. 2002

J Cellular Molecular Medi

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We investigated the time‐dependence of apoptotic events in EL4 cells by monitoring plasma membrane changes in correlation to DNA fragmentation and cell shrinkage. We applied three apoptosis inducers (staurosporine, tubericidine and X‐rays) and we looked at various markers to follow the early‐to‐late apoptotic events: phospholipid translocation (identified through annexin V‐fluorescein assay and propidium iodide), lipid package (via merocyanine assay), membrane fluidity and anisotropy (via fluorescent measurements), DNA fragmentation by the fluorescence‐labeling test and cell size measurements. The different apoptotic inducers caused different reactions of the cells: staurosporine induced apoptosis most rapidly in a high number of cells, tubercidine triggered apoptosis only in the S phase cells, while X‐rays caused a G2/M arrest and subsequently apoptosis. Loss of lipid asymmetry is promptly detectable after one hour of incubation time. The phosphatidylserine translocation, decrease of lipid package and anisotropy, and the increase of membrane fluidity appeared to be based on the same process of lipid asymmetry loss. Therefore, the DNA fragmentation and the cell shrinkage appear to be parallel and independent processes running on different time scales but which are kinetically inter‐related. The results indicate different signal steps to apoptosis dependent on inducer characteristics but the kinetics of “early‐to‐late” apoptosis appears to be a fixed program.

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Section: Discussionmentioning

confidence: 99%

Kinetics of apoptotic markers in exogeneously induced apoptosis of EL4 cells

Jessel

Haertel

Socaciu

et al. 2002

J Cellular Molecular Medi

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“…Several authors have reported a good quantitative inverse relationship between micronucleus frequency and clonogenic survival (Wandl et al, 1989;Jamali and Trott, 1996;Mariya et al, 1997); however, there are also several reports in which such a correlation was not found (Bush and McMillan, 1993;Slavotinek et al, 1993;Villa et al, 1994). Some authors have reported an inverse correlation between apoptotic frequency and cell survival (Radford and Murphy, 1994;Olive and Durand, 1997;Guo et al, 1999), whereas others found no correlation (Yangihara et al, 1995;McKenna et al, 1996).…”

mentioning

confidence: 89%

Relationship between clonogenic radiosensitivity, radiation-induced apoptosis and DNA damage/repair in human colon cancer cells

Dunne¹,

Price²,

Mothersill³

et al. 2003

Br J Cancer

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The intrinsic radiation sensitivity of normal and tumour tissue is a major determinant of the outcome of radiotherapy. There is currently no established test that can be used routinely to measure the radiosensitivity of the cells in an individual patient's cancer in a manner that can inform treatment planning. The purpose of this study was to evaluate, in four human colorectal adenocarcinoma cell lines, two possible end points as surrogate markers of radiation response -apoptosis and induction of DNA single-strand breaksand to compare the results with those of a conventional clonogenic assay. Cell lines (SW707 SW480, SW48 and HT29) known to differ in radiosensitivity were exposed to single doses of X-rays ranging from 0.5 to 5 Gy and cell survival was measured using the clonogenic assay. Apoptosis was determined on the basis of morphology under fluorescent microscopy and DNA damage/repair was measured, as tail moment, using an adaptation of the alkaline comet assay. The relationship between surviving fraction at 2 Gy (SF 2 ) and the percentage of apoptotic cells 24 h after the same dose was complex, but apoptosis accurately predicted the order of radiosensitivities as measured by SF 2 . Initial damage measured after 2 Gy using the alkaline comet assay gave a close correlation with SF 2 (r 2 ¼ 0.95), whereas there was no correlation between initial DNA damage repair rate and SF 2 .

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“…In experimental animal tumors, apoptosis has been shown to occur following treatment with irradiation. 4,5) One such study reported that an acute apoptotic response after irradiation may be a feature of the radiosensitive tumor. 6) Spontaneous apoptosis is a mechanism of cell loss in untreated tumors, 3) so irradiation probably enhances the process of apoptosis that results in tumor cell death in irradiated patients.…”

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confidence: 99%

Detection of Apoptosis and Expression of Apoptosis‐associated Proteins as Early Predictors of Prognosis after Irradiation Therapy in Stage IIIb Uterine Cervical Cancer

Yuki

Fujimura

Yamakawa

et al. 2000

Japanese Journal of Cancer Research

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We investigated the proportion of apoptotic cells and the expression of apoptosis-associated proteins after the delivery of the first week of irradiation for stage IIIb uterine cervical cancer. Thirty patients with stage IIIb squamous cell carcinoma of the uterine cervix who received only irradiation therapy were registered in this study. Specimens were obtained before irradiation therapy and at the end of the first week of irradiation. The apoptotic index (AI) of each tissue specimen was calculated by counting the apoptotic cells and expressed as a percentage. Immunohistochemical evaluation for apoptosis-related proteins, p53, Bcl-2, Bax, caspase-1 and caspase-3 was also performed. The AI was 0.8 ± ± ± ±0.9% (mean ± ± ± ± SD) before irradiation and 1.7 ± ± ± ±1.3% at the end of the first week of irradiation. We observed that the patients who survived more than 5 years had AI levels of 2.1 ± ± ± ±1.3% at the end of their first week of therapy. This rate was significantly higher than the rate of 1.1 ± ± ± ±0.8% (P = = = =0.02) of the patients who died within 5 years. When the cut-off value of the AI was set at 1.7%, the sensitivity, specificity, positive predictive value, and negative predictive value for the prediction of patients' prognosis after irradiation therapy were 73.4%, 72.4%, 82.4%, and 61.5%, respectively. In 17 of the AI-positive cases, expressions of Bax (P = = = =0.006), caspase-1 (P = = = =0.045), and caspase-3 (P = = = =0.013) at the end of the first week were significantly higher than before irradiation. The proportion of apoptotic cells and the expression of apoptosis-associated proteins, Bax, caspase-1, and caspase-3, at the end of the first week of irradiation could be useful predictors of the prognosis in stage IIIb squamous cell carcinoma of the uterine cervix treated by irradiation therapy.

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Radiation Response of Mouse Lymphoid and Myeloid Cell Lines. Part III. Different Signals Can Lead to Apoptosis and May Influence Sensitivity to Killing by DNA Double-strand Breakage

Cited by 102 publications

References 16 publications

Kinetics of apoptotic markers in exogeneously induced apoptosis of EL4 cells

Kinetics of apoptotic markers in exogeneously induced apoptosis of EL4 cells

Relationship between clonogenic radiosensitivity, radiation-induced apoptosis and DNA damage/repair in human colon cancer cells

Detection of Apoptosis and Expression of Apoptosis‐associated Proteins as Early Predictors of Prognosis after Irradiation Therapy in Stage IIIb Uterine Cervical Cancer

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