Radiation-Induced Acute Immediate Nuclear Abnormalities in Oral Cancer Cells

Bhattathiri, Narayanan V.; Bindu, L.; Remani, Prathapan; Bharathykkutty, Chandralekha; Nair, Krishnan M.

doi:10.1159/000332093

Cited by 25 publications

(14 citation statements)

References 13 publications

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“…The mitotic catastrophe is generally considered a consequence of premature or improper entry of a cell into mitosis and can be induced by a multitude of DNA-damaging agents including radiation. The mitotic catastrophe is executed by most non-hematopoietic tumor cells in response to ionizing radiation [68] and is frequently observed in experimental tumors following radiotherapy and radioimmunotherapy [69][70][71][72][73]. Mitotic catastrophe is today considered to be the major cell death mechanism by which solid tumors respond to clinical radiotherapy.…”

Section: Radiation-induced Mitotic Catastrophementioning

confidence: 99%

Radiation-induced cell death mechanisms

2010

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The main goal when treating malignancies with radiation therapy is to deprive tumor cells of their reproductive potential. One approach to achieve this is by inducing tumor cell apoptosis. Accumulating evidences suggest that induction of apoptosis alone is insufficient to account for the therapeutic effect of radiotherapy. It has become obvious in the last few years that inhibition of the proliferative capacity of malignant cells following irradiation, especially with solid tumors, can occur via alternative cell death modalities or permanent cell cycle arrests, i.e., senescence. In this review, apoptosis and mitotic catastrophe, the two major cell deaths induced by radiation, are described and dissected in terms of activating mechanisms. Furthermore, treatment-induced senescence and its relevance for the outcome of radiotherapy of cancer will be discussed. The importance of p53 for the induction and execution of these different types of cell deaths is highlighted. The efficiency of radiotherapy and radioimmunotherapy has much to gain by understanding the cell death mechanisms that are induced in tumor cells following irradiation. Strategies to use specific inhibitors that will manipulate key molecules in these pathways in combination with radiation might potentiate therapy and enhance tumor cell kill.

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Section: Radiation-induced Mitotic Catastrophementioning

confidence: 99%

Radiation-induced cell death mechanisms

2010

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“…Nuclear morphologic changes in U251MG or D54MG cells were evaluated using Giemsa staining, as described elsewhere (Bhattathiri et al, 1998a, b;Bhattathiri, 2001). U251MG and D54MG cells were irradiated with a dose of 4 Gy, and were infected with Axmock, Ax-hp16 or Ax-p21 as described above.…”

Section: Evaluation Of Nuclear Morphologymentioning

confidence: 99%

“…The frequency of micronucleated, nuclear budded, binucleated and multinucleated tumour cells was evaluated. The criteria for identification of these cells are described elsewhere (Bhattathiri et al, 1998a, b;Bhattathiri, 2001). Briefly, micronucleated cells contain small round bodies of nuclear material within the cytoplasm, separate from the main nucleus (the cells indicated with one arrow in Figure 4D and E).…”

Section: Evaluation Of Nuclear Morphologymentioning

confidence: 99%

p16 gene transfer increases cell killing with abnormal nucleation after ionising radiation in glioma cells

et al. 2003

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It is well established that cells synchronised at the G1 -S phase are highly radiosensitive. In this study, p16-null human glioma cell lines were induced into G1 cell cycle arrest by adenovirus-mediated p16 gene transfer, and examined for radiation-induced cell killing. Clonogenic analysis and trypan blue extraction test showed that the p16 gene transfer enhanced radiation-induced cell killing in p16-null glioma cell lines. TUNEL assays and pulse-field gel electrophoresis confirmed that the radiation-induced cell killing of p16-transfected cells could be caused by a nonapoptotic mechanism. Gimsa staining demonstrated that irradiation alone or Ax-mock infection plus irradiation results in a slight increase in the frequency of cells with abnormal nucleus, compared to unirradiated uninfected or Ax-mock infected cells. However, Ax-hp16 or Ax-hp21 infection alone modestly increased the frequency of cells with abnormal nucleus (especially bi-and multinucleation), and 4-Gy irradiation of Ax-hp16 or Ax-hp21 infected cells substantially enhanced this frequency. These results suggest that there exists some unknown interaction between radiation and p16 in cytoplasm/ membranes, which decreases cytokinesis and promotes abnormal nucleation. Thus, p16 expression prevented radiation-induced apoptosis by promoting abnormal nucleation, thereby leading to another mode of cell death.

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“…The most important data of 4 papers in Table 2 are presented concerning the studied cells with no sign of pathology [23][24][25][26] presented (Table 3) [27][28][29][30]. Both in normal and tumor cells a significant increase of MN was observed due to radiation.…”

Section: The Data Concerning Possibility To Use Micronuclei (Mn) Levementioning

confidence: 99%

“…In 4 papers MN level was studied in cervix and oral mucosa tumor cells (Table 3) [24,[27][28][29][30]. In some cases MN frequencies in the tumor cells were higher than in the normal mucosa cells (e. g., 15 ‰ [27] and 11 ‰ [28] compared with the healthy subjects from India -0.7-4.0 ‰ [32]).…”

Section: The Data Concerning Possibility To Use Micronuclei (Mn) Levementioning

confidence: 99%

Biomonitoring of the cytogenetic effect of antitumor therapy by means of micronucleus assay in exfoliated epithelial cells

Nersesyan

2007

Cytol. Genet.

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Radiation-Induced Acute Immediate Nuclear Abnormalities in Oral Cancer Cells

Cited by 25 publications

References 13 publications

Radiation-induced cell death mechanisms

Radiation-induced cell death mechanisms

p16 gene transfer increases cell killing with abnormal nucleation after ionising radiation in glioma cells

Biomonitoring of the cytogenetic effect of antitumor therapy by means of micronucleus assay in exfoliated epithelial cells

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