Hypersensitivity to radiation-induced non-apoptotic and apoptotic death in cell lines from patients with the ICF chromosome instability syndrome

Author(s):  
Ajita Narayan ◽  
Cathy Tuck-Muller ◽  
Karen Weissbecker ◽  
Dominique Smeets ◽  
Melanie Ehrlich
2017 ◽  
Author(s):  
Y.A. Eidelman ◽  
S.V. Slanina ◽  
V.S. Pyatenko ◽  
I.K. Khvostunov ◽  
S.G. Andreev

ABSTRACTThe experimental observations demonstrate that different cell lines reveal various shape of dynamic curves for radiation-induced chromosomal instability (RICI). We analyzed our own and published data on RICI for three cell lines, CHO-K1, V79 and TK6, on the basis of the mechanistic RICI model. We demonstrate that all three dynamic curves can be successfully described by the proposed model with partially cell line specific parameters.


2021 ◽  
Vol 22 (3) ◽  
pp. 1418
Author(s):  
Elham Shahhoseini ◽  
Masao Nakayama ◽  
Terrence J. Piva ◽  
Moshi Geso

This study examined the effects of gold nanoparticles (AuNPs) and/or ionizing radiation (IR) on the viability and motility of human primary colon epithelial (CCD841) and colorectal adenocarcinoma (SW48) cells as well as human primary epidermal melanocytes (HEM) and melanoma (MM418-C1) cells. AuNPs up to 4 mM had no effect on the viability of these cell lines. The viability of the cancer cells was ~60% following exposure to 5 Gy. Exposure to 5 Gy X-rays or 1 mM AuNPs showed the migration of the cancer cells ~85% that of untreated controls, while co-treatment with AuNPs and IR decreased migration to ~60%. In the non-cancerous cell lines gap closure was enhanced by ~15% following 1 mM AuNPs or 5 Gy treatment, while for co-treatment it was ~22% greater than that for the untreated controls. AuNPs had no effect on cell re-adhesion, while IR enhanced only the re-adhesion of the cancer cell lines but not their non-cancerous counterparts. The addition of AuNPs did not enhance cell adherence. This different reaction to AuNPs and IR in the cancer and normal cells can be attributed to radiation-induced adhesiveness and metabolic differences between tumour cells and their non-cancerous counterparts.


PLoS Genetics ◽  
2017 ◽  
Vol 13 (4) ◽  
pp. e1006707 ◽  
Author(s):  
Signe Penner-Goeke ◽  
Zelda Lichtensztejn ◽  
Megan Neufeld ◽  
Jennifer L. Ali ◽  
Alon D. Altman ◽  
...  

2007 ◽  
Vol 178 (2) ◽  
pp. 283-296 ◽  
Author(s):  
Yohei Niikura ◽  
Amruta Dixit ◽  
Ray Scott ◽  
Guy Perkins ◽  
Katsumi Kitagawa

The spindle checkpoint that monitors kinetochore–microtubule attachment has been implicated in tumorigenesis; however, the relation between the spindle checkpoint and cell death remains obscure. In BUB1-deficient (but not MAD2-deficient) cells, conditions that activate the spindle checkpoint (i.e., cold shock or treatment with nocodazole, paclitaxel, or 17-AAG) induced DNA fragmentation during early mitosis. This mitotic cell death was independent of caspase activation; therefore, we named it caspase-independent mitotic death (CIMD). CIMD depends on p73, a homologue of p53, but not on p53. CIMD also depends on apoptosis-inducing factor and endonuclease G, which are effectors of caspase-independent cell death. Treatment with nocodazole, paclitaxel, or 17-AAG induced CIMD in cell lines derived from colon tumors with chromosome instability, but not in cells from colon tumors with microsatellite instability. This result was due to low BUB1 expression in the former cell lines. When BUB1 is completely depleted, aneuploidy rather than CIMD occurs. These results suggest that cells prone to substantial chromosome missegregation might be eliminated via CIMD.


2014 ◽  
Vol 9 (1) ◽  
pp. 15 ◽  
Author(s):  
Belinda Maroschik ◽  
Anne Gürtler ◽  
Anne Krämer ◽  
Ute Rößler ◽  
Maria Gomolka ◽  
...  

1983 ◽  
Vol 3 (9) ◽  
pp. 1675-1679
Author(s):  
P Jolicoeur ◽  
E Rassart ◽  
P Sankar-Mistry

Using the Southern procedure, we have studied the presence of ecotropic-specific murine leukemia viral sequences in genomic DNA isolated from primary X-ray-induced thymomas, from lymphoid cell lines established from them, or from secondary tumors passaged in vivo. We found that primary radiation-induced thymomas and infiltrated spleens do not harbor newly acquired ecotropic provirus. However, additional ecotropic proviruses (which appear recombinant in the gagpol region) could be detected in most of the tumorigenic cell lines established in vitro from them and in tumors arising from subcutaneous transplantation of the primary thymomas. These results suggest that primary radiation-induced thymomas may not be clonal. They also indicate a strong correlation between the presence of ecotropic recombinant proviruses in the genome and the growth ability, both in vitro and in vivo, of specific cells within these thymomas, suggesting a possible mitogenic function for murine leukemia virus.


2006 ◽  
Vol 1 (3) ◽  
pp. 451-462 ◽  
Author(s):  
Jianshe Yang ◽  
Xigang Jing ◽  
Zhuanzi Wang ◽  
Wenjian Li

AbstractThree human malignancy cell lines were irradiated with 60Co γ-rays. Initial chromatid breaks were measured by using the chemically induced premature chromosome condensation technique. Survival curves of cells exposed to gamma rays was linear-quadratic while the efficiency of Calyculin A in inducing PCC of G2 PCC was about five times more than G1 PCC. A dose-dependent increase in radiation-induced chromatid/isochromatid breaks was observed in G1 and G2 phase PCC and a nearly positive linear correlation was found between cell survival and chromatin breaks. This study implies that low LET radiation-induced chromatid/isochromatid breaks can potentially be used to predict the radiosensitivity of tumor cells either in in vitro experimentation or in in vivo clinical radiotherapy.


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