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Chromosomal end fusion resulting from telomere erosion increases susceptibility to radiation via multinucleation: Effect of p53
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ju, Yeun-Jin | - |
dc.contributor.author | Park, Jeong Eun | - |
dc.contributor.author | Juhn, Kyoung Mi | - |
dc.contributor.author | Keong, Jaemin | - |
dc.contributor.author | Yun, Miyong | - |
dc.contributor.author | Park, Myung | - |
dc.contributor.author | Park, Gil-Hong | - |
dc.contributor.author | Choi, Kang-Yell | - |
dc.contributor.author | Cho, Myung-Haing | - |
dc.contributor.author | Wong, Kwok-Kin | - |
dc.contributor.author | Park, Won-Bong | - |
dc.contributor.author | Lee, Kee-Ho | - |
dc.date.accessioned | 2009-08-07T03:02:46Z | - |
dc.date.available | 2009-08-07T03:02:46Z | - |
dc.date.issued | 2006 | - |
dc.identifier.citation | International Journal of Oncology 29: 753-763, 2006 | en |
dc.identifier.issn | 1019-6439 | - |
dc.identifier.uri | http://www.spandidos-publications.com/ijo/article.jsp?article_id=ijo_29_4_753 | - |
dc.identifier.uri | https://hdl.handle.net/10371/6482 | - |
dc.description.abstract | and telomerase activation are frequently found in human cancers. p53 inactivation, however, eliminates or attenuates the biological responses to telomerase inhibition and the eventual telomere erosion. We show that telomere erosion can increase the susceptibility to radiation, irrespective of p53 status. Both telomerase inhibition and critically shortened telomere with significant change of chromosomal end-to-end fusion were essential for the enhancement of radiosensitivity. The enhancement was correlated with greater formation of multinucleated cells. p53 inactivation did not eliminate the observed generation of chromosomal fusion and multinucleation, and the resulting increased susceptibility to radiation, as opposed to the previously proved role of p53 in mediating cellular responses to telomere dysfunction. The present findings suggest the importance of chromosomal end fusion in modulating radiosensitivity rather than p53 DNA damage signaling. Thus, the suggested anticancer radiotherapeutic strategy combined with telomerase inhibition could clinically be applicable to cancers, irrespective of p53 status. | en |
dc.description.sponsorship | We thank Professor Woon Ki Paik for critical reading of the
manuscript and Eun-Ju Lee for assistance in the preparation of the manuscript. This work was supported by a grant from National Nuclear R&D program and Human Genome Project (FG-1-1), Korean Ministry of Science and Technology. | en |
dc.language.iso | en | - |
dc.publisher | Spandidos Publications | en |
dc.subject | chromosome | en |
dc.subject | fusion | en |
dc.subject | p53 | en |
dc.subject | radiosensitivity | en |
dc.subject | telomerase | en |
dc.title | Chromosomal end fusion resulting from telomere erosion increases susceptibility to radiation via multinucleation: Effect of p53 | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 주은진 | - |
dc.contributor.AlternativeAuthor | 박정은 | - |
dc.contributor.AlternativeAuthor | 전경미 | - |
dc.contributor.AlternativeAuthor | 정재민 | - |
dc.contributor.AlternativeAuthor | 윤미용 | - |
dc.contributor.AlternativeAuthor | 박명진 | - |
dc.contributor.AlternativeAuthor | 박길홍 | - |
dc.contributor.AlternativeAuthor | 최강열 | - |
dc.contributor.AlternativeAuthor | 조명행 | - |
dc.contributor.AlternativeAuthor | 박원봉 | - |
dc.contributor.AlternativeAuthor | 이기호 | - |
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