Frontiers in Radiation Oncology

The mode of action by radiation is postulated to be the production of double strand breaks of DNA. The repair of double strand breaks occurs through non homologous end joining through acetylation of histone proteins by histone acetyltransferases (HATs). The fixation of double strand breaks through H...

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collection Directory of Open Access Books
description The mode of action by radiation is postulated to be the production of double strand breaks of DNA. The repair of double strand breaks occurs through non homologous end joining through acetylation of histone proteins by histone acetyltransferases (HATs). The fixation of double strand breaks through HAT inhibitors is a promising application for radiation sensitization in the clinic. P53 is a tumour suppressor gene and its mutation has been implicated in 60% of human cancers. As one of the pivotal anticancer genes, P53 controls the transcription and translation of a series of genes. The kinetics of DNA double strand break generation and their co relation to P53 status, ATM and ARF activation are computed and modelled for understanding the potential of such research.
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publishDate 2021
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spelling doab-20.500.12854ir-665752024-03-31T22:43:40Z Frontiers in Radiation Oncology Kataria, Tejinder Radiotherapy thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCL Oncology The mode of action by radiation is postulated to be the production of double strand breaks of DNA. The repair of double strand breaks occurs through non homologous end joining through acetylation of histone proteins by histone acetyltransferases (HATs). The fixation of double strand breaks through HAT inhibitors is a promising application for radiation sensitization in the clinic. P53 is a tumour suppressor gene and its mutation has been implicated in 60% of human cancers. As one of the pivotal anticancer genes, P53 controls the transcription and translation of a series of genes. The kinetics of DNA double strand break generation and their co relation to P53 status, ATM and ARF activation are computed and modelled for understanding the potential of such research. 2021-04-20T15:47:13Z 2021-04-20T15:47:13Z 2013 book ONIX_20210420_9789535111634_1934 9789535111634 9789535171706 https://directory.doabooks.org/handle/20.500.12854/66575 eng image/jpeg n/a https://www.intechopen.com/books https://mts.intechopen.com/storage/books/2693/authors_book/authors_book.pdf IntechOpen IntechOpen 10.5772/3065 10.5772/3065 78a36484-2c0c-47cb-ad67-2b9f5cd4a8f6 9789535111634 9789535171706 IntechOpen 228 open access
spellingShingle Radiotherapy
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCL Oncology
Frontiers in Radiation Oncology
title Frontiers in Radiation Oncology
title_full Frontiers in Radiation Oncology
title_fullStr Frontiers in Radiation Oncology
title_full_unstemmed Frontiers in Radiation Oncology
title_short Frontiers in Radiation Oncology
title_sort frontiers in radiation oncology
topic Radiotherapy
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCL Oncology
topic_facet Radiotherapy
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCL Oncology
url ONIX_20210420_9789535111634_1934