This book offers a profound and thorough illumination of the clinical aspects of radiation oncology. It is believed that radiation's mode of action contributes to the development of double strand breaks in DNA. Due to the acetylation of histone proteins by histone acetyltransferases, double strand breaks are repaired by non-homologous end joining (HATs). When it comes to radiation sensitivity in therapeutic settings, this repair may prove to be helpful. Sixty percent of human malignancies are related to the transformation of the tumor suppressor gene P53, which limits the transcription and translation of a certain set of genes.
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- SKU: 9781632420824
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