Status of H2AX and TP53 (Non- phosphorylation) for DNA Damage in Cancer Patients on Radiotherapy-A Case-Control Study | Abstract

International Journal of Medical Research & Health Sciences (IJMRHS)
ISSN: 2319-5886 Indexed in: ESCI (Thomson Reuters)


Status of H2AX and TP53 (Non- phosphorylation) for DNA Damage in Cancer Patients on Radiotherapy-A Case-Control Study

Author(s):Alkhansa S. Mahmoud*, Omer M. Abdalla, Amna A. Ali, Nuha M. Hassan, Amna A. Yousif, Fawzia E. Elbashir, Ahmed Omer, Raheel Mussa and Ammar ME. Hassan

Introduction: Radiotherapy is widely used in the treatment of cancer patients, and some genes affect the response to radiotherapy. In addition, phosphorylation is a hallmark of DNA damage response. In this study, we aim to investigate the status of H2AX and the non-phosphorylation forms of tumor suppressor p53 (TP53) before and after radiotherapy to reveal their roles in DNA damage response and radio-sensitivity. Materials and Methods: ELISA technique was used to determine the H2AX concentration and TP53 expression status in plasma of 29 cancer patients and 29 healthy individuals of the same age and sex as a control group. Patients were treated with radiotherapy, while the control group was not irradiated. H2AX and TP53 were measured before the start of radiotherapy on the first day of treatment and then 30 minutes after radiotherapy on the last day. Results: Both H2AX and TP53 had higher levels in cancer patients before radiotherapy than in healthy subjects. In 21 patients, H2AX levels were significantly decreased after radiotherapy compared with levels before radiotherapy (p=0.002), and TP53 levels were significantly increased after radiotherapy compared with levels before radiotherapy (p=0.0008). In eight patients (n=8), H2AX levels were increased after radiotherapy and TP53 expression was decreased after radiotherapy. Conclusion: The results show that both H2AX and TP53 can be induced by DNA damage. The decrease of H2AX level after radiotherapy refers to the conversion of this histone protein to the phosphorylated form (gamma-H2AX) after radiotherapy, so H2AX can be used as an indicator of DNA damage response and radiation sensitivity by the phosphorylation form (gamma-H2AX) in early exposure. While TP53 is activated by radiotherapy because its expression is increased after radiotherapy in cancer patients, indicating that TP53 is not yet phosphorylated, TP53 can also be used as a marker to indicate DNA damage response in early radiation exposure.

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