%0 Journal Article %T P53/P21 Expression Increment as Predisposing Factor for Cancer Development in Hypertensive Patients in Al-Diwaniyah Province, Iraq %J Journal of Medicinal and Chemical Sciences %I Sami Publishing Company (SPC) %Z 2651-4702 %A Alebady, Zainab Adnan Hatem %A Hatem, Oraas Adnan %A Abd AL-Hamza, Tabarak %A Sarhan, Fatima Mushtaq %A Raham, Mohammed Mrauh %D 2023 %\ 03/01/2023 %V 6 %N 3 %P 472-479 %! P53/P21 Expression Increment as Predisposing Factor for Cancer Development in Hypertensive Patients in Al-Diwaniyah Province, Iraq %K Hypertension %K p53 %K p21 %K Apoptosis %K Antihypertensive drugs %R 10.26655/JMCHEMSCI.2023.3.3 %X Hypertension has been linked to a higher risk of getting some malignancies and a higher cancer-related mortality rate. Furthermore, many anticancer medicines have been linked to developing new high blood pressure or deteriorating previously well-controlled hypertension. The P53 tumor antigen is a mutation-hosting antigen. It is also one of the human tumors’ most common genetic changes. Tumor growth is thought to be produced by several stages of genetic damage, which can lead to a breakdown in cell cycle regulatory systems. The objective of this study was to investigate the relationship between high blood pressure and cancer development markers represented by p53, the guardian of the genome, protein expression and its downstream regulator, p21. 20 hypertensive patients (46-70 years of age) were included in this study. Blood samples were collected from two study groups. ELISA Technique was used to detect the protein levels of P53 and P21. The data presented in this study indicate the effect of high blood pressure on cell cycle progression and suggest that programmed cell death is triggered by hypertension, which was reflected by the high expression of P53 and its downstream regulator p21. It is suggested by the data that high blood pressure could be considered a driving force in tumor development through indirect stimulation of cell proliferation to compensate the cell loss by apoptosis which can also drive the development of tumor cells. %U https://www.jmchemsci.com/article_156860_aa316cd44e8c93f4928282afc05f5b04.pdf