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Coronavirus disease 2019 (COVID-19) has rapidly spread across the globe since its outbreak in Wuhan, China, in 2019. Clinical evidence suggests higher oxidative stress in COVID-19 patients, and this worsening redox status which may contribute to disease progression. The present study aimed to investigate the oxidative Deoxyribonucleic acid damage in patients with mild and severe COVID-19 infection and to evaluate its relationship to the disease progression and severity. A case-control study was conducted from September 2021 to January 2022 in Duhok city, Kurdistan Region-Iraq. 180 individuals have participated. Among 88 COVID-19 cases, 92 healthy volunteers as the control group, with ages ranging (18-45) years. Patients were divided into two groups according to the severity of infection (mild cases, severe cases). Serum level of 8-OHdG and malondialdehyde (MDA) were assessed as oxidative stress biomarkers. Serum levels of 8-OHdG were considerably higher in patients with COVID-19 infection in comparison to the control group, (p

p53 is a tumor suppressor that prevents the emergence of transformed cells by inducing apoptosis or senescence, among other responses. Its functions are regulated tightly by posttranslational modifications. Here we show that Bruton's tyrosine kinase (BTK) is a novel modulator of p53. We found that BTK is induced in response to DNA damage and p53 activation. BTK induction leads to p53 phosphorylation, which constitutes a positive feedback loop that increases p53 protein levels and enhances the transactivation of its target genes in response to stress. Inhibiting BTK reduced both p53-dependent senescence and apoptosis. Further, BTK expression also upregulated DNA damage signals and apoptosis. We conclude that despite being involved in oncogenic signals in blood malignancies, BTK has antineoplastic properties in other contexts, such as the enhancement of p53's tumor suppressor responses. Along with evidence that BTK expression correlates with good prognosis in some epithelial tumors, our findings may encourage a reevaluation of the clinical uses of BTK inhibitors in cancer therapy. Cancer Res; 76(18); 5405–14. ©2016 AACR.

Supplementary Figure 2. p53 phosphorylation.

Legends for supplementary figures

Supplementary Figure 1.p53 expression and phosphorylation.

Supplementary Figure 3. BTK and apoptosis.