Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways
Elwakkad, A., Gamal El Din, A., Hebishy, M., Abou-Seif, H. (2024). Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways. EKB Journal Management System, 23(2), 184-198.
Amany Elwakkad; Amina A. Gamal El Din; Mohamed A. Hebishy; Howida S. Abou-Seif. "Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways". EKB Journal Management System, 23, 2, 2024, 184-198.
Elwakkad, A., Gamal El Din, A., Hebishy, M., Abou-Seif, H. (2024). 'Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways', EKB Journal Management System, 23(2), pp. 184-198.
Elwakkad, A., Gamal El Din, A., Hebishy, M., Abou-Seif, H. Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways. EKB Journal Management System, 2024; 23(2): 184-198.

Apoptosis as a therapeutic strategy for breast cancer: the role of Thymax, a gross thymic extract, in modulating cell death pathways

Egyptian Pharmaceutical Journal
Volume 23, Issue 2, April 2024, Page 184-198  XML PDF (4.97 MB)
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Authors
Amany Elwakkad; Amina A. Gamal El Din; Mohamed A. Hebishy; Howida S. Abou-Seif
Abstract
Background
Breast cancer is a prevalent disease in women and a leading cause of cancer-related health issues. Thymax, a thymic extract, has shown potential for inducing breast cancer cell apoptosis in vitro.
Objective
This study aims to investigate how Thymax induces apoptosis and inhibits breast cancer growth and metastasis in vivo.
Materials and methods
Thymax treatment was divided into five groups: the first group (negative control) − normal rats without tumors. In the second group (positive control), rats were injected subcutaneously in the mammary gland with a single dose of 50 mg/kg b.w. of 7,12-Dimethylbenz(a)anthracene (in 2 ml of corn oil) and allowed to develop tumors for 120 days. Group 3: Thymax was orally administered 6 days a week to tumor-bearing rats (0.4 mg/rat) and continued for 5 weeks. Tumor-bearing rats in group 4 (Thymax injection) received 0.1 ml of Thymax solution through intraperitoneal injection twice weekly for 5 weeks. The last group was Thymax mix (oral and injection); tumor-bearing rats received Thymax solution by dual routes: orally with 0.4 ml six times per week and intraperitoneally with 0.1 ml twice weekly for 5 weeks. Thymax treatment, beginning after 120 days of tumor induction, continued for 5 weeks.
Results and conclusion
Thymax- induced apoptosis in breast cancer cells by increasing cytochrome c, tumor necrosis factor receptor type 1-associated death domain protein (TRADD), and Fas associated death domain (FADD) levels. It also activated the mitochondrial-dependent pathway with up-regulation of tumor protein gene (P53) expression and cysteine-dependent, aspartate-specific peptidase (caspase-8) activation. Thymax restored normal renal and hepatic cell function and enhanced the immune system by improving total antioxidant levels and inhibiting malondialdehyde levels in treated animals. Histopathological results showed a significant apoptotic effect in the group receiving Thymax injections, demonstrating its capability to induce apoptosis without tumors or atypia in mammary glands.
Keywords
apoptosis; breast cancer; Caspase-8; in vivo; Oxidative Stress; Thymax
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