Thesis Type: Postgraduate
Institution Of The Thesis: Gazi University, Sağlık Bilimleri Enstitüsü, BİYOKİMYA (ECZ) ANA BİLİM DALI, Turkey
Approval Date: 2021
Thesis Language: Turkish
Student: Kader Kübra DEMİRDÖĞEN
Supervisor: Aymelek Gönenç
Abstract:
The impaired apoptosis mechanism participate in formation of breast cancer, which is the most common type of cancer among women in the world. Changes in levels of TNF-associated apoptosis inducing ligand (TRAIL), one of the extrinsic apoptotic pathway elements. TRAIL and its receptors, DR4 and DR5, are associated with the prognosis of cancer. YKL-40 and urokinase type plasminogen activator receptor (uPAR) has antiapoptotic activity. CCL5 is a one of chemokines triggering formation cancer microenvironment. In our study, serum sTRAIL, DR4, DR5, uPAR, CCL5 and YKL-40 levels were measured using ELISA kits in breast cancer patients. The sample collected from 62 healthy individuals and 62 patients with breast cancer newly diagnosed and untreated in General Surgery Department of Gazi Hospital. While the levels of TRAIL receptors DR4 and DR5 increased in breast cancer patients, no significant difference was found between the two groups in terms of serum TRAIL level (p <0.05, p <0.01, p> 0.05, respectively). Serum uPAR and YKL-40 levels were significantly lower in the patient group compared to the control group (p <0.01, p <0.01, respectively). While there was no difference between the patient and control groups in terms of serum CCL5 levels, it was found to be lower in Grade 3 patients than Grade 1 patients (p <0.05). A positive correlation was found between TRAIL levels and DR5 levels in breast cancer patients and healthy controls. It is thought that the increase of serum DR4 and DR5 levels in breast cancer may be a compensatory mechanism by which death receptor-mediated apoptosis is induced. The effect of this pathway on the cancer developing will be elucidated by clinical studies which in TRAIL and receptor expressions, including metastatic breast cancer, will be accessed together.
Key Words
: Apoptosis, sTRAIL, TRAIL’s receptors, chemokines, breast cancer