Glioblastoma ve oligodendroglioma'da CD47 ekspresyonunun incelenmesi: Tümör mikrosistemi ve tedavi stratejileri açısından olası etkiler

Glioblastoma (GBM) is the most common and aggressive type of primary malignant brain tumor with a median survival time of 16 to 19 months The diagnosis of GBM is typically made by imaging techniques such as magnetic resonance imaging (MRI) and confirmed by biopsy. Treatment is mainly surgery, but also includes radiation therapy and supportive chemotherapy. Surgical resection is the most decisive factor in patient survival, but the use of temozolomide chemotherapy in combination with radiotherapy has been shown to improve the 2-year survival rate. GBM is characterized by its rapid growth and infiltrative nature, making it difficult to completely remove by surgery. Despite advances in treatment modalities, GBM remains largely incurable and has a high rate of recurrence even after treatment, which contributes to its poor prognosis. Alternative treatment modalities for GBM are needed because current treatment options such as surgery, adjuvant chemotherapy and radiation therapy have limited effectiveness in improving long-term survival. While these treatments can help manage symptoms and prolong survival to some extent, they are not curative. CD47 is a membrane protein belonging to the immunoglobulin superfamily and is known as the "don't eat me" signal. It plays a role in immune evasion by inhibiting phagocytosis, the process by which immune cells engulf and destroy cancer cells. In cancer, high levels of CD47 expression have been observed in several tumor types, including prostate carcinoma, ovarian cancer, clear cell renal cell carcinoma, non-small cell lung cancer ,endometrial carcinoma, breast cancer, bladder cancer and more. In these cancers, CD47 expression has been associated with adverse clinicopathological features such as higher tumor grade, lymphovascular invasion and advanced disease stages, revealing a link between expression level and poor prognosis and reduced survival rates. Between 2004 and 2013, only a limited number of studies have examined the level and role of CD47 in GBM. In these studies, in summary, high CD47 levels were associated with radiotherapy and temozolomide resistance, targeted inhibition of CD47 was shown to suppress tumor growth in vitro, CD47 was shown to work together with SIRPalpha, calreticulin, Tenascin C molecules in GBM and to be associated with PI3K/Akt pathway, and PDL-1 and VEGF inhibition in addition to CD47 inhibition was shown to be synergistic in suppressing tumor growth. Our aim in this study is to add to the literature on the role of CD47 in GBM in different aspects by revealing the concentration and prevalence of CD47 levels in pathology specimens and its relationship with patient survival, treatment resistance and tumor grade.