Introduction
Wilm’s Tumor (WT), also called nephroblastoma, is the most common genitourinary system tumor in children and is caused by mutations or deletions of Wilms Tumor Gene-1 (WT1) located on the short arm of chromosome 111. This tumor with an incidence of 1 in 10,000 children accounts for 6% of all childhood cancers2. It usually occurs before 5 years of age in a single kidney and equally in both genders3. Although there has been an increase in the survival rate in recent years, the survival rate is still low with 50% in patients with metastasis and recurrence despite intensive treatment regimens3. In survived children, late survival and secondary malignancies are observed due to chemo-radiotherapy side effects4. Understanding the pathogenesis, progression and metastasis-related factors of this malignancy, which has a high mortality and morbidity rate, is of crucial importance for the development of new treatments. Although it is known that WT1 and kat-catenin mutations are effective in the tumorigenesis of WT, factors effective in the progression are not exactly known5. Therefore, new studies are needed to be conducted on this subject.
There are studies suggesting that prostoglandins (PG) have effects on immune system, cell proliferation, apoptosis, and angiogenesis. The cyclooxygenase (COX) enzyme, which plays a role in the synthesis of PGs, has two known isoforms. COX-1 is responsible for the normal physiological effect and found in almost all tissues, while COX-2 can be induced by trauma, inflammatory cytokines, growth factors, and oncogenes. COX-2 increase is responsible for decreased apoptosis, immunosuppression, increased tumor cell proliferation, angiogenesis and metastasis potential in cancerous tissues6. Over-expression of COX-2 has been reported in many malignancies, but there are few studies on its role in WT. Therefore, in our study, we aimed to determine the prognostic significance of COX-2 in this tumor and its effects on tumor formation.