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.