Resumen de Cyclooxygenase‑2 expression as a prognostic factor in pediatric classical Hodgkin lymphoma
Y. Elborai, A. Elgammal, Ahmed A. K. Salama, M. Fawzy, E. D. El Desouky, I. Antía, L.M. Shalaby
Purpose Cyclooxygenase-2 (COX-2) is an inflammation-related enzyme that has been shown to have a role in tumor initia- tion, angiogenesis, and proliferation. It has been demonstrated that COX-2 expression is increased in many tumors and is a negative prognostic parameter. Our objective is to investigate the prognostic value of COX-2 expression in pediatric patients with classical Hodgkin lymphoma (CHL).
Methods This was a retrospective analysis in pediatric patients ( n = 127) diagnosed with CHL and treated at the pediatric oncology department, National Cancer Institute, Cairo University, January 2005–June 2013. We correlated COX-2 immu- nostaining in Reed–Sternberg (RS) cells with clinical variables and outcome.
Results COX-2 was expressed on 38.6% of RS cells. The median follow-up time was 48.4 months (range 4–114 months).
The 5-year OS and PFS, in COX-2(+ve) versus COX-2(−ve) was 85.3% versus 96.0% ( p = 0.248) and 78.6% versus 84.3% ( p = 0.354), respectively. A multivariate analysis showed that COX-2(+ve) was not significantly associated with the 5-year OS (HR = 2.9; 95% CI 0.7–12.4, p = 0.149) or with the 5-year PFS (HR = 1.4; 95% CI 0.6–3.2, p = 0.490). High-risk patients in the COX-2(+ve) group had a significantly lower 5-year OS ( p = 0.021). The 5-year PFS was significantly lower in the COX-2(+ve) group with B symptoms ( p = 0.023) and bulky disease ( p = 0.028). Radiotherapy was given only to high-risk patients; survival was much better in radiation-treated children in both the Cox-2(+ve) and Cox-2(−ve) groups. The magni- tude of the radiotherapy effect was also greater in the Cox-2(+ve) group, but this difference was not statistically significant.
Conclusion COX-2 expression showed a tendency to be a poor prognostic factor, but it failed to provide meaningful independ - ent information. Further larger studies are needed to investigate COX-2 as a prognostic factor and potential therapeutic target.
