We hypothesized that patterns of CTNNB1 (β-
catenin) mutations would affect the outcome of
conservative therapy in patients with
desmoid tumors. This study aimed to determine the significance of CTNNB1 (β-
catenin) mutations in predicting the treatment outcome in patients with
desmoid tumors treated with
meloxicam, a
cyclooxygenase-2 (COX-2) selective inhibitor. Between 2003 and 2012, consecutive thirty-three patients with extra-peritoneal sporadic
desmoid tumors were prospectively treated with
meloxicam as the initial systemic medical
therapy. The efficacy of
meloxicam was evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST).
DNA was isolated from frozen tissue or
formalin-fixed materials. CTNNB1 mutation analysis was performed by direct sequencing. Positivity of nuclear β-
catenin staining by immunohistochemistry was compared with the status of CTNNB1 mutations. The correlation between the efficacy of
meloxicam treatment and status of CTNNB1 mutations was analyzed. Of the 33 patients with
meloxicam treatment, one showed complete remission (CR), 7 partial remission (PR), 12 stable disease (SD), and 13 progressive disease (PD). The following 3 point mutations were identified in 21 of the 33 cases (64%): T41A (16 cases), S45F (4 cases) and S45P (one case). The nuclear expression of β-
catenin correlated significantly with CTNNB1 mutation status (p = 0.035); all four cases with S45F mutation exhibited strong nuclear expression of β-
catenin. S45F mutation was significantly associated with a poor response (all cases; PD) (p = 0.017), whereas the other mutations had no impact on efficacy. The CTNNB1 mutation status was of significant prognostic value for
meloxicam treatment in patients with sporadic
desmoid tumors.