Celecoxib

In Apcᵐⁱⁿ⁄⁺ mice, a model of spontaneous intestinal tumorigenesis, dietary zinc deficiency significantly increased colon tumor formation. This effect was mediated by upregulation of pro‑inflammatory mediators, including COX‑2, TNF‑α, and multiple CCL, CXCL, and IL chemokines. Administration of the selective COX‑2 inhibitor celecoxib reduced both the inflammatory response and tumor burden. The authors conclude that zinc deficiency promotes colon cancer through an inflammatory mechanism and that celecoxib can attenuate this effect, suggesting a potential prevention strategy for zinc‑deficient populations.

Fig. 1 Celecoxib attenuated ZD-promoted tumorigenesis through suppressing inflammations. (Yin X, et al., 2021)

In a post hoc analysis of the phase 3 CALGB/SWOG 80702 trial (940 patients with stage III colon cancer), postoperative ctDNA status was highly prognostic: ctDNA‑positive patients had markedly worse disease‑free and overall survival (aHR ~6 for both). Among ctDNA‑positive patients, adjuvant celecoxib significantly improved DFS (aHR 0.61) and OS (aHR 0.62) compared to placebo. No such benefit was seen in ctDNA‑negative patients. ctDNA status may inform which patients should receive celecoxib alongside conventional chemotherapy.

Fig. 2 Disease-Free Survival (DFS) and Overall Survival (OS) Estimates, by Assigned Oral Agent (Celecoxib vs. Placebo) and Postoperative Circulating Tumor DNA (ctDNA) Status. (Zhang GQ, et al., 2026)