To illustrate and document the tenuous connection between the Wilcoxon–Mann–Whitney (WMW) procedure and medians, its relationship to mean ranks is first contrasted with the relationship of a t-test to means. The quantity actually tested: $\widehat{\mathrm{Pr}}(X_1<X_2)+\widehat{\mathrm{Pr}}(X_1=X_2)/2$ is then described and recommended as the basis for an alternative summary statistic that can be employed instead of medians. In order to graphically represent an estimate of the quantity: Pr(X₁ < X₂) + Pr(X₁ = X₂)/2, use of a bubble plot, an ROC curve and a dominance diagram are illustrated. Several counter-examples (real and constructed) are presented, all demonstrating that the WMW procedure fails to be a test of medians. The discussion also addresses another, less common and perhaps less clear cut, but potentially even more important misconception: that the WMW procedure requires continuous data in order to be valid. Discussion of other issues surrounding the question of the WMW procedure and medians is presented, along with the authors' teaching experience with the topic. SAS code used for the examples is included as supplementary material.

2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid (CDDO), a synthetic analog of oleanolic acid, and its C28 methyl ester derivative (CDDO-Me), have shown potent antitumorigenic activity against a wide range of cancer cell lines, including prostate cancer cells in vitro, and inhibited the development of liver and lung cancer in vivo. In the present study, we examined the efficacy of CDDO-Me in preventing the development and progression of prostate cancer in the transgenic adenocarinoma of the mouse prostate (TRAMP) model. CDDO-Me inhibited the growth of murine TRAMPC-1 prostate cancer cells by inducing apoptosis through the inhibition of antiapoptotic p-Akt, p-mTOR and NF-κB. Early intervention with CDDO-Me (7.5 mg/kg) initiated at five weeks of age for 20 wk inhibited the progression of the preneoplastic lesions (low-grade PIN and high-grade-PIN) to adenocarcinoma in the dorsolateral prostate (DLP) and ventral prostate (VP) lobes of TRAMP mice. Even delayed administration of CDDO-Me started at 12 wk of age for 12 wk inhibited the development of adenocarcimona of the prostate. Both early and late treatment with CDDO-Me inhibited the metastasis of tumor to the distant organs. Treatment with CDDO-Me inhibited the expression of prosurvival p-Akt and NF-κB in the prostate and knocking-down Akt in TRAMPC-1 tumor cells sensitized them to CDDO-Me. These findings indicated that Akt is a target for apoptoxicity in TRAMPC-1 cells in vitro and potentially a target of CDDO-Me for inhibition of prostate cancer in vivo.