Table 3.

The number of colonic ACF or intestinal polyps in mouse models of intestinal tumorigenesis following either genetic deletion or pharmacologic inhibition of EP receptor subtypes or COX isoforms

ReceptorAzoxymethane-Induced ACF Development*ApcMin/+ Mouse PolyposisApcΔ716 Mouse Polyposis
EP165% (GD; ref. 70)56% (P; ref. 70)No difference (GD; ref. 68)
65% (P; refs. 70, 71)No Δ polyp size
EP2NDND58% (GD; ref. 68)
EP3No difference (GD; ref. 67)NDNo difference (GD; ref. 68)
EP456% (GD; ref. 67)69% (P; ref. 67)No difference (EP4+/− only; ref. 68)
67% (P; ref. 67)Polyp size decreased
COX-160% (P; ref. 72)23% (GD; ref. 5)59% (P; ref. 72)
COX-263% (P; ref. 73)16% (GD; ref. 5)14% (GD; ref. 76)
3%§ (P; ref. 74)29% (P; ref. 75)45% (P; refs. 77, 78)
Anti-PGE2 antibodyND67% (63)ND
No Δ polyp size
  • NOTE: ND, not determined.

  • * Azoxymethane-induced ACF number following either genetic deletion (GD) or pharmacologic inhibition (P) as a percentage of wild-type or control ACF multiplicity.

  • Polyp (or adenoma) number following either genetic deletion (GD) or pharmacologic inhibition (P) as a percentage of wild-type or control polyp multiplicity. Δ, change.

  • The Apc1309 mouse model of familial adenomatous polyposis was used in this study.

  • § Percentage of azoxymethane-induced tumor (not ACF) multiplicity in untreated rats.