Nflammation models [40-42]. Results from this study demonstrate that V2O5 functions as an in vivo lung tumor promoter in both A/J and BALB mice. Further, we demonstrate a positive relationship between tumor promotion and susceptibility to V2O5-induced inflammation, involving the induction of the chemokines KC and MCP-1, the transcription factors NFB and cFos, as well as sustained activation of ERK