Mutations in the ras oncogenes have been linked to many different canc
ers, In contrast to the extensive body of knowledge related to the gen
etics of ras activation, relatively little is known of the transcripti
onal events triggered by ras, In previous work we have used differenti
al display to identify Mob-1, a member of alpha-chemokine family, as o
ne of the immediate transcriptional targets following Ras activation,
Here, we provide additional experimental evidence to support this find
ing by the use of an inducible H-ras expression system, the treatment
of Ras farnesyl transferase inhibitor and activation of endogenous Ras
by serum growth factors, We further demonstrate that IP-10, the human
homolog of Mob-1, is overexpressed in the majority of colorectal canc
ers.