ABSTRACT
Mycosis fungoides [MF] is usually an indolent disease that, after a variable period of time in a stable phase, evolves into a tumoral form with aggressive behavior. Knowledge about the molecular mechanisms involved in the pathogenesis of tumoral progression in MIF is still scarce. Alterations of p16[ink4a] and retinoblastonia [Rb] have been demonstrated in a wide range of human tumors, p16[ink4a] inhibits Rb protein and thus acts as a negative cell cycle regulator. This prompted us to investigate their hypothetical role in MF progression. Twenty-five patients with MF of different clinicopatholgical stages were studied. p16[ink4a] expression was absent in 28% of the studied cases, where it was more lost in tumoral lesions than in patches and plaques lesions and in higher clinical stages than in low stages and the difference was statistically highly significant [P<0.001]. Therefore, the loss of p16[ink4a] is associated with the aggressive forms of MF. The results of the present study also showed a significant reciprocal relationship between p16[ink4a] and Rb proteins in most MF cases. However, alterations of Rb protein were not correlated with any of the clinicopathological features of the studied cases. In conclusion, this study demonstrated that lack of p16[ink4a], expression is a sensitive and specific marker of advanced cases of MF in comparison to Rb and thus p16[ink4a] could he used as a marker for poor prognostic patients with MF