Molecular 'palpation' of BPH: a tale of MAPK signalling?

Benign prostatic hyperplasia (BPH) is a very common cause of hospitalizatio n and surgery is currently the most effective therapy. MAP kinases (MAPKs) are a group of protein kinases with an important function in integrating ph ysiological and pathological stimuli that might impact on cellular growth, differentiation and programmed cell death (apoptosis). Certain components o f the MAPK signal-transduction pathways are involved in stimulus-specific f ine-tuning of the activities mediated by the various MAPK families. As home ostasis is impaired in the hyperplastic prostate, aberrant coordination of the MAPK cascades might be implicated in a proliferative-apoptotic imbalanc e. Here, we hypothesize that the pathogenesis of BPH might be facilitated b y functional anomalies in the MAPK circuitry and postulate that pharmacolog ical 'rewiring' of MAPK pathways offers a potentially exciting new avenue f or improved therapeutic control of clinical BPH.