作者: Carmen Berasain
DOI: 10.1016/J.JHEP.2010.01.020
关键词:
摘要: Cellular senescence is a process characterized by permanent cell cycle arrest. It the consequence of finite proliferative capacity normal cells (replicative senescence) and response to stress damage from exogenous endogenous sources. Several years ago it was shown that an innate tumour suppressive mechanism associated with activation oncogenes, which limits progression pre-malignant lesions [1]. As consequence, escape prerequisite for malignancy. There are three main mechanisms trigger cellular must be quelled in cancer cells: p53 pathway, upregulation CDKN2A locus, telomere shortening [2]. Genetic epigenetic aberrations any or all these pathways common marks types human cancer. However, resistance transformed reversible [3], senescence-inducing drugs could represent ideal opportunity increase arsenal anti-cancer weapons In present issue The Journal Hepatology work Menard et al. describes new example blockage linked induction replicative xenograft model liver [4]. Hepatocellular carcinoma (HCC) fifth most world poor prognosis. many cases no effective therapy at can offered patients HCC [5]. Surgical interventions such as ablation transplantation restricted selected group very specific clinical features, non-resectable tumours resistant conventional chemotherapy. New strategies radiotherapy gene alone combination early stages development [6]. Given survival benefits molecular inhibitor Sorafenib advanced [7] use single combined targeted therapies appears promising therapeutic alternative. Recent studies demonstrate existence increasing number might altered profiling identification patient subclasses according drug responsiveness will lead more per-