What controls PTEN and what it controls (in prostate cancer)

• 来源期刊: 亚洲男性学杂志（英文版）
• 年，卷（期）: 2012,（1）
• 页码范围: 130-131
• 页数: 2页
• 语种: 英文
• DOI: 10.1038/aja.2011.122

摘要

The standard of care for metastatic prostate cancer (PCa) is androgen deprivation therapy since almost all PCa growth is initially reliant on the androgen receptor (AR).However,almost all patients develop resistance to this therapy within 18-24months,and current treatment for castration-resistant prostate cancer (CRPC) is extremely limited,despite the advent of new drugs that target the AR,such as ahiraterone and MDV3100.1 Multiple studies have associated the loss of phosphatase and tensin homolog deleted on chromosome 10(PTEN),a dual lipid and protein phosphatase that is frequently lost in prostate cancer,with the development of CRPC.2,3 Yet,multiple studies have shown that at least 20％-40％of primary PCa,which are almost always androgen sensitive,experience a loss of PTEN,4,5 while as many as 30％ of CRPC tumors are PTEN-positive.6 The broad questions then facing researchers are:(i) How does PTEN loss cause CRPC?;(ii) What is the mechanism of CRPC development in PTEN+/+ tumors?;and (iii) How can CRPC tumors be inhibited in PTEN-null cells?Three new publications in recent times have come up with mechanisms that answer these questions.7-9 Two of these,both in Cancer Cell eadier this year,from the laboratories of Dr Charles Sawyers and Dr Hong Wu,address a novel negative feedback regulation between AR and PTEN,and all three,including the one from Dr Damu Tang,show that the loss of PTEN function is likely the first step towards the development of CRPC.