作者: William G. Nelson , Karen S. Sfanos , Angelo M. DeMarzo , Srinivasan Yegnasubramanian
DOI: 10.1007/978-1-60761-259-9_6
关键词: Neoplastic transformation 、 Corpora amylacea 、 Statin 、 Cancer research 、 Prostatitis 、 Prostate cancer 、 Prostate 、 Carcinogenesis 、 PCA3 、 Medicine
摘要: Both prostate cancer and prostatic inflammation have reached epidemic proportions among men in the United States developed world. New insights from molecular pathology analyses of human tissues, animal models, hinted that a diverse collection factors, ranging infectious agents to estrogenic hormones dietary carcinogens, can inflict damage epithelium elicit inflammatory responses evolve into chronic or recurrent condition. When infiltrates collect near urethra, symptomatic prostatitis likely ensues, driving as many two million physician visits each year US. Asymptomatic inflammation, an insidious condition is far more common than prostatitis, tends affect peripheral zone prostate, creating tissue microenvironment prone promote development. This environment leads formation focal atrophy lesions epithelium, replete with corpora amylacea, stroma infiltrated by cells. The mechanism inflammation-driven carcinogenesis appears involve epigenetic gene silencing neoplastic transformation proliferative lesions, type represents earliest precursor lesions. With accumulating evidence supporting causal association between cancer, attention has turned potential use anti-inflammatory drugs for prevention. From epidemiology studies, aspirin statin drugs, both properties, seem protect against development, especially when taken combination. contribution pathogenesis will be reviewed.