REVIEW

Molecular pathology of prostate cancer

C Hughes¹, A Murphy¹, C Martin¹, O Sheils¹ and J O’Leary²

¹ Pathology Department, Trinity College Dublin and Coombe Women’s Hospital, Dublin, Ireland
² Pathology Department, Coombe Women’s Hospital, Dublin 8, Ireland

Correspondence to:
Correspondence to:
Professor J O’Leary
Pathology Department, Coombe Women’s Hospital, Dublin 8, Ireland; olearyjj{at}tcd.ie

The molecular pathology of prostate cancer is complex; not only are multiple genes involved in its pathogenesis, but additional environmental factors such as diet and inflammation are also involved. The exhaustive research into prostate cancer to date has demonstrated a complex interaction of multiple genes and environmental factors, some of which may be more important in individual prostate cancer cases. This is an exciting era, with the emergence of new investigative tools such as DNA microarray technology and the application of the field of proteomics to the study of human cancers. Knowledge of genetic changes underlying the initiation, development, and progression of prostate cancer is accumulating rapidly. With increasing knowledge, it may be possible to distinguish indolent from aggressive prostate tumours by molecular fingerprinting. This review discusses the most consistently reported molecular pathological findings in hereditary and sporadic prostate cancer, together with new concepts and technologies.

Abbreviations: AMACR, -methylacyl coenzyme A racemase; AR, androgen receptor; GSTP1, glutathione S-transferase; IFN, interferon; IL-6, interleukin 6; KLF, Kruppel-like factor; MAPK, mitogen activated protein kinase; P13K–Akt, phosphatidylinositol 3'-kinase–protein kinase B; PIN, prostate intraepithelial neoplasia; PSA, prostate specific antigen; PTEN, phosphatase and tensin homologue; Rb, retinoblastoma; STAT, signal transducer and activator of transcription; VDR, vitamin D receptor

Keywords: prostate; cancer; review; molecular; pathology

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