Prostate cancer

Research output: Contribution to journalArticle

Abstract

Genes, dietary factors, and lifestyle-related factors contribute to the development of prostate cancer. Two inherited susceptibility genes, RNASEL and MSR1, may have roles in responses to infections, raising the possibility that prostate infection or inflammation initiates prostatic carcinogenesis. A new prostate-cancer-precursor lesion, proliferative inflammatory atrophy, may be another link between prostatic inflammation and prostate cancer. Loss of the GSTP1 caretaker function, as cells of proliferative inflammatory atrophy give rise to cells of prostatic intraepithelial neoplasia and to prostate-cancer cells, increases the prostate's vulnerability to genomic damage caused by inflammatory oxidants and dietary carcinogens. Somatic targets of genomic damage include NKX3.1, a candidate gatekeeper gene, as well as PTEN and AR, genes that may modulate the progression of prostate cancer. Inherited polymorphic variants of genes mediating androgen action, AR, CYP17, and SRD5A2, also influence the development and progression of prostate cancer.

Original languageEnglish (US)
Pages (from-to)366-381
Number of pages16
JournalNew England Journal of Medicine
Volume349
Issue number4
DOIs
StatePublished - Jul 24 2003

Fingerprint

Prostatic Neoplasms
Genes
Atrophy
Prostate
Prostatic Intraepithelial Neoplasia
Steroid 17-alpha-Hydroxylase
Inflammation
Infection
Oxidants
Carcinogens
Androgens
Life Style
Carcinogenesis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Prostate cancer. / Nelson, William G; Demarzo, Angelo Michael; Isaacs, William B.

In: New England Journal of Medicine, Vol. 349, No. 4, 24.07.2003, p. 366-381.

Research output: Contribution to journalArticle

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