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Pathological and molecular mechanisms of prostate carcinogenesis: Implications for diagnosis, detection, prevention, and treatment
Journal of cellular biochemistry, 2004-02, Vol.91 (3), p.459-477
De Marzo, Angelo M.
DeWeese, Theodore L.
Platz, Elizabeth A.
Meeker, Alan K.
Nakayama, Masashi
Epstein, Jonathan I.
Isaacs, William B.
Nelson, William G.
2004
Details
Autor(en) / Beteiligte
De Marzo, Angelo M.
DeWeese, Theodore L.
Platz, Elizabeth A.
Meeker, Alan K.
Nakayama, Masashi
Epstein, Jonathan I.
Isaacs, William B.
Nelson, William G.
Titel
Pathological and molecular mechanisms of prostate carcinogenesis: Implications for diagnosis, detection, prevention, and treatment
Ist Teil von
Journal of cellular biochemistry, 2004-02, Vol.91 (3), p.459-477
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2004
Link zum Volltext
Quelle
Wiley Online Library All Journals
Beschreibungen/Notizen
Prostate cancer is an increasing threat throughout the world. As a result of a demographic shift in population, the number of men at risk for developing prostate cancer is growing rapidly. For 2002, an estimated 189,000 prostate cancer cases were diagnosed in the U.S., accompanied by an estimated 30,200 prostate cancer deaths [Jemal et al., 2002]. Most prostate cancer is now diagnosed in men who were biopsied as a result of an elevated serum PSA (>4 ng/ml) level detected following routine screening. Autopsy studies [Breslow et al., 1977; Yatani et al., 1982; Sakr et al., 1993], and the recent results of the Prostate Cancer Prevention Trial (PCPT) [Thompson et al., 2003], a large scale clinical trial where all men entered the trial without an elevated PSA (<3 ng/ml) were subsequently biopsied, indicate the prevalence of histologic prostate cancer is much higher than anticipated by PSA screening. Environmental factors, such as diet and lifestyle, have long been recognized contributors to the development of prostate cancer. Recent studies of the molecular alterations in prostate cancer cells have begun to provide clues as to how prostate cancer may arise and progress. For example, while inflammation in the prostate has been suggested previously as a contributor to prostate cancer development [Gardner and Bennett, 1992; Platz, 1998; De Marzo et al., 1999; Nelson et al., 2003], research regarding the genetic and pathological aspects of prostate inflammation has only recently begun to receive attention. Here, we review the subject of inflammation and prostate cancer as part of a “chronic epithelial injury” hypothesis of prostate carcinogenesis, and the somatic genome and phenotypic changes characteristic of prostate cancer cells. We also present the implications of these changes for prostate cancer diagnosis, detection, prevention, and treatment. © 2003 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0730-2312
eISSN: 1097-4644
DOI: 10.1002/jcb.10747
Titel-ID: cdi_crossref_primary_10_1002_jcb_10747
Format
–
Schlagworte
Atrophy - physiopathology
,
benign prostatic hyperplasia
,
DNA-Binding Proteins
,
Gene Expression Regulation, Neoplastic
,
Genes, Tumor Suppressor
,
Homeodomain Proteins - genetics
,
Humans
,
inflammation
,
Inflammation - physiopathology
,
Male
,
Phosphoproteins - genetics
,
Phosphoric Monoester Hydrolases - genetics
,
prostate cancer
,
prostateatrophy
,
Prostatic Neoplasms - genetics
,
Prostatic Neoplasms - pathology
,
Prostatic Neoplasms - therapy
,
prostatitis
,
Proteins - genetics
,
PTEN Phosphohydrolase
,
Racemases and Epimerases - genetics
,
Receptors, Androgen - genetics
,
Serine Endopeptidases - genetics
,
Signal Transduction
,
Telomere - genetics
,
Telomere - physiology
,
Trans-Activators - genetics
,
Transcription Factors - genetics
,
Tumor Suppressor Proteins - genetics
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