title: Differences between latent and clinical prostate carcinomas: lower cell proliferation activity in latent cases.
abstract: BACKGROUND
  Biological significance of prostate latent cancers as early phase of clinical cancers has been controversial. The characterization of the latent cancer may be important to investigate differences between latent and clinical prostate cancers.
  
  
  METHODS
  Latent cancers of the prostate, discovered at autopsy in men with no prior treatment for prostate disease and clinical prostate cancers, were compared for cell proliferation activities with parameters such as markers Ag-nucleolar organizer regions (AgNOR), topoisomerase II-alpha, and Ki-67. We also immunohistochemically studied alpha-methylacyl-CoA racemase (AMACR) expression that was recently identified as a possible positive marker of the prostate cancers. We analyzed 50 latent cancers and 50 clinical cancers, and samples were analyzed with Gleason grades or tumor volume.
  
  
  RESULTS
  In the latent cancers, Gleason grades 1-4 were observed, but in the clinical cancers Gleason grades 2-5 were recognized. Cell proliferation activities were significantly lower in the latent cancers in Gleason grade 3, and similar results were obtained but without statistical significance in Gleason grades 2 and 4. When analysis was performed according to the tumor size, it was shown that the growth activities of the tumor of the clinical cancer were higher than the latent cancer.
  
  
  CONCLUSIONS
  These results indicate that proliferation activities of the latent cancers were lower than the clinical cancers at the same Gleason grades. The data also suggest that latent cancers are just of preclinical stage and there is a possibility to progress to clinical ones by changing life style and longer life expectancy.
authors.affiliation: Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Kawasumi, Nagoya, Japan. seishiro@med.nagoya-cu.ac.jp
authors.forename: Seishiro
authors.initials: S
authors.lastname: Takahashi
authors.forename: Shugo
authors.initials: S
authors.lastname: Suzuki
authors.forename: Satoru
authors.initials: S
authors.lastname: Takahashi
authors.forename: Shingo
authors.initials: S
authors.lastname: Inaguma
authors.forename: Makoto
authors.initials: M
authors.lastname: Asamoto
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Shirai
mesh_terms: D000951:Antigens, Neoplasm / Q000032:analysis; D034961:Antigens, Nuclear / Q000032:analysis; D001344:Autopsy; D049109:Cell Proliferation; D004250:DNA Topoisomerases, Type II / Q000032:analysis; D004268:DNA-Binding Proteins / Q000032:analysis; D018450:Disease Progression; D006801:Humans; D007150:Immunohistochemistry; D015994:Incidence; D033162:Incidental Findings; D019394:Ki-67 Antigen / Q000032:analysis; D008017:Life Expectancy; D008019:Life Style; D008297:Male; D009687:Nuclear Proteins / Q000032:analysis; D011471:Prostatic Neoplasms / Q000737:chemistry / Q000175:diagnosis* / Q000453:epidemiology / Q000473:pathology*; D019998:Racemases and Epimerases / Q000032:analysis
chemical_list: D000951:Antigens, Neoplasm; D034961:Antigens, Nuclear; D004268:DNA-Binding Proteins; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; C051963:nucleolar organizer region associated proteins; D019998:Racemases and Epimerases; C108352:alpha-methylacyl-CoA racemase; D004250:DNA Topoisomerases, Type II