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  • Rubin, Mark A. (författare)

Decreased alpha-methylacyl CoA racemase expression in localized prostate cancer is associated with an increased rate of biochemical recurrence and cancer-specific death

  • Artikel/kapitelEngelska2005

Förlag, utgivningsår, omfång ...

  • 2005
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:oru-15600
  • https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-15600URI
  • https://doi.org/10.1158/1055-9965.EPI-04-0801DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:1939193URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:12539626URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:12476100URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • alpha-Methylacyl CoA racemase (AMACR) is overexpressed in prostate cancer relative to benign prostatic tissue. AMACR expression is highest in localized prostate cancer and decreases in metastatic prostate cancer. Herein, we explored the use of AMACR as a biomarker for aggressive prostate cancer. AMACR protein expression was determined by immunohistochemistry using an image analysis system on two localized prostate cancer cohorts consisting of 204 men treated by radical prostatectomy and 188 men followed expectantly. The end points for the cohorts were time to prostate-specific antigen (PSA) failure (i.e., elevation > 0.2 ng/mL) and time to prostate cancer death in the watchful waiting cohort. Using a regression tree method, optimal AMACR protein expression cutpoints were determined to best differentiate prostate cancer outcome in each of the cohorts separately. Cox proportional hazard models were then employed to examine the effect of the AMACR cutpoint on prostate cancer outcome, and adjusted for clinical variables. Lower AMACR tissue expression was associated with worse prostate cancer outcome, independent of clinical variables (hazard ratio, 3.7 for PSA failure; P = 0.018; hazard ratio, 4.1 for prostate cancer death, P = 0.0006). Among those with both low AMACR expression and high Gleason score, the risk of prostate cancer death was 18-fold higher (P = 0.006). The AMACR cutpoint developed using prostate cancer-specific death as the end point predicted PSA failures independent of Gleason score, PSA, and margin status. This is the first study to show that AMACR expression is significantly associated with prostate cancer progression and suggests that not all surrogate end points may be optimal to define biomarkers of aggressive prostate cancer.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Bismar, Tarek A. (författare)
  • Andrén, OveÖrebro universitet,Hälsoakademin(Swepub:oru)oan (författare)
  • Mucci, Lorelei (författare)
  • Kim, Robert (författare)
  • Shen, Ronglai L. (författare)
  • Ghosh, Debashis (författare)
  • Wei, John T. (författare)
  • Chinnaiyan, Arul M. (författare)
  • Adami, Hans-OlovKarolinska Institutet (författare)
  • Kantoff, Philip W. (författare)
  • Johansson, Jan-Erik (författare)
  • Örebro universitetHälsoakademin (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Cancer Epidemiology, Biomarkers and Prevention18, s. 162A-162A1055-99651538-7755
  • Ingår i:LABORATORY INVESTIGATION18, s. 162A-162A0023-6837
  • Ingår i:MODERN PATHOLOGY18, s. 162A-162A0893-3952

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