title: Involvement of decreased Galectin-3 expression in the pathogenesis and progression of prostate cancer.
abstract: BACKGROUND
  Altered expression or loss of function of Galectin-3 (Gal-3) was suggested to be involved in the pathogenesis and progression of various human cancer entities. The aim of the present study is to determine the expression of Gal-3 in prostate tissue emerging from a benign to a malignant, in the beginning hormone-sensitive and finally hormone-refractory status to further elucidate the role of this carbohydrate-binding protein for the pathogenesis and/or progression of malignant prostatic disease.
  
  
  METHODS
  Five hundred and eighty three tissue samples from malignant, tumor adjacent benign, and histologically benign intra-prostatic areas, retrieved out of 25 whole mounted prostate cancer (CaP) specimens and additional 95 samples of hormone-refractory CaP, were processed to tissue microarrays. Immunohistochemical Gal-3 expression was correlated with clinicopathological parameters among the different tissue entities.
  
  
  RESULTS
  Gal-3 expression was significantly decreased in the hormone-sensitive CaP specimens when compared with the respective benign tissue either localized far distant from the malignant lesion (P < 0.0001, Wilcoxon test) or directly neighboring the primary tumor (P < 0.0001). The staining reaction in the benign tissue areas directly neighboring the primary cancerous lesions differed significantly from the benign glands localized distant from the primary tumors (P < 0.001). A statistically highly significant, almost complete loss of Gal-3 was observed in the hormone-refractory when compared with the hormone-sensitive tumors (P < 0.0001; mean staining score: 27.7% vs. 8.5%).
  
  
  CONCLUSIONS
  The present investigation clearly indicates decreased expression of Gal-3 to be substantially involved in the pathogenesis and further progression of CaP from benign prostate glands to a finally hormone-refractory malignant disease.
authors.affiliation: Department of Urology, Eberhard Karls University Tübingen, Germany.
authors.forename: Axel S
authors.initials: AS
authors.lastname: Merseburger
authors.forename: Mario W
authors.initials: MW
authors.lastname: Kramer
authors.forename: Jörg
authors.initials: J
authors.lastname: Hennenlotter
authors.forename: Perikles
authors.initials: P
authors.lastname: Simon
authors.forename: Judith
authors.initials: J
authors.lastname: Knapp
authors.forename: Jörg T
authors.initials: JT
authors.lastname: Hartmann
authors.forename: Arnulf
authors.initials: A
authors.lastname: Stenzl
authors.forename: Jürgen
authors.initials: J
authors.lastname: Serth
authors.forename: Markus A
authors.initials: MA
authors.lastname: Kuczyk
mesh_terms: D000368:Aged; D000728:Androgens / Q000502:physiology; D018450:Disease Progression; D037502:Galectin 3 / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000378:metabolism* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D040081:Protein Array Analysis
chemical_list: D000728:Androgens; D037502:Galectin 3