title: Macrophage migration inhibitory factor in prostatic adenocarcinoma: correlation with tumor grading and combination endocrine treatment-related changes.
abstract: BACKGROUND
  Macrophage migration inhibitory factor (MIF) is a ubiquitary cytokine whose expression has been investigated in tumors, showing a correlation between tumor aggressiveness and production of this protein by neoplastic cells. The aim of our study was to correlate MIF expression with tumor grade (Gleason scoring system) and histopathological changes after combined endocrine treatment (CET) of prostate adenocarcinoma.
  
  
  METHODS
  We analyzed MIF immunoreactivity in 124 paired needle biopsies and radical prostatectomy specimens from 62 prostate cancer patients, of which 20 had been treated with CET.
  
  
  RESULTS
  In untreated prostates, MIF expression significantly correlated with tumor grading, being stronger in low-grade than in high-grade adenocarcinoma. In treated prostates, histopathological changes also correlated with MIF immunoreactivity, but not in a significant manner.
  
  
  CONCLUSIONS
  The results of the current study demonstrated that with histological dedifferentiation, prostate adenocarcinoma cells show a reduced MIF expression. This finding may be the consequence of a reduced MIF synthesis or the result of an enhanced and altered secretion by tumor cells into the surrounding stroma. The consequent abnormal interaction between MIF and environmental factors might influence tumor growth and diffusion. On the other hand, the minor but not significantly reduced MIF expression by tumor cells after CET seems to exclude a hormonal regulation of MIF secretion.
authors.affiliation: Institute of Pathological Anatomy and Histology, University of Siena, Siena, Italy.
authors.forename: M T
authors.initials: MT
authors.lastname: del Vecchio
authors.forename: S A
authors.initials: SA
authors.lastname: Tripodi
authors.forename: F
authors.initials: F
authors.lastname: Arcuri
authors.forename: L
authors.initials: L
authors.lastname: Pergola
authors.forename: L
authors.initials: L
authors.lastname: Hako
authors.forename: R
authors.initials: R
authors.lastname: Vatti
authors.forename: M
authors.initials: M
authors.lastname: Cintorino
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D000368:Aged; D000726:Androgen Antagonists / Q000008:administration & dosage; D000728:Androgens / Q000502:physiology; D018931:Antineoplastic Agents, Hormonal / Q000008:administration & dosage; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D001707:Biopsy, Needle; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D005485:Flutamide / Q000008:administration & dosage; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists; D006801:Humans; D007150:Immunohistochemistry; D008263:Macrophage Migration-Inhibitory Factors / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D011379:Prognosis; D011467:Prostate / Q000378:metabolism; D019048:Prostatic Intraepithelial Neoplasia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*
chemical_list: D000726:Androgen Antagonists; D000728:Androgens; D018931:Antineoplastic Agents, Hormonal; D008263:Macrophage Migration-Inhibitory Factors; D007987:Gonadotropin-Releasing Hormone; D005485:Flutamide