title: Analysis of the capillary architecture in the precursors of prostate cancer: recent findings and new concepts.
abstract: OBJECTIVE
  To report on recent findings and new concepts in the remodeling of the capillary architecture in the precursors of prostate cancer.
  
  
  METHODS
  Immunohistochemical methods have been adopted in prostate cancer and in its precursors (prostatic intra-epithelial neoplasia) to investigate capillary pattern changes-which were mainly analyzed as capillary frequency- and the degree of endothelial cell proliferation. Several features related to the capillary architecture have been considered. Manual, semiautomatic, and automatic (machine vision) types of evaluation have been used to quantify the features.
  
  
  RESULTS
  The data available indicate that: (1) Going from normal prostate through prostatic intra-epithelial neoplasia up to invasive adenocarcinoma, an increasing proportion of capillaries becomes shorter, with open lumen and undulated external contour and with greater proliferation of the endothelial cells and greater expression of type IV collagenase. The highest proportion of touching capillaries is seen in normal prostate, while the lowest is found in invasive adenocarcinoma, being intermediate in prostatic intra-epithelial neoplasia. (2) When total androgen ablation is induced, there is no proliferation of the endothelium, whereas the capillaries are reduced in frequency and represented by small vessels lined by flat endothelial cells and with an open lumen. (3) Automation in the evaluation of the capillary architecture is feasible with a machine vision system.
  
  
  CONCLUSIONS
  The progression in prostate carcinogenesis is associated with changes in the capillary architecture. There are some preliminary data indicating that total androgen ablation can inhibit the angiogenesis in precursors of prostate cancer.
authors.affiliation: Institute of Pathological Anatomy and Histopathology, University of Ancona, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Montironi
authors.forename: L
authors.initials: L
authors.lastname: Diamanti
authors.forename: D
authors.initials: D
authors.lastname: Thompson
authors.forename: H G
authors.initials: HG
authors.lastname: Bartels
authors.forename: P H
authors.initials: PH
authors.lastname: Bartels
mesh_terms: D002455:Cell Division / Q000502:physiology; D017364:Collagenases / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology / Q000201:enzymology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D020780:Matrix Metalloproteinase 9; D009389:Neovascularization, Pathologic; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis* / Q000235:genetics; D011467:Prostate / Q000166:cytology / Q000473:pathology / Q000648:ultrastructure; D019048:Prostatic Intraepithelial Neoplasia / Q000098:blood supply / Q000235:genetics / Q000473:pathology*; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D017364:Collagenases; D020780:Matrix Metalloproteinase 9