title: Angiogenesis and tumor progression of melanoma. Quantification of vascularity in melanocytic nevi and cutaneous malignant melanoma.
abstract: BACKGROUND
  The capacity of cutaneous malignant melanoma (CMM) to induce angiogenesis is well established. In addition, dysplastic melanocytic nevi (DMN) have been reported to display prominent vascularity relative to common acquired nevi; but this observation has never been verified objectively.
  
  
  METHODS
  In the following studies, papillary dermal or tumor vascularity was quantified in 10 examples of normal skin, and in a series of 18 melanocytic nevi, 29 DMN, 37 primary CMM and 5 melanoma metastases. Microvessels were identified with the lectin Ulex europaeus agglutinin I. The number of microvessels were counted with an ocular grid (area 7.84 x 10(-2) mm2) at x400 magnification, and the mean vascularity recorded for five fields for each specimen.
  
  
  RESULTS
  Mean vascular counts were as follows: normal skin 5.9, common acquired nevus 9.1, nevus with features of DMN 10.3, DMN, slight atypia 11.8; DMN, moderate atypia 12.2; DMN, severe atypia 14.8; primary CMM 25.4; and metastatic melanoma 29.5). Significant differences were recorded for DMN, severe atypia versus melanoma (p less than 0.01), DMN, severe versus common nevi (p less than 0.02) and versus nevi with features of DMN (P less than 0.05). When microvessel counts from CMM in the radial growth phase were compared with those from CMM in the vertical growth phase, or CMM less than 1.0 mm versus those greater than 1.0 mm, no significant differences were found. However, CMM in radial growth did differ from severely atypical DMN (22.4 versus 14.8, p less than 0.05).
  
  
  CONCLUSIONS
  These results quantify for the first time a gradual rise in vascularity with tumor progression in the melanocytic system and onset of angiogenesis during the radial growth phase of CMM. Other than severely atypical DMN, DMN did not differ substantially from common nevi with reference to overall vascularity.
authors.affiliation: Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston.
authors.forename: R L
authors.initials: RL
authors.lastname: Barnhill
authors.forename: K
authors.initials: K
authors.lastname: Fandrey
authors.forename: M A
authors.initials: MA
authors.lastname: Levy
authors.forename: M C
authors.initials: MC
authors.lastname: Mihm
authors.forename: B
authors.initials: B
authors.lastname: Hyman
mesh_terms: D002196:Capillaries / Q000648:ultrastructure; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D037102:Lectins; D008545:Melanoma / Q000098:blood supply* / Q000503:physiopathology; D009362:Neoplasm Metastasis; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D009508:Nevus, Pigmented / Q000098:blood supply* / Q000503:physiopathology; D037121:Plant Lectins; D012878:Skin Neoplasms / Q000098:blood supply* / Q000503:physiopathology
chemical_list: D037102:Lectins; D037121:Plant Lectins; C036850:Ulex europaeus lectins