title: Microvessel density in pituitary adenomas and carcinomas.
abstract: Tumor growth depends on several factors, including angiogenesis. Tumors cannot grow if new vessels are not formed to supply the cells with oxygen and other nutrients and to remove waste products. Increased angiogenesis can be correlated with tumor growth and metastatic potential in many tumor types, indicating that neoformation of vessels is a prognostic indicator of tumor behavior. We evaluated microvessel densities in 157 various pituitary adenoma types and seven pituitary carcinomas using immunocytochemistry for CD-34 antigen, a reliable marker of endothelial cells. The lowest percentage of microvessel density was found in growth hormone-producing adenomas, the highest level in pituitary carcinomas. In general, no major correlation was found between MIB-1 index (an indicator of cell proliferation) and microvessel density. The statistical study also demonstrated no gender-dependent changes in the microvessel density of pituitary tumors. Although the microvessel density was not significantly different in relation to invasiveness of pituitary tumors, our results demonstrate a tendency of invasive pituitary tumors to be more highly vascularized than non-invasive ones. Dopamine agonist and long-acting somatostatin analog treatment compared with untreated tumors did not significantly affect microvessel densities. Statistical differences were demonstrated in the microvessel density of macroadenomas between patients older and patients younger than 40 years. Significant differences were also apparent in the microvessel densities between microadenomas and macroadenomas diagnosed in young patients but not in the older age group. The strongly positive correlation observed between microvessel density and age is consistent with the view that age of the host may have an influence on the extent of neovascularization of pituitary adenomas.
authors.affiliation: Department of Anatomy, Campus Universitario de Lugo, Spain. svidal@lugo.usc.es
authors.forename: S
authors.initials: S
authors.lastname: Vidal
authors.forename: K
authors.initials: K
authors.lastname: Kovacs
authors.forename: E
authors.initials: E
authors.lastname: Horvath
authors.forename: B W
authors.initials: BW
authors.lastname: Scheithauer
authors.forename: T
authors.initials: T
authors.lastname: Kuroki
authors.forename: R V
authors.initials: RV
authors.lastname: Lloyd
mesh_terms: D000236:Adenoma / Q000098:blood supply* / Q000737:chemistry / Q000188:drug therapy / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018952:Antigens, CD34 / Q000032:analysis; D034961:Antigens, Nuclear; D001971:Bromocriptine / Q000627:therapeutic use; D002277:Carcinoma / Q000098:blood supply* / Q000737:chemistry / Q000188:drug therapy / Q000473:pathology; D002648:Child; D018491:Dopamine Agonists / Q000627:therapeutic use; D005260:Female; D006728:Hormones / Q000627:therapeutic use; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen; D008297:Male; D008833:Microcirculation / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D008875:Middle Aged; D009361:Neoplasm Invasiveness / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology*; D009687:Nuclear Proteins / Q000032:analysis; D015282:Octreotide / Q000627:therapeutic use; D010911:Pituitary Neoplasms / Q000098:blood supply* / Q000737:chemistry / Q000188:drug therapy / Q000473:pathology
chemical_list: D018952:Antigens, CD34; D034961:Antigens, Nuclear; D018491:Dopamine Agonists; D006728:Hormones; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D001971:Bromocriptine; D015282:Octreotide