title: Gains of chromosome 22 by fluorescence in situ hybridization in the context of an hyperdiploid karyotype are associated with aggressive clinical features in meningioma patients.
abstract: BACKGROUND
  Meningiomas usually are considered to be benign tumors; however, 10-20% of cases recur. Few disease characteristics have proved to have prognostic impact for predicting disease free survival. The objective of the current study was to explore the prognostic value of numeric abnormalities of chromosome 22 for meningioma patients.
  
  
  METHODS
  In this study, the authors prospectively analyzed the incidence of numeric chromosome abnormalities of chromosome 22 by interphase fluorescence in situ hybridization, using a specific probe for the bcr gene located in chromosome 22q11.2, on a total of 88 consecutive meningioma patients. The authors also analyzed its correlation with both the clinicobiologic characteristics at presentation and the patient's outcome.
  
  
  RESULTS
  The authors' results show that monosomy 22 was present in 49% of the cases and that this numeric chromosomal abnormality is not associated with other prognostic features of the disease. In contrast, gains (trisomy/tetrasomy) of chromosome 22 were detected in 8 (9%) cases who simultaneously showed gains for other chromosomes and represent an adverse prognostic factor regarding disease free survival (P = 0.001); in addition, trisomy/tetrasomy 22 was more frequently related to younger patients (P = 0.001), aggressive histopathologic features (P < 0.000), a greater incidence of DNA aneuploidy (P =0.006), and a higher proportion of S-phase tumor cells (P = 0.02).
  
  
  CONCLUSIONS
  In summary, the authors conclude that loss of a copy of chromosome 22 is a frequent finding in meningioma tumors, but it does not affect the clinical outcome of these patients. In contrast, gains (trisomy/tetrasomy) of chromosome 22, in the context of an hyperdiploid karyotype, although much less frequent, are associated with a more aggressive disease course.
authors.affiliation: Neurosurgery Service, Hospital Universitario de Salamanca, Salamanca, Spain. maillo2@teleline.es
authors.forename: A
authors.initials: A
authors.lastname: Maíllo
authors.forename: P
authors.initials: P
authors.lastname: Díaz
authors.forename: J M
authors.initials: JM
authors.lastname: Sayagués
authors.forename: A
authors.initials: A
authors.lastname: Blanco
authors.forename: M D
authors.initials: MD
authors.lastname: Tabernero
authors.forename: J
authors.initials: J
authors.lastname: Ciudad
authors.forename: A
authors.initials: A
authors.lastname: López
authors.forename: J M
authors.initials: JM
authors.lastname: Gonçalves
authors.forename: A
authors.initials: A
authors.lastname: Orfao
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology; D002453:Cell Cycle; D002869:Chromosome Aberrations / Q000235:genetics* / Q000473:pathology; D025063:Chromosome Disorders; D002892:Chromosomes, Human, Pair 22 / Q000235:genetics*; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D007621:Karyotyping; D019656:Loss of Heterozygosity; D008297:Male; D008875:Middle Aged; D011123:Polyploidy; D011379:Prognosis