Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

Wiley - Tập 50 Số 3 - Trang 153-159 - 2002
José María Sayagués1, María Dolores Tabernero2,1, A. Maíllo3,1, P. Díaz3,1, Ana Rasillo1, Bortoluci Aglae1, J.A. Gómez-Moreta3,1, Ángel Santos‐Briz4, Francisco Morales3, Alberto Órfão1
1Servicio General de Citometría, Departmento de Medicina y Centro de Investigaciones del Cáncer, Universidad de Salamanca, Salamanca, Spain
2Hospital Universitario de Salamanca, Unidad de Investigación, Salamanca, Spain
3Neurosurgery Service, Hospital Universitario de Salamanca, Salamanca, Spain
4Departament of Pathology, Hospital Universitario de Salamanca, Salamanca, Spain

Tóm tắt

AbstractObjective: Although information on the cytogenetic characteristics of meningioma tumors has accumulated progressively over the past few decades, information on the genetic heterogeneity of meningiomas is still scanty. The aim of the present study was to analyze by interphase fluorescence in situ hybridization (FISH) the incidence of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y in a group of 70 consecutive meningioma tumors. Another goal was to establish the potential associations among the altered chromosomes, as a way to assess both intertumoral and intratumoral heterogeneity. Methods: For the purpose of the study, 70 patients diagnosed with meningioma were analyzed. Interphase FISH for the detection of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y was applied to fresh tumor samples from each of the patients studied. Results: The overall incidence of numerical abnormalities was 76%. Chromosome Y in males and chromosome 22 in the whole series were the most common abnormalities (46% and 61%, respectively). Despite the finding that monosomy of chromosome 22/22q‐ deletions are the most frequent individual abnormality (53%), we have observed that chromosome gains are significantly more common than chromosome losses (60% versus 40%). Chromosome gains corresponded to abnormalities of chromosomes 1 (27%), 9 (25%), 10 (23%), 11 (22%), 14 (33%), 15 (22%), 17 (23%), and X in females (35%) and males (23%) whereas chromosome losses apart from chromosome 22 frequently involved chromosomes 14 (19%), X in males (23%), and Y in males (32%). Although an association was found among most gained chromosomes on one side and chromosome losses on the other side, different association patterns were observed. Furthermore, in the latter group, monosomy 22/22q‐ was associated with monosomy X in females and monosomy 14/14q‐ was associated with nulisomy Y in males. In addition, chromosome losses usually involved a large proportion of the tumor cells whereas chromosome gains were restricted to small tumor cell clones, including tetraploid cells. Conclusions: Our results show that meningiomas are genetically heterogeneous tumors that display different patterns of numerical chromosome changes, as assessed by interphase FISH. Cytometry (Clin. Cytometry) 50:153–159, 2002. © 2002 Wiley‐Liss, Inc.

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Wiley

Tập 50 Số 3

153-159

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