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LETTERS TO THE EDITOR Chromosomal Alterations in a Case of Ganglioglioma
Gangliogliomas are low-grade primary CNS tumors composed of mixed populations of glial elements and an admixture of neuroblasts [1]. In this study, we present a 51-year-old woman, who underwent surgical resection of a cerebral tumor (2.5-×-3.0 -cm in size) of the right parietal region in June 1992. The patient remains asymptomatic. Based on histopathology and ultrastructure, the tumor was diagnosed as a ganglioglJoma (Fig. 1). Cytogenetic analysis of the tumor tissue was ]performed after short-term culturo Figure I Histopathology of tumor, a) Synaptophysin immunohistochemistry showing nuraerous immunopositive neuronal cells; × 100. b) Electronmicrograph of tumor cells showing a neuronal process containing abundant dense-core vesicles surrounded by astrocytic processes; × 12000.
ing, harvesting, and G-banding as previously described [2]. The subsequent karyotypic analysis and nomenclature met the criteria of the ISCN [3]. The karyotype 43,XX, der(1)t(1;5)(q21;q12),- 5,der(8;13)(q10;q10),- 9,i(10)(q10) was found in seven cells (Fig. 2), five cells displayed nonclonal chromosome changes, and the remaining 14 mitoses were normal. Gangliogliomas, clinically benign tumors of the complex entity, have been reported to display a predominantly normal karyotype [4-6}. In our tumor, the chromosomal changes display some similarity to those frequently seen in the malignant gliomas. Particularly, the changes leading to the partial or total loss of chromosomes 9 and 10 are frequently seen in tumors of astrocytic origin [7]. Loss of chromosome 10 precedes transition from benign astrocytoma to glioblastoma [8]. In addition, partial m o n o s o m y of chromosome 9 may also represent a chromosome change associated with tumor progression, but chromosome 9 abnormalities are not exclusive to high-grade astrocytic tumors [9]. Gangliogliomas are benign tumors but occasionally they undergo malignant transformation [1]. It is a glial component that can progress into malignant tumor. Since our patient remains asymptomatic, one may speculate that the loss of the chromosome 9 and the short arm of chromosome 10 (the consequence of isochromosome formation), were not critical for the progression of glial cells bearing these changes to the malignant ones. Follow-up of our patient is pending. This paper was supported by the research grant from the Polish State Research Committee. MARIA DEBIEC-RYCHTER PAWEL P. LIBERSKI JANUSZ ALWASIAK ANDRZEJ KLIMEK
Laboratory of Tumor Biology Department of Tumor Pathology, Medical Academy of Lodz, Department of Neurology, Regional Multidisciplinary Hospital (Copernicus Hospital), Lodz, Poland.
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Figure 2 GTG-banded karyotype displaying three marker chromosomes: M1, der(1)t(1;5)(q21;q12); M2,der (8;13) (ql0;ql0); and M3, i(lO)(qlO).
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