RESUMO
Allelic loss on chromosome 10 is a frequent event in high grade gliomas. Earlier studies have shown that in most cases a complete copy of chromosome 10 is lost in the tumor. To define more accurately and specifically the region of common deletion on chromosome arm 10p, we have screened a large series of gliomas for allelic losses that exclusively affect this part of the chromosome. Allelic loss profiles were determined for 127 gliomas, including 118 astrocytomas of various malignancy grades. Seventeen tumors displayed loss of part of chromosome 10. In three of these, only chromosome arm 10p sequences were lost. The interval between loci D10S559 and D10S435 in 10p15, with a length of approximately 800 kilobase pairs, was commonly deleted in the latter tumors, suggesting that this region may harbor a tumor suppressor gene important in glioma tumorigenesis. Comparison of the allelic loss profiles in the low and high grade astrocytomas revealed that astrocytoma progression is associated with increased loss of chromosome 10 sequences.
Assuntos
Neoplasias Encefálicas/genética , Cromossomos Humanos Par 10/genética , Glioma/genética , Astrocitoma/genética , Deleção Cromossômica , Mapeamento Cromossômico , DNA de Neoplasias/análise , Ganglioneuroma/genética , Genes Supressores de Tumor , Humanos , Perda de Heterozigosidade , Repetições de Microssatélites , Reação em Cadeia da PolimeraseRESUMO
Ependymomas are glial cell-derived tumors. They are, in contrast to other gliomas (astrocytomas, oligodendrogliomas, and oligoastrocytomas), ill-defined with respect to the genes and chromosomal segments important in their tumorigenesis. In this study, we extensively screened 17 ependymomas for genetic changes characteristic of other gliomas. Allelic loss was detected on chromosome arm 22q in three tumors; on chromosome 10 in two tumors; on chromosome arm 17p in two tumors; and on chromosome arms 6q, 9p, 13q, and 19q, each in one tumor. No allelic losses were found on chromosome arms 1p and 16q. None of the tumors had EGFR gene amplification. In each case, the chromosomal segment affected by the deletion included the region known to harbor a tumor suppressor gene important in glioma tumorigenesis. We conclude that ependymomas resemble the other glial neoplasms with respect to type and location of the chromosomal changes involved. Given the relatively infrequent occurrence of these genetic changes, ependymomas should be considered genetically as low-grade gliomas.
