TY - JOUR
T1 - Deletion mapping of the long arm of chromosome 22 in human meningiomas
AU - Akagi, Kenzo
AU - Kurahashi, Hiroki
AU - Arita, Norio
AU - Hayakawa, Toru
AU - Monden, Morito
AU - Mori, Takesada
AU - Takai, Shinichiro
AU - Nishisho, Isamu
PY - 1995/1/17
Y1 - 1995/1/17
N2 - Cytogenetic and molecular genetic analyses have shown that a tumor‐suppressor gene for human meningioma is located on the long arm of chromosome 22. Recently, somatic mutations of the NF2 gene have been identified in sporadic meningiomas. However, tumorigenesis of certain cases of meningioma cannot be fully explained by inactivation of the NF2 gene alone. Thus, to obtain some indication as to the existence of another tumorsuppressor gene, it seemed important to re‐examine the loss of heterozygosity (LOH) on 22q in sporadic meningioma. A total of 46 sporadic meningiomas was examined for LOH at 20 loci on 22q. LOH was observed in 29 tumors (63%), of which 13 (28%) showed different patterns of a partial loss of 22q. However, the NF2 locus was retained in one tumor that lost a more distal part of 22q. Moreover, 27 of the 28 tumors which showed LOH at the NF2 locus also lost alleles at more telomeric loci. These results raise the possibility that another tumor‐suppressor gene for meningioma may exist on 22q and that its localization may be distal to the D22S102 locus. © 1995 Wiley‐Liss, Inc.
AB - Cytogenetic and molecular genetic analyses have shown that a tumor‐suppressor gene for human meningioma is located on the long arm of chromosome 22. Recently, somatic mutations of the NF2 gene have been identified in sporadic meningiomas. However, tumorigenesis of certain cases of meningioma cannot be fully explained by inactivation of the NF2 gene alone. Thus, to obtain some indication as to the existence of another tumorsuppressor gene, it seemed important to re‐examine the loss of heterozygosity (LOH) on 22q in sporadic meningioma. A total of 46 sporadic meningiomas was examined for LOH at 20 loci on 22q. LOH was observed in 29 tumors (63%), of which 13 (28%) showed different patterns of a partial loss of 22q. However, the NF2 locus was retained in one tumor that lost a more distal part of 22q. Moreover, 27 of the 28 tumors which showed LOH at the NF2 locus also lost alleles at more telomeric loci. These results raise the possibility that another tumor‐suppressor gene for meningioma may exist on 22q and that its localization may be distal to the D22S102 locus. © 1995 Wiley‐Liss, Inc.
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U2 - 10.1002/ijc.2910600208
DO - 10.1002/ijc.2910600208
M3 - Article
C2 - 7829212
AN - SCOPUS:0028909493
SN - 0020-7136
VL - 60
SP - 178
EP - 182
JO - International Journal of Cancer
JF - International Journal of Cancer
IS - 2
ER -