Jacoby L B, Jones D, Davis K, Kronn D, Short M P, Gusella J, MacCollin M
Neurosurgical Service, Massachusetts General Hospital, Charlestown 02129, USA.
Am J Hum Genet. 1997 Dec;61(6):1293-302. doi: 10.1086/301633.
Patients with multiple schwannomas without vestibular schwannomas have been postulated to compose a distinct subclass of neurofibromatosis (NF), termed "schwannomatosis." To compare the molecular-genetic basis of schwannomatosis with NF2, we examined the NF2 locus in 20 unrelated schwannomatosis patients and their affected relatives. Tumors from these patients frequently harbored typical truncating mutations of the NF2 gene and loss of heterozygosity of the surrounding region of chromosome 22. Surprisingly, unlike patients with NF2, no heterozygous NF2-gene changes were seen in normal tissues. Examination of multiple tumors from the same patient revealed that some schwannomatosis patients are somatic mosaics for NF2-gene changes. By contrast, other individuals, particularly those with a positive family history, appear to have an inherited predisposition to formation of tumors that carry somatic alterations of the NF2 gene. Further work is needed to define the pathogenetics of this unusual disease mechanism.
患有多发性施万细胞瘤但无前庭神经鞘瘤的患者被假定构成神经纤维瘤病(NF)的一个独特亚类,称为“施万细胞瘤病”。为了比较施万细胞瘤病与NF2的分子遗传学基础,我们检测了20名无亲缘关系的施万细胞瘤病患者及其患病亲属的NF2基因座。这些患者的肿瘤经常携带NF2基因典型的截短突变以及22号染色体周围区域的杂合性缺失。令人惊讶的是,与NF2患者不同,在正常组织中未发现杂合性NF2基因改变。对同一患者的多个肿瘤进行检测发现,一些施万细胞瘤病患者是NF2基因改变的体细胞镶嵌体。相比之下,其他个体,尤其是那些有阳性家族史的个体,似乎具有形成携带NF2基因体细胞改变的肿瘤的遗传易感性。需要进一步开展工作来明确这种不寻常疾病机制的发病机制。