Däschner K, Assum G, Eisenbarth I, Krone W, Hoffmeyer S, Wortmann S, Heymer B, Kehrer-Sawatzki H
Abteilung Humangenetik, University of Ulm, Germany.
Biochem Biophys Res Commun. 1997 May 19;234(2):346-50. doi: 10.1006/bbrc.1997.6645.
LOH at the NF1 locus was investigated in 38 neurofibromas of 26 NF1 patients. Only in one of these tumors LOH was observed. In this plexiform neurofibroma of a NF1 patient with a constitutional one base-pair insertion in NF1 exon 4b, a non-random X-inactivation pattern was found, strongly suggesting a clonal origin of the tumor cells. The analysis of X-inactivation patterns allowed the classification of some of the other neurofibromas with regard to the detectability of clonal LOH. In 3 of 6 neurofibromas without LOH amenable to this analysis, a comparable X-inactivation pattern was found in constitutional and neurofibroma derived DNA. A clonal LOH would not have been detected in these tumors. However, we observed a nonrandom pattern in 3 of the 6 neurofibromas, suggesting a clonal origin of the tumor cells. LOH was not detected in these tumors, but could, however, have occurred by mutational events below the level of large somatic deletions, loss of a whole chromosome 17 or somatic recombination.
在26例神经纤维瘤病1型(NF1)患者的38个神经纤维瘤中研究了NF1基因座的杂合性缺失(LOH)。这些肿瘤中仅在1例观察到LOH。在1例NF1患者的丛状神经纤维瘤中,其NF1基因第4b外显子存在一个构成性的单碱基对插入,发现了一种非随机的X染色体失活模式,强烈提示肿瘤细胞的克隆起源。通过分析X染色体失活模式,可根据克隆性LOH的可检测性对其他一些神经纤维瘤进行分类。在6例可进行此分析且无LOH的神经纤维瘤中,有3例在构成性DNA和神经纤维瘤衍生的DNA中发现了类似的X染色体失活模式。在这些肿瘤中无法检测到克隆性LOH。然而,我们在6例神经纤维瘤中的3例中观察到了非随机模式,提示肿瘤细胞的克隆起源。在这些肿瘤中未检测到LOH,但它可能是由低于大片段体细胞缺失、整条17号染色体丢失或体细胞重组水平的突变事件引起的。