Castresana J S, Barrios C, Gómez L, Kreicbergs A
Department of Tumor Pathology, Karolinska Hospital, Stockholm, Sweden.
Diagn Mol Pathol. 1992 Dec;1(4):235-8.
The genomic organization of four oncogenes, i.e., c-myc, c-myb, c-Ha-ras, and c-fms, was investigated in fresh surgical specimens from 10 patients with cartilaginous tumors. Among nine chondrosarcomas, six were primary lesions and three local recurrences. The remaining case was a chondroblastoma. Amplification of the c-myc proto-oncogene was the sole abnormality detected in this series, occurring in two chondrosarcomas (four- and eight-fold). No other genetic alteration such as oncogene rearrangement was found. Nor was there any amplification of the other oncogenes studied. Both c-myc-amplified tumors were primary lesions and histologically classified as grade II; according to flow DNA cytometry, one was diploid and the other aneuploid. In our limited series, there was no overall relationship between c-myc amplification, on the one hand, and histologic subtype, malignancy grade, surgical stage, or ploidy level, on the other. Our study shows that amplification of the c-myc oncogene, presumed to be involved in the development of malignancy, is encountered in occasional human chondrosarcomas, however, without any relationship to other well-known features of this tumor entity. The clinical significance of this gene amplification remains to be established.
在10例软骨肿瘤患者的新鲜手术标本中，研究了4种癌基因，即c-myc、c-myb、c-Ha-ras和c-fms的基因组结构。9例软骨肉瘤中，6例为原发性病变，3例为局部复发。其余1例为软骨母细胞瘤。c-myc原癌基因的扩增是该系列中检测到的唯一异常，发生在2例软骨肉瘤中（分别为4倍和8倍扩增）。未发现其他基因改变，如癌基因重排。所研究的其他癌基因也未出现扩增。两个c-myc扩增的肿瘤均为原发性病变，组织学分级为II级；根据流式细胞仪DNA分析，一个为二倍体，另一个为非整倍体。在我们有限的病例系列中，一方面，c-myc扩增与另一方面的组织学亚型、恶性程度、手术分期或倍体水平之间没有总体相关性。我们的研究表明，推测与恶性肿瘤发生有关的c-myc癌基因扩增在偶发的人类软骨肉瘤中出现，然而，与该肿瘤实体的其他已知特征没有任何关系。这种基因扩增的临床意义尚待确定。
