Stenman G, Mark J, Ekedhal C
Tumour Biol. 1984;5(2):103-17.
By banding methods the chromosomes were studied in 20 cultured benign mixed salivary gland tumors. The results were considered together with the findings in 61 previously studied adenomas. About 55% of the 81 adenomas had a normal stemline. A total of 39 abnormal stemlines were found in the remaining 36 cases. The abnormal stemlines could be divided into four groups: 1) A large group with chromosome 8 involvement, mostly translocations of segments distal to 8q12; 2) A small group with chromosome 12 involvement, usually translocations of segments distal to 12q13-15;3) A small group with translocations and/or deletions affecting a distal segment of either the short or the long arm of chromosome 3; 4) A heterogeneous and small group with deviations related to those seen in variant cells in cases with normal stemlines. Comparisons with the known localization of proto-oncogenes revealed that almost 60% of the abnormal stemlines showed anomalies which could fit with oncogene activation. Future mapping studies of proto-oncogenes, as well as studies of combined actions of proto-oncogenes, different viral genes and some poorly understood oncogenic factors, will no doubt, enable a more complete characterization of the roles played by oncogenes in the genesis and progression of mixed tumors.
通过显带方法对20例培养的涎腺良性混合瘤的染色体进行了研究。将结果与之前研究的61例腺瘤的结果综合考虑。81例腺瘤中约55%具有正常的干系。在其余36例中总共发现了39条异常干系。异常干系可分为四组:1)一大组涉及8号染色体,大多是8q12远端片段的易位;2)一小组涉及12号染色体,通常是12q13 - 15远端片段的易位;3)一小组有影响3号染色体短臂或长臂远端片段的易位和/或缺失;4)一小类异质性的组,其偏差与正常干系病例中变异细胞所见的偏差有关。与原癌基因已知定位的比较显示,几乎60%的异常干系显示出可能与癌基因激活相符的异常。原癌基因的未来定位研究,以及原癌基因、不同病毒基因和一些尚不清楚的致癌因素联合作用的研究,无疑将能够更全面地描述癌基因在混合瘤发生和发展中所起的作用。