Nakashima T, Masuda A, Sekiguchi T, Nishimoto T, Uemura T
Department of Otorhinolaryngology, Faculty of Medicine, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812, Japan.
Eur Arch Otorhinolaryngol. 1994;251 Suppl 1:S87-90. doi: 10.1007/BF02565228.
The genesis and progression of malignant tumors may be related to certain somatic mutations and the accumulation of multiple chromosomal alterations. Using four freshly resected malignant tumors, we investigated the relationship between chromosomal alteration and expression of cell cycle regulatory genes. Specimens of thyroid hyperplasia and normal thyroid tissue were also investigated. As cell cycle regulating genes, we chose the cdc2 gene that encodes the p34cdc2 protein kinase, a major kinase of the cell cycle, and the RCC1 gene that is essential for coupling between S and M phases. Three of the malignant tumors contained cells with chromosomal alterations, including one polyploid and two aneuploid. The DNA content of cells in thyroid hyperplasia was the same as in the normal gland. The amount of p34cdc2 protein was very low in cells of both normal thyroid and hyperplastic tissue, and grew very slowly as compared with malignant tumors. There was no significant relationship between the amount of RCC1 and ploidy pattern.
恶性肿瘤的发生和进展可能与某些体细胞突变以及多种染色体改变的积累有关。我们使用四个新切除的恶性肿瘤，研究了染色体改变与细胞周期调节基因表达之间的关系。还研究了甲状腺增生和正常甲状腺组织的标本。作为细胞周期调节基因，我们选择了编码p34cdc2蛋白激酶（细胞周期的主要激酶）的cdc2基因，以及对S期和M期之间的偶联至关重要的RCC1基因。三个恶性肿瘤含有染色体改变的细胞，包括一个多倍体细胞和两个非整倍体细胞。甲状腺增生细胞的DNA含量与正常腺体相同。正常甲状腺和增生组织细胞中的p34cdc2蛋白量非常低，与恶性肿瘤相比生长非常缓慢。RCC1的量与倍性模式之间没有显著关系。
