Morita R, Hikiji K, Yamakawa K, Nakamura Y
Department of Genetic Research Laboratory, SRL Inc.
Nihon Rinsho. 1992 Dec;50(12):3100-5.
Several rodent studies based on molecular biology have suggested that accumulation of genetic alterations in cancer-associated genes is required to convert a normal cell into a malignant cell. Activation of oncogenes and inactivation of tumor suppressor genes appear to be involved in carcinogenesis. In renal cell carcinomas, we have recently implied that the presence of tumor suppressor genes at chromosome 3p13-14.3 and 21.3, the regions where are also commonly deleted in adenocarcinoma of the lung; at chromosome 5q21, the region where the MCC (mutated in colorectal cancer) gene and APC (adenomatous polyposis coli) gene are located; at chromosome 6q27; and at 10q 21-23. We have also indicated that genes on 3p is probably important for development of RCCs and genes on 5q, 6q, and 10q may be associated with progression of RCCs.
几项基于分子生物学的啮齿动物研究表明，癌症相关基因中遗传改变的积累是将正常细胞转化为恶性细胞所必需的。癌基因的激活和肿瘤抑制基因的失活似乎参与了致癌过程。在肾细胞癌中，我们最近暗示在染色体3p13 - 14.3和21.3存在肿瘤抑制基因，这些区域在肺癌腺癌中也常发生缺失；在染色体5q21，即MCC（在结直肠癌中发生突变）基因和APC（腺瘤性息肉病 coli）基因所在的区域；在染色体6q27；以及在10q 21 - 23。我们还指出3p上的基因可能对肾细胞癌的发生发展很重要，而5q、6q和10q上的基因可能与肾细胞癌的进展有关。
