Qin Lun-Xiu
Liver Cancer Institute Zhongshan Hospital, Fudan University, Shanghai, China.
World J Gastroenterol. 2002 Oct;8(5):769-76. doi: 10.3748/wjg.v8.i5.769.
The central role of sequential accumulation of genetic alterations during the development of cancer has been firmly established since the pioneering cytogenetic studies successfully defined recurrent chromosome changes in specific types of tumor. In the course of carcinogenesis, cells experience several genetic alterations that are associated with the transition from a preneoplastic lesion to an invasive tumor and finally to the metastatic state. Tumor progression is characterized by stepwise accumulation of genetic alterations. So does the dominant metastatic clone. Modern molecular genetic analyses have clarified that genomic changes accumulate during the development and progression of cancers. In comparison with the corresponding primary tumor, additional events of chromosomal aberrations (including gains or allelic losses) are frequently found in metastases, and the incidence of combined chromosomal alterations in the primary tumor, plus the occurrence of additional aberrations in the distant metastases, correlated significantly with decreased postmetastatic survival. The deletions at 3p, 4p, 6q, 8p, 10q, 11p, 11q, 12p, 13q, 16q, 17p, 18q, 21q, and 22q, as well as the over-representations at 1q, 8q, 9q, 14q and 15q, have been found to associate preferentially with the metastatic phenotype of human cancers. Among of them, the deletions on chromosomes 8p, 17p, 11p and 13p seem to be more significant, and more detail fine regions of them, including 8p11, 8p21-12, 8p22, 8p23, 17p13.3, 11p15.5, and 13q12-13 have been suggested harboring metastasis-suppressor genes. During the past decade, several human chromosomes have been functionally tested through the use of microcell-mediated chromosome transfer (MMCT), and metastasis-suppressor activities have been reported on chromosomes 1, 6, 7, 8, 10, 11, 12, 16, and 17. However, it is not actually known at what stage of the metastatic cascade these alterations have occurred. There is still controversial with the association between the chromosomal aberrations and the metastatic phenotype of cancer. As the progression of human genome project and the establishment of more and more new techniques, it is hopeful to make clear the genetic mechanisms involved in the tumor metastasis in a not very long future, and provide new clues to predicting and controlling the metastasis.
自开创性的细胞遗传学研究成功确定特定类型肿瘤中反复出现的染色体变化以来,基因改变的顺序积累在癌症发展过程中的核心作用已得到确凿证实。在致癌过程中,细胞经历多种基因改变,这些改变与从癌前病变向侵袭性肿瘤的转变以及最终向转移状态的转变相关。肿瘤进展的特征是基因改变的逐步积累。优势转移克隆也是如此。现代分子遗传学分析已阐明,基因组变化在癌症的发生和发展过程中不断积累。与相应的原发性肿瘤相比,转移灶中经常发现额外的染色体畸变事件(包括增加或等位基因缺失),原发性肿瘤中染色体联合改变的发生率以及远处转移灶中额外畸变的发生与转移后生存率降低显著相关。已发现3p、4p、6q、8p、10q、11p、11q、12p、13q、16q、17p、18q、21q和22q的缺失,以及1q、8q、9q、14q和15q的过度表达与人类癌症的转移表型优先相关。其中,8p、17p、11p和13p染色体上的缺失似乎更为显著,并且有人提出它们的更精细区域,包括8p11、8p21 - 12、8p22、8p23、17p13.3、11p15.5和13q12 - 13含有转移抑制基因。在过去十年中,通过微细胞介导的染色体转移(MMCT)对几条人类染色体进行了功能测试,并报道了1、6、7、8、10、11、12、16和17号染色体具有转移抑制活性。然而,实际上尚不清楚这些改变发生在转移级联的哪个阶段。染色体畸变与癌症转移表型之间的关联仍存在争议。随着人类基因组计划的推进以及越来越多新技术的建立,有望在不久的将来阐明肿瘤转移所涉及的遗传机制,并为预测和控制转移提供新线索。