Cobaleda C, Pérez-Losada J, Sánchez-García I
Departamento de Diferenciación y Proliferación Celular, CSIC/Universidad de Salamanca, Spain.
Bioessays. 1998 Nov;20(11):922-30. doi: 10.1002/(SICI)1521-1878(199811)20:11<922::AID-BIES7>3.0.CO;2-O.
This article highlights the recent advances in our understanding of the molecular structure and function of proteins that are activated or created by chromosomal abnormalities and discusses their possible role in tumor development. The molecular characterization of these proteins has revealed that tumor-specific fusion proteins are the consequence of the majority of chromosomal translocations associated with leukemias and solid tumors. A common theme that emerges is that creation of these proteins disrupts the normal development of tumor-specific target cells by blocking apoptosis. These insights identify these chromosomal translocation-associated genes as potential targets for improved cancer therapies.
本文重点介绍了我们在理解由染色体异常激活或产生的蛋白质的分子结构和功能方面的最新进展，并讨论了它们在肿瘤发展中可能发挥的作用。对这些蛋白质的分子特征分析表明，肿瘤特异性融合蛋白是大多数与白血病和实体瘤相关的染色体易位的结果。一个共同的主题是，这些蛋白质的产生通过阻断细胞凋亡破坏了肿瘤特异性靶细胞的正常发育。这些见解将这些与染色体易位相关的基因确定为改进癌症治疗的潜在靶点。
