Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.
Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.
复制标题
DOI：
10.1155/2015/183590
复制
发表时间：
2015
影响因子：
--
通讯作者：
Nicot C
中科院分区：
文献类型：
--
作者：
Nicot C
肿瘤抑制功能对于控制细胞增殖、激活细胞凋亡或衰老途径以消除不需要的细胞、将 DNA 损伤信号与细胞周期停滞检查点联系起来、激活适当的 DNA 修复途径以及防止粘附丧失以抑制转移的发生至关重要。因此，抑癌基因对于维持遗传和基因组完整性是不可或缺的。因此，体细胞突变或表观遗传机制导致的肿瘤抑制因子失活常常与肿瘤的发生和发展相关。相反，肿瘤抑制功能的重新激活可以有效逆转转化的表型并导致细胞周期停滞或癌细胞死亡，并可用作治疗策略。成人 T 细胞白血病/淋巴瘤 (ATLL) 是一种侵袭性淋巴组织增生性疾病，与人类 T 细胞白血病病毒 1 型 (HTLV-I) 感染 CD4 T 细胞相关。 HTLV-I相关的T细胞转化是多步骤致癌过程的结果，其中病毒最初诱导慢性T细胞增殖并改变细胞途径，导致遗传缺陷的积累和病毒感染细胞的生长失调。本综述将重点关注 HTLV-I 发病机制中调节肿瘤抑制因子失活的遗传和表观遗传机制的当前知识。
Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to inhibit initiation of metastases. Therefore, tumor suppressor genes are indispensable to maintaining genetic and genomic integrity. Consequently, inactivation of tumor suppressors by somatic mutations or epigenetic mechanisms is frequently associated with tumor initiation and development. In contrast, reactivation of tumor suppressor functions can effectively reverse the transformed phenotype and lead to cell cycle arrest or death of cancerous cells and be used as a therapeutic strategy. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease associated with infection of CD4 T cells by the Human T-cell Leukemia Virus Type 1 (HTLV-I). HTLV-I-associated T-cell transformation is the result of a multistep oncogenic process in which the virus initially induces chronic T-cell proliferation and alters cellular pathways resulting in the accumulation of genetic defects and the deregulated growth of virally infected cells. This review will focus on the current knowledge of the genetic and epigenetic mechanisms regulating the inactivation of tumor suppressors in the pathogenesis of HTLV-I.
登录
查看更多内容
影响因子：
5.4
作者：
Dewan, M. Zahidunnabi;Takamatsu, Naofumi;Morishita, Kazuhiro
通讯作者：
Morishita, Kazuhiro
影响因子：
2.7
作者：
Cheng, JH;Zhang, DS;Marasco, WA
通讯作者：
Marasco, WA
影响因子：
37.3
作者：
Chaib-Mezrag, Hassiba;Lemacon, Delphine;Nicot, Christophe
通讯作者：
Nicot, Christophe
影响因子：
11.2
作者：
Caldwell, GM;Jones, C;Morton, DG
通讯作者：
Morton, DG
影响因子：
20.3
作者：
Bellon, Marcia;Lepelletier, Yves;Nicot, Christophe
通讯作者：
Nicot, Christophe