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首页> 外文期刊>Cell cycle >New tricks from an old oncogene: gene fusion and copy number alterations of MYB in human cancer.
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New tricks from an old oncogene: gene fusion and copy number alterations of MYB in human cancer.

机译：旧癌基因的新技巧：人类癌症中MYB的基因融合和拷贝数改变。

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摘要

MYB is a leucine zipper transcription factor that is essential for hematopoesis and for renewal of colonic crypts. There is also ample evidence showing that MYB is leukemogenic in several animal species. However, it was not until recently that clear evidence was presented showing that MYB actually is an oncogene rearranged in human cancer. In a recent study, a novel mechanism of activation of MYB involving gene fusion was identified in carcinomas of the breast and head and neck. A t(6;9) translocation was shown to generate fusions between MYB and the transcription factor gene NFIB. The fusions consistently result in loss of the 3'-end of MYB, including several highly conserved target sites for microRNAs that negatively regulate MYB expression. Deletion of these target sites may disrupt the repression of MYB, leading to overexpression of MYB-NFIB transcripts and protein and to transcriptional activation of critical MYB target genes associated with apoptosis, cell cycle control, cell growth/angiogenesis and cell adhesion. This study, together with previous and recent data showing rearrangements and copy number alterations of the MYB locus in T-cell leukemia and certain solid tumors, will be the main focus of this review.
机译：MYB是亮氨酸拉链的转录因子，对于造血和结肠隐窝的更新至关重要。也有大量证据表明，MYB在几种动物中具有致白血病作用。但是，直到最近，才提出了明确的证据，证明MYB实际上是在人类癌症中重排的致癌基因。在最近的一项研究中，在乳腺癌和头颈部癌中发现了一种涉及基因融合的MYB激活新机制。显示了t（6; 9）易位，可在MYB和转录因子基因NFIB之间产生融合。融合始终导致MYB 3'末端丢失，包括负调控MYB表达的microRNA的几个高度保守的靶位点。这些靶位点的缺失可能破坏MYB的阻遏，导致MYB-NFIB转录物和蛋白质的过表达以及与细胞凋亡，细胞周期控制，细胞生长/血管生成和细胞粘附相关的关键MYB靶基因的转录激活。这项研究以及以前和最近的数据显示了T细胞白血病和某些实体瘤中MYB基因座的重排和拷贝数变化，将是本综述的主要重点。

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