TEL基因在白血病的发生中起重要的作用，但TEL基因易位通过不同的分子机制引起白血病发生机制尚不完全清楚。其他TEL基因易位发生较少，如t(5;12)(q31;p13)，t(6;12;17)(p21;p13;q25)，t(7;12)(p15;p13)，t(7;12)(p12;p13)，t(7;12)(q36;p13)t(12;13)(p13;q12)易位，分别在伴有明显嗜酸性粒细胞增多的CML、儿童AML、MDS、ALL及非何杰金淋巴瘤病人中检测到。12p13的断裂点多发生在TEL基因5′端上游外显子编码的HLH结构域处。
3 问题与展望
经过数年的努力，对TEL基因在白血病发病机制中的作用做了大量的研究，为阐明白血病的发病机制打开了一扇光明之门，然而TEL基因仍给我们留下许多问题。如TEL基因的分子机制是什么？如何抑制AML1调控基因的表达？能否通过抑制激酶活性而进行白血病治疗？这些问题的解决将有助于深入了解TEL相关白血病的发病机制，并为临床的治疗提供新的思路。
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