Romana S P, Mauchauffé M, Le Coniat M, Chumakov I, Le Paslier D, Berger R, Bernard O A
U 301 de l'Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
Blood. 1995 Jun 15;85(12):3662-70.
Analysis of a growing number of chromosomal translocations in human tumors have shown that they frequently result in gene fusions encoding chimeric proteins. We have characterized the recurrent t(12;21)(p12;q22) translocation present in human B-lineage acute leukemias. This translocation fused two genes, tel and AML1, that have previously been described in chromosomal translocations specific for myeloid malignancies. These two genes therefore belong to an increasing number of human genes that are involved in a variety of hematopoietic malignant disorders and can be rearranged with numerous partners. Interestingly, in these acute leukemias, deletion of the other tel allele from the normal chromosome 12 was associated with the tel rearrangement, whereas both tel alleles were present in the chronic leukemias bearing a t(5;12) that we have tested.
对人类肿瘤中越来越多的染色体易位分析表明,它们常常导致编码嵌合蛋白的基因融合。我们已经对人类B系急性白血病中存在的常见t(12;21)(p12;q22)易位进行了特征描述。这种易位融合了两个基因,即tel和AML1,这两个基因先前已在髓系恶性肿瘤特有的染色体易位中被描述过。因此,这两个基因属于越来越多的人类基因,这些基因参与了多种造血系统恶性疾病,并且可以与众多伙伴发生重排。有趣的是,在这些急性白血病中,正常12号染色体上另一个tel等位基因的缺失与tel重排相关,而在我们检测过的携带t(5;12)的慢性白血病中,两个tel等位基因都存在。