Soenen V, Preudhomme C, Roumier C, Laï J L, Lepelley P, Facon T, Pagniez D, Fenaux P
Laboratoire d'Hématologie, CHU Lille, France.
Leukemia. 1998 Feb;12(2):238-41. doi: 10.1038/sj.leu.2400909.
We report a case of myelodysplastic syndrome (MDS) occurring during the course of multiple myeloma (MM) treated by alkylating agents. Karyotype showed unbalanced t(5;17), resulting in 17p deletion. Dysgranulopoïesis typical of the '17p-syndrome' and p53 mutation and overexpression were present. A combination of FISH and immunophenotype analysis (FICTION, analysis) showed that 17p deletion was restricted to myeloid cells, and that p53 overexpression was also restricted to myeloid cells. These findings strongly argue against a common clonal origin of MM and MDS, and support the hypothesis that MM and MDS were clonally unrelated, and that MDS was indeed secondary to treatment with alkylating agents.
我们报告了1例在接受烷化剂治疗的多发性骨髓瘤（MM）病程中发生的骨髓增生异常综合征（MDS）。核型显示不平衡的t(5;17)，导致17p缺失。存在典型的“17p综合征”的异常粒细胞生成以及p53突变和过表达。荧光原位杂交（FISH）和免疫表型分析（FICTION分析）相结合显示，17p缺失仅限于髓系细胞，p53过表达也仅限于髓系细胞。这些发现有力地反驳了MM和MDS有共同克隆起源的观点，并支持MM和MDS克隆无关以及MDS确实继发于烷化剂治疗的假说。
