Xiao H, Baer M R, Block A W, Sait S N, Kakati S
Clinical Cytogenetics Laboratory, Roswell Park Cancer Institute, Buffalo, N.Y 14263.
Cancer Genet Cytogenet. 1993 Jun;67(2):141-4. doi: 10.1016/0165-4608(93)90168-l.
We describe a patient with acute myeloid leukemia (AML) who had a deletion of chromosome 22 at q11 as a sole chromosomal abnormality, resulting in the karyotype 46,XY,del(22)(q11). Southern blot analysis showed no bcr rearrangement and fluorescence in situ hybridization indicated no juxtaposition of c-abl. This study indicates that molecular events other than bcr rearrangement and c-abl juxtaposition were involved in leukemogenesis in this patient. We hypothesize that a tumor suppressor candidate gene may be located on the long arm of chromosome 22; its loss may lead to malignant transformation.
我们描述了一名急性髓系白血病（AML）患者，其22号染色体q11处缺失是唯一的染色体异常，导致核型为46,XY,del(22)(q11)。Southern印迹分析显示无bcr重排，荧光原位杂交表明无c-abl并列。本研究表明，该患者白血病发生涉及bcr重排和c-abl并列以外的分子事件。我们推测，一个肿瘤抑制候选基因可能位于22号染色体长臂上；其缺失可能导致恶性转化。
