Ohyashiki K, Ohyashiki J H, Kinniburgh A J, Toyama K, Ito H, Minowada J, Sandberg A A
Department of Internal Medicine, Tokyo Medical College, Japan.
Cancer Genet Cytogenet. 1988 Jul 1;33(1):83-92. doi: 10.1016/0165-4608(88)90053-2.
Molecular and cytogenetic analyses were performed on human T-cell leukemia cell lines (PEER and MOLT-4) with the 6q- anomaly. The PEER cells contained an interstitial deletion of the long arm of chromosome 6, that is, del(6)(q13q21), as well as other changes. The MOLT-4 cells showed a terminal deletion of the long arm of chromosome 6, that is, del(6)(q24). The 700-bp BamHI/XbaI-digested c-myb probe hybridized to a 4.3-kb fragment in EcoRI digested DNAs from these two cell lines, showing no deletion, rearrangement, or amplification. On the other hand, ML cells [ML-1, -2 and -3; human myeloid/T-cell biphenotypic leukemia cell lines with del(6)(q24)] showed an amplification of the c-myb gene and had a high level of the c-myb-related mRNA at 3.5 kb. Though no amplification of the c-myb at the DNA level was noted in the PEER or MOLT-4 cell lines, apparent high expression of the c-myb was detected in these human T-cell neoplastic lines. These results indicate that high c-myb expression is related to lineage of hematopoietic neoplasia rather than to the 6q- change.
对具有6号染色体长臂异常(6q-)的人T细胞白血病细胞系(PEER和MOLT-4)进行了分子和细胞遗传学分析。PEER细胞含有6号染色体长臂的中间缺失,即del(6)(q13q21),以及其他变化。MOLT-4细胞显示6号染色体长臂的末端缺失,即del(6)(q24)。用700bp的BamHI/XbaI消化的c-myb探针与来自这两种细胞系的EcoRI消化的DNA中的一个4.3kb片段杂交,未显示缺失、重排或扩增。另一方面,ML细胞[ML-1、-2和-3;具有del(6)(q24)的人髓系/T细胞双表型白血病细胞系]显示c-myb基因扩增,并且在3.5kb处有高水平的c-myb相关mRNA。虽然在PEER或MOLT-4细胞系中未观察到DNA水平上c-myb的扩增,但在这些人T细胞肿瘤细胞系中检测到明显的c-myb高表达。这些结果表明,c-myb高表达与造血肿瘤的谱系有关,而不是与6q-变化有关。