Morris C M, Fitzgerald P H, Kennedy M A, Hollings P E, Garry M, Corbett G M
Cytogenetic and Molecular Oncology Unit, Christchurch Hospital, New Zealand.
Br J Haematol. 1989 Apr;71(4):481-6. doi: 10.1111/j.1365-2141.1989.tb06306.x.
A patient whose leukaemic cells carried the rare t(7;11)(p15;p15) was diagnosed as having acute myelomonocytic leukaemia (AML-M4), and supports the association of this specific translocation with forms of acute myeloid leukaemia showing differentiation. Blast phase chronic myeloid leukaemia was excluded by lack of involvement of the ABL and BCR genes. Chromosome in situ hybridization studies showed that both the HRAS1 and INS genes were present on the terminal part of chromosome 11p which was translocated to chromosome 7p. Neither HRAS1 nor INS were structurally rearranged. Field inversion gel electrophoresis showed that a 400 kb fragment encompassing HRAS1 was structurally entire in leukaemic DNA. Because the INS gene, which was also translocated, is probably located proximal to HRAS1 on chromosome 11p, it is unlikely that HRAS1 was near the chromosome 11 breakpoint or involved in this leukaemia.
一名白血病细胞携带罕见的t(7;11)(p15;p15)的患者被诊断为急性粒单核细胞白血病（AML-M4），这支持了这种特定易位与表现出分化的急性髓系白血病形式之间的关联。由于ABL和BCR基因未受累，排除了急变期慢性髓系白血病。染色体原位杂交研究表明，HRAS1和INS基因都位于11号染色体p末端，该末端易位至7号染色体p。HRAS1和INS在结构上均未重排。脉冲场凝胶电泳显示，白血病DNA中包含HRAS1的400 kb片段在结构上是完整的。由于同样发生易位的INS基因可能位于11号染色体p上HRAS1的近端，因此HRAS1不太可能靠近11号染色体断点或参与该白血病。
