Sheer D, Hiorns L R, Stanley K F, Goodfellow P N, Swallow D M, Povey S, Heisterkamp N, Groffen J, Stephenson J R, Solomon E
Proc Natl Acad Sci U S A. 1983 Aug;80(16):5007-11. doi: 10.1073/pnas.80.16.5007.
Somatic cell hybrids have been constructed between a thymidine kinase-deficient mouse cell line and blood leukocytes from a patient with acute promyelocytic leukemia showing the 15q+;17q- chromosome translocation frequently associated with this disease. One hybrid contains the 15q+ translocation chromosome and very little other human material. We have shown that the c-fes oncogene, which has been mapped to chromosome 15, is not present in this hybrid and, therefore, probably is translocated to the 17q- chromosome. Analysis of the genetic markers present in this hybrid has enabled a more precise localization of the translocation breakpoints on chromosomes 15 and 17. Our experiments also have enabled an ordering and more precise mapping of several genetic markers on chromosomes 15 and 17.
已经在一个缺乏胸苷激酶的小鼠细胞系与一名急性早幼粒细胞白血病患者的血液白细胞之间构建了体细胞杂种,该患者表现出15q+;17q-染色体易位,这种易位常与该疾病相关。一个杂种含有15q+易位染色体且几乎没有其他人类物质。我们已经表明,已定位于15号染色体的c-fes癌基因在这个杂种中不存在,因此,它可能已易位到17q-染色体上。对这个杂种中存在的遗传标记的分析使得能够更精确地定位15号和17号染色体上的易位断点。我们的实验还使得能够对15号和17号染色体上的几个遗传标记进行排序和更精确的定位。