Jin X M, Miao J, Xu Y, Deng G R
Beijing Cancer Institute, Beijing.
Zhonghua Zhong Liu Za Zhi. 1988 May;10(3):167-70.
DNA of peripheral blood or bone marrow leukocytes from 8 normal subjects, 7 cases of acute lymphocytic leukemia (ALL), 2 of acute myelogenous leukemia (AML) and 1 of chronic myelogenous leukemia (CML), having been digested by endonuclease Eco RI or Pst I separately, was hybridized with the probes of 3' fragment (Pst I/Hind III) or 5' fragment (Hinc II/Pst I) of Abelson murine leukemia virus (A-MuLV) oncogene v-abl. The proto-oncogene c-abl, which is homologous to v-abl, was found amplified in 4 ALL, 1 CML and 1 AML. In one of these 4 ALL, c-abl was amplified even over 100 times. A new c-abl BamH I fragment with 6.7 kilobase pairs (kb) in length was observed in 2 ALL and 1 CML out of these 6 cases with amplification, but none of this fragment was found in the normal subjects or other leukemia patients. These 3 patients with the presence of 6.7 kb fragment were high risk ones and 2 of them had died, suggesting that 6.7 kb fragment be the index of poor prognosis. The amplification and rearrangement of c-abl imply the activation of proto-oncogene in leukemogenesis.
分别用内切酶Eco RI或Pst I消化8名正常受试者、7例急性淋巴细胞白血病（ALL）、2例急性髓细胞白血病（AML）和1例慢性髓细胞白血病（CML）的外周血或骨髓白细胞的DNA，然后与Abelson鼠白血病病毒（A-MuLV）癌基因v-abl的3'片段（Pst I/Hind III）或5'片段（Hinc II/Pst I）探针杂交。发现与v-abl同源的原癌基因c-abl在4例ALL、1例CML和1例AML中发生扩增。在这4例ALL中的1例中，c-abl扩增甚至超过100倍。在这6例发生扩增的病例中的2例ALL和1例CML中观察到一个新的长度为6.7千碱基对（kb）的c-abl BamH I片段，但在正常受试者或其他白血病患者中均未发现该片段。这3例存在6.7 kb片段的患者为高危患者，其中2例已死亡，提示6.7 kb片段是预后不良的指标。c-abl的扩增和重排意味着原癌基因在白血病发生过程中被激活。
