Browett P J, Ganeshaguru K, Hoffbrand A V, Norton J D
Department of Haematology, Royal Free Hospital School of Medicine, London, U.K.
Leuk Res. 1988;12(1):25-31. doi: 10.1016/s0145-2126(98)80005-2.
By using a combination oligonucleotide probe hybridization and restriction enzyme polymorphism analysis, a series of 48 cases of B-cell chronic lymphocytic leukemia were investigated for activating point mutations at codons 12, 13 and 61 of the K-ras proto-oncogene. A small series of acute leukemias (seven with acute lymphoblastic leukemia (ALL), 11 with acute myeloid leukemia (AML)) were examined in parallel. None of the cases of B-CLL contained detectable activating mutations of the K-ras gene at codon 12 (GGT-gly----GCT-ala) was detected at presentation. In both cases of acute leukemia, the mutation was restricted to one allele and could not be detected in remission samples. Those data suggest that activation of members of the ras oncogene family, typified by K-ras, may be less important in disease pathogenesis in leukemias such as B-CLL that arise from a more committed progenitor.
通过联合使用寡核苷酸探针杂交和限制性内切酶多态性分析，对48例B细胞慢性淋巴细胞白血病患者进行了研究，以检测K-ras原癌基因第12、13和61密码子处的激活点突变。同时对一小系列急性白血病患者（7例急性淋巴细胞白血病（ALL）、11例急性髓细胞白血病（AML））进行了检测。在初诊时，未在任何B-CLL病例中检测到K-ras基因第12密码子（GGT-甘氨酸----GCT-丙氨酸）的可检测激活突变。在两例急性白血病病例中，该突变仅限于一个等位基因，且在缓解期样本中未检测到。这些数据表明，以K-ras为代表的ras癌基因家族成员的激活，在诸如B-CLL等源自更定向祖细胞的白血病的疾病发病机制中可能不那么重要。
