Transforming genes in human leukemia cells.
Transforming genes in human leukemia cells.
复制标题
转化人类白血病细胞中的基因。
作者：
H. Hirai;S. Tanaka;M. Azuma;Y. Anraku;Y. Kobayashi;M. Fujisawa;T. Okabe;A. Urabe;F. Takaku
采用NIH/3T3细胞，采用dna介导的基因转移技术，检测32例新鲜白血病患者骨髓细胞的高分子量dna是否存在可传播的活化转化基因。32例患者中4例的骨髓细胞dna诱导NIH/3T3细胞转化。四个病例中的两个，慢性骨髓性白血病和急性淋巴细胞白血病，含有活化的N-ras癌基因。分子克隆和核苷酸序列分析表明，在这两种情况下，导致转化活性的病变都定位于预测蛋白密码子12中从鸟嘌呤到胸腺嘧啶的单核苷酸转变。这些观察结果表明，N-ras癌基因的激活与细胞分化的特定阶段或白血病表型无关。另外两个与急性骨髓性白血病和急性淋巴细胞性白血病相关的转化基因既不与ras基因家族成员同源，也不与人类blim -1基因同源。因此，NIH/3T3转染法在人类白血病中经常检测到活化的N-ras癌基因，而其他与ras基因家族不同的转化基因可以通过转染法在某些白血病中检测到。
High-molecular weight DNAs of fresh bone marrow cells from 32 patients with fresh leukemia were assayed for the presence of transmissible activated transforming genes by a DNA-mediated gene transfer technique using NIH/3T3 cells. DNAs of bone marrow cells from four of the 32 patients induced transformation of NIH/3T3 cells. Two of the four cases, a chronic myelogenous leukemia and an acute lymphocytic leukemia, contained activated N-ras oncogenes. Molecular cloning and nucleotide sequence analysis revealed that the lesion responsible for the transforming activity was localized to a single nucleotide transition from guanine to thymine in codon 12 of the predicted protein in each of the two cases. These observations indicate that activation of N-ras oncogenes is independent of the specific stage of cell differentiation or the leukemia phenotype. The other two transforming genes associated with an acute myelogenous leukemia and an acute lymphocytic leukemia showed homology neither with members of the ras gene family nor with the human Blym-1 gene. Thus, the NIH/3T3 transfection assay frequently detects activated N-ras oncogenes in human leukemias, while other transforming genes, distinct from the ras gene family, can be detected in some leukemias by the transfection assay.
DOI：
10.1073/pnas.80.2.383
发表时间：
1983-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
SHIMIZU, K;GOLDFARB, M;WIGLER, M
通讯作者：
WIGLER, M